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3,200 |
6171208-1
| 30,402,317 |
comm/PMC006xxxxxx/PMC6171208.xml
|
Endoprosthetic Reconstruction for a Displaced Atypical Femoral Fracture in a Cancer Patient with Poor Prognosis
|
A 48-year-old woman with breast cancer underwent mastectomy (histology: invasive ductal carcinoma, histology grade 2; estrogen receptor: positive; progesterone receptor: positive; HER2: positive; Ki67: 10%, n+[27/28]) at the department of surgery in a previous hospital. Subsequently, she underwent chemotherapy with paclitaxel and doxifluridine and hormonal therapy with tamoxifen. Six years after surgery, bone metastasis was noted in the vertebra, and she was treated with a combination of radiotherapy and chemotherapy with trastuzumab. However, the metastatic disease progressed. Liver metastasis was also noted at 57 years of age, and the treatment was switched to capecitabine plus lapatinib, which was shortly discontinued because of adverse effects. Disease progression continued, although fulvestrant was also added. Eventually, she underwent chemotherapy with trastuzumab emtansine (T-DM1).\nFor the inhibition of bone metastasis, zoledronate was initiated at 54 years of age and was continued for 5 years until renal failure. After discontinuation of zoledronate, denosumab was used for 3 years until the detection of AFFs in both proximal femurs on the bone scintigraphy at 62 years of age (). Eventually, BMAs had been administered for 8 years. Right hip pain occurred temporarily, whereas left hip pain persisted for a long time. She experienced a left displaced femoral subtrochanteric fracture after falling at the age of 63 years (). At that point, the doctors in the previous hospital made a diagnosis of a pathological fracture caused by bone metastasis and consulted with our department for specialized treatment. After the patient was transferred to our hospital, we examined whether that fracture was due to bone metastasis, but no metastatic lesion was noted at the fracture site. In addition, radiography of the fracture area exhibited a beak on the lateral side of the fracture site associated with cortical bone sclerosis, which was characteristic of an AFF () []. Considering the long-term administration of BMAs, the fractures were diagnosed as AFFs.\nFor treating the displaced AFF, we could select either IMN or prosthetic reconstruction. For appropriate selection, evaluation of the patient's prognosis is required because recovery of ADL/QOL is the priority in cancer patients with limited life expectancy. The Katagiri score as a predictor of prognosis in patients with skeletal metastasis was high () [], and similarly, the score of another scoring system for metastatic breast cancer was also high () []. Thus, both predicted a poor prognosis. IMN is a less invasive approach, and it might successfully induce bone healing. However, delayed union/nonunion and implant failure are possible issues. To achieve early weight bearing and avoid these issues, we performed endoprosthetic reconstruction (Zimmer Biomet, OSS Proximal Femur) on the seventh day after the injury (). Two weeks after surgery, she achieved walker-assisted gait. After subsequent rehabilitation, prophylactic IMN was performed for the right incomplete AFF (). Six months after surgery, the Musculoskeletal Tumor Society (MSTS) score recovered (47%) to almost the preoperative level (50%) before the injury (). However, she died of breast cancer 1 year and 2 months after the endoprosthetic reconstruction.
|
[[48.0, 'year']]
|
F
|
{'8965890': 1, '25044999': 1, '24932278': 1, '26980645': 1, '25998535': 1, '23712442': 1, '26195566': 1, '23523494': 1, '22643705': 1, '15855375': 1, '27818818': 2, '23365544': 1, '27627968': 1, '24368402': 1, '28009615': 1, '21610533': 1, '27708978': 1, '30402317': 2}
|
{'5080486-1': 1}
|
3,201 |
6171214-1
| 30,327,743 |
comm/PMC006xxxxxx/PMC6171214.xml
|
Surgical Treatment of Idiopathic Enlargement of the Right Atrium
|
A 23-year-old man (weight 65 kg, height 175 cm, and BSA 1.8 m2) with a diagnosis of primitive right atrial enlargement from foetal age was referred to our Centre for cardiological evaluation. Cardiac examination showed increased heart size on percussion and a grade II/VI Levine systolic murmur. No significant pathological findings were found on pulmonary examination. Electrocardiography showed a regular sinus rhythm with a rate of approximately 60 beats/min associated with an abnormal morphology and duration of P wave (enlargement of P wave with duration of 130 msec), together with a low amplitude of QRS complexes in the limb leads. All routine laboratory studies were within normal limits. Chest radiography showed an abnormal cardiac silhouette with increased convexity in the lower half of the right cardiac border and cardiomegaly ().\nTransthoracic two-dimensional echocardiography demonstrated a huge right atrium of about 6.2 cm and a volume of 230 ml/m2, with a thick smoke pattern and mild tricuspid regurgitation. The pulmonary arterial pressure was normal (). The tricuspid valve was normal without significant annular dilation. No stenosis or abnormal displacement of the tricuspid valve leaflets was detected. No significant regurgitation of the tricuspid valve was found despite a partial distortion of the anterior leaflet and compression of the right ventricle inflow. The right ventricle appeared small and compressed anteriorly by the right atrium (area of RV: 11 cm2).\nCardiac magnetic resonance imaging showed a marked right atriomegaly (right atrium area: 66.50 cm2, volume: 220 ml/m2) and normal size of the left atrium (left atrium area: 7.02 cm2). The right ventricle was regular in size and global contractility but was partially compressed and dislocated posteriorly, due to the massive enlargement of the right atrium. The left ventricle was regular in dimension, thickness of the wall, and global/segmental contractility (FE VS = 61%). No evident transvalvular jets or areas of late gadolinium enhancement were found. The pericardium was visualized without focal abnormalities or pericardial effusion ().\nDue to the high risk of arrhythmias and thrombus formation in the right atrium, which is a potential risk for pulmonary embolism, the patient underwent cardiac surgery. Through a median sternotomy, cardiopulmonary bypass was established with standard aorta and bicaval cannulation. After the pericardium was opened, the entire anterior surface of the heart was found to be covered with a thin wall in continuity with the right atrium. No atrial appendage as such was apparent. The right atrium was fully opened. The inferior border of the atriotomy was sewn around the anterior part of the tricuspid annulus, and the superior border was brought over the lateral wall of the right atrium as a flap and sewn near the interatrial groove. This provided adequate reduction of the atrial size and reinforcement of the atrial wall ().\nThe histology of the resected atrial wall showed focal hyperplasic areas of smooth muscle cells with polymorphic nuclei surrounded by a few scattered areas of hypertrophic fibrous tissue.\nPostoperative transesophageal echocardiogram showed a significant reduction of the right atrium area (23 cm2, volume: 93 ml).\nThe patient was extubated 11 hours after surgery. Complications arose postoperatively with the early appearance of pericardial effusion with leukocytosis and elevated inflammatory markers. This was resistant to conventional medical therapy, which in the end required surgical drainage. Medical therapy of the postpericardiotomy syndrome (ibuprofen 600 mg/TID and colchicine 1 mg/OD) was continued over the subsequent 6 follow-up months without further recurrence of pericardial effusion.
|
[[23.0, 'year']]
|
M
|
{'10858411': 1, '14484255': 1, '3970788': 1, '16214503': 1, '23626440': 2, '15486129': 1, '34418966': 1, '25441791': 1, '11326142': 1, '23663418': 1, '24569332': 1, '30327743': 2}
|
{'3634252-1': 1}
|
3,202 |
6171215-1
| 30,327,739 |
comm/PMC006xxxxxx/PMC6171215.xml
|
Diagnostic Quandary: Salmonella Agbeni Vertebral Osteomyelitis and Epidural Abscess
|
A 54-year-old Caucasian male with past medical history positive only for diverticulitis with a resultant sigmoidectomy presented to a pain management specialist with progressively worsening bilateral low back, buttock, and radicular leg pain, weakness, and numbness for five weeks after falling from an 8 ft. ladder onto concrete. At the time of the fall, no notable injury was sustained and the patient reported only minimal low back pain without radiculopathy. Over the next several days, the patient began to experience numbness and weakness of the bilateral lower extremities. Evaluation in the ER, which included a hip X-ray and MRI of the lumbar spine (seen in ), revealed only mild lumbar facet arthropathy and moderate left neural foraminal stenosis at L3-L4 without any concomitant hip or spine fracture.\nFollowing discharge, the patient reported worsening low back pain and bilateral lower extremity weakness in both L5 and S1 distributions. Several weeks after the initial fall, the patient was referred to pain management where he was evaluated and eventually underwent a radionuclide bone scan. This revealed mildly increased uptake at L5/S1 but was suspected to be a result of facet osteoarthritis. The patient denied any fever at this time, constitutional symptoms, or recent illness. Review of symptoms and physical exam were unremarkable aside from mild paraspinal tenderness and lumbosacral radiculopathy. The rest of the patient's neurologic exam was normal. The patient was instructed to follow up in one week's time. At the return visit, he reported continued worsening of symptoms with no relief. At this point in time, the patient mentioned that he had been experiencing shaking chills at night. Other review of symptoms and physical exam remained unchanged, and the patient was noted to be afebrile. A CT scan () and subsequent MRI of the lumbar spine () were conducted which revealed extensive findings of discitis/osteomyelitis at L5–S1 as well as an epidural abscess resulting in severe narrowing of the central spinal canal. An emergent decompression laminectomy and discectomy was performed at L5–S1 with evacuation of the epidural abscess. Intraoperative tissue and wound cultures revealed Salmonella enterica serovar Agbeni. The patient recovered well and was discharged on eight weeks of IV ceftriaxone as dictated by culture sensitivities. Patient has recovered well with no neurologic deficits.
|
[[54.0, 'year']]
|
M
|
{'9709878': 1, '13452006': 1, '27034871': 2, '20800526': 1, '30327739': 2}
|
{'4806280-1': 1}
|
3,203 |
6171225-1
| 30,285,830 |
comm/PMC006xxxxxx/PMC6171225.xml
|
Late presentation, MR imaging features and surgical treatment of Herlyn-Werner-Wunderlich syndrome (classification 2.2); a case report
|
A 19-year-old, unmarried woman presented with complaint of chronic pelvic pain and a palpable mass at the lower pelvic midline region. On physical examination, a mobile and painless mass was palpated at the lower pelvic midline region. The external genitalia were normal in appearance. Transabdominal ultrasonography reported a cystic structure in the lower pelvic region communicating with the uterus (likely dilated vagina) with endometrial cavities and absent right kidney. A cystic structure with internal septae was also reported in the left adnexal region.\nMR imaging with contrast was performed and showed duplication of the uterine bodies, endometrial canals, uterine cervices and vaginal canals. The right vaginal canal was significantly dilated. There was communication between the two cervices well seen in the axial T2W sequence. A small tubular structure with internal fluid signal along the anterolateral aspect of the dilated right hemivagina represented blind ectopic ureter (the mesonephric remnants) (Figs. and ). Right kidney was not visualized in included sections of the upper abdomen (Fig. ).\nA heterogeneous cystic structure was seen in the left ovary with hemorrhagic components.\nThe patient underwent surgery under general anesthesia. The septum was excised and hematocolpos was drained. The hemorrhagic, infected left adnexal cyst was also excised.
|
[[19.0, 'year']]
|
F
|
{'33840015': 1, '25591566': 1, '34745901': 2, '20734166': 1, '22405336': 2, '25932973': 1, '17503029': 1, '31105948': 2, '24347855': 2, '34367397': 1, '16677898': 1, '28058067': 1, '30285830': 2}
|
{'3314562-1': 1, '3314562-2': 1, '3314562-3': 1, '6501474-1': 1, '8556507-1': 1, '3843333-1': 1}
|
3,204 |
6171255-1
| 30,327,740 |
comm/PMC006xxxxxx/PMC6171255.xml
|
Intraoperative Local Administration of Platelet-Rich Plasma (PRP) during Neurolysis Surgery for the Treatment of Digital Nerve Crush Injury
|
The patient was a healthy 28-year-old woman who works as a book binder with no history of interest to this report. The fingers of her dominant hand were caught in a binding machine during work. Immediately after the injury, sensory disturbance and numbness occurred and persisted. Furthermore, she experienced severe neuropathic pain and anesthesia of her index finger. The patient came to our clinic 2 weeks after the injury.\nA wound scar was observed near the distal interphalangeal (DIP) joint of the ulnar side of the index finger (). Sensory examination revealed hypoesthesia in the thumb, index, middle, and little fingers. In the index finger, in particular, the area of the ulnar side beyond the wound was red (indicating loss of protective sensation) based on Semmes-Weinstein monofilament score used by tactile and contact force tester (2SA01, Kono Seisakusho Co. Ltd., Japan) [] (). Tinel's sign was observed, consistent with the wound. Severe neuropathic pain was observed both at rest and during movement. The visual analog scale (VAS) for pain was 10/10 mm. There were no radiological findings suggestive of fracture (). The range of motion of the index finger (injured/healthy side) was restricted due to neuropathic pain: metacarpophalangeal (MP) joint: 0°/70°, proximal interphalangeal (PIP) joint: 0°/40°, and DIP joint: 0°/60°. The total active range of motion (TAM) was 63%.\nIn a sensory nerve conduction study (NCS), we attempted to derive sensory nerve action potentials (SNAPs) of the thumb, index, and middle fingers. Using the antegrade recording method, SNAPs were collected by stimulating the digital nerve; they were derived from the forearm just above the median nerve using a surface electrode. No derivation of SNAP was observed in the distal area of the index finger (). We also attempted to use ultrasound for diagnosis, but definitive diagnosis proved difficult due to the small size of the digital nerve.\nNeurotmesis was suspected based on clinical findings and NCS. Although we attempted to control her neuropathic pain, her symptoms were uncontrollable by conservative therapy. If neurotmesis was not denied by NCS, we recommended the patient to conduct intraoperative diagnosis in our facility. Surgery under general anesthesia was performed 5 weeks after injury. Intraoperative findings revealed severe adhesion around the digital nerve, but the nerve preserved its continuity. The intraoperative diagnosis was nerve crush injury. After undergoing neurolysis, 0.5 ml of PRP was intraneurally injected at two locations of the injured area that was identified based on intraoperative findings (total administration volume = 1 ml) (). A 25-gauge needle was used for infiltration, and PRP was injected from the proximal side of the injured site under direct vision.\nAfter 1 week of immobilization, rehabilitation of active finger motion was initiated. A decrease in neuropathic pain was observed immediately after surgery (). Improvement of restricted finger range of motion was recognized from 2 weeks postoperatively and became normal 4 weeks after surgery. In the Semmes-Weinstein monofilament test, the sensory disorder recovered gradually and completely recovered 6 months postoperatively (–(d)). The derivation of SNAP was confirmed 3 months postoperatively, and it became normal 9 months postoperatively (Figures and ). Neuropathic pain disappeared 9 months after surgery.\nPRP was elaborated according to PRGF-Endoret technology (BTI Biotechnology Institute, Vitoria-Gasteiz, Spain) in the cell-processing factory unit of our hospital which fulfills the criteria for good manufacturing product (GMP). Briefly, a total of 36 ml of peripheral venous blood was withdrawn into four tubes of 9 ml containing 3.8% (w/v) sodium citrate. Blood was centrifuged at 580 g for 8 minutes at room temperature (24–26°C). The upper volume of plasma (platelet-poor plasma; PPP), which contains a similar platelet count to that of peripheral blood, was drawn off and discarded in a collection tube. The 2 ml plasma fraction (PRP) located immediately above the sediment of red blood cells, but not including the buffy coat, was collected from each tube (total 8 ml PRP) and transferred to another tube. This tube was taken to the operation room ready for use. This plasma contains a moderate enrichment of platelets (two- to threefold the platelet count of peripheral blood) with scarce leukocytes, being a P2-x-Bβ PRP according to the classification system proposed by DeLong et al. []. The concentration rate of administered PRP in this case was 2.23 (). To initiate clotting, calcium chloride (10% w/v) was added to the liquid PRP aliquots just before injection. All procedures were performed under sterile conditions.
|
[[28.0, 'year']]
|
F
|
{'23780535': 1, '29094404': 1, '20422684': 1, '21712738': 1, '25230270': 1, '23840657': 1, '3805636': 1, '23723151': 1, '14641648': 1, '26807124': 1, '1640150': 1, '9371122': 1, '23472861': 1, '23801419': 1, '11681796': 1, '20505591': 1, '33229720': 1, '18583097': 1, '23519544': 1, '21244302': 1, '27845852': 1, '21488817': 1, '23833487': 1, '15509939': 1, '8393905': 1, '26876895': 1, '26048672': 1, '9638695': 1, '24901030': 1, '22738751': 1, '21029038': 1, '24838385': 1, '26745165': 1, '19187989': 1, '30327740': 2}
|
{}
|
3,205 |
6171295-1
| 30,285,777 |
comm/PMC006xxxxxx/PMC6171295.xml
|
Intravesical migration of female urethral dilator: a case report of a new urologic emergency in the era of e-commerce
|
A 47-year-old white female was referred at 1 AM to our Urology department from the Emergency Room for admitted migration inside the bladder of a metallic urethral dilator used for sexual stimulation. The patient stated that she had bought the object through a dedicated internet site. An ultrasound study revealed a partially full bladder with an echogenic internal structure (Fig. ). An X-ray plate of the pelvis clearly visualized the presence of a high-density object shaped like a rifle bullet about 6 cm long, placed obliquely above the pubic symphysis. It was referred by the Radiologist as “likely intrauterine device” (Fig. ).\nSince the patient had no symptoms, she opted to return home under oral antibacterial treatment with Ciprofloxacin, and endoscopic extraction was planned in 2 days time, with the program of introducing through the urethra under sedation a 24 F nephroscope and to extract the dilator placing it in line with the instrument axis and retrieving it with a 3-pronged rigid grasper.\nThe following day, when contacted by telephone again, the patient refused hospitalization, stating that she had be able to self-manipulate retrogradely the dilator through the urethra outside the bladder (Table ). An US and X-ray study of the pelvis confirmed the absence of the foreign body (Fig. ).
|
[[47.0, 'year']]
|
F
|
{'17563678': 1, '17687134': 1, '18658011': 1, '27790300': 1, '10893567': 1, '30285777': 2}
|
{}
|
3,206 |
6171728-1
| 30,345,024 |
comm/PMC006xxxxxx/PMC6171728.xml
|
Case Report: Severe back pain, epigastric distress and refractory nausea; an unusual presentation of mediastinal bronchogenic cyst
|
A 44-year-old Hispanic female presented with a three-week history of recurrent sharp interscapular pain radiating to the mid-sternal and epigastric region associated with refractory nausea and vomiting. She underwent cholecystectomy for intermittent epigastric pain two years ago. CT abdomen at that time showed a subcarinal mass measuring 5.4 X 5.0 cm (\n). Subsequent EUS diagnosed it as a bronchogenic cyst. EBUS guided aspiration resulted in an incomplete drainage and she was discharged after partial improvement.\nCurrent physical examination showed a heart rate of 126/min (normal range: 60–100/min) and respiratory rate of 20/min (normal range: 12–20/min). Initial labs showed white cell count of 10.58X10\n3/uL (normal range: 4000–11X10\n3uL), elevated inflammatory markers [ESR of 63mm/hr (normal range: 0–20 mm/hr); CRP of 116 mg/L (normal range: <3.0 mg/L)], and hypokalemic metabolic alkalosis. Electrocardiogram showed non-specific T wave changes. Chest X-ray showed right posterior mediastinal mass (\n).\nCT chest showed an increase in the size of the bronchogenic cyst (9.64 X 7.7 cm) with small right pleural effusion (\n).\nThe X-ray and CT findings were consistent with partial cyst rupture or an infected cyst. X-ray esophagogram ruled out esophageal compression or contrast extravasation. The patient’s symptoms were refractory to conservative analgesic and antiemetic measure like Dilaudid (hydromorphone) 1 mg IV every 3 hourly and Zofran (Ondansetron) 4 mg IV every 4 hourly for pain and nausea/vomiting respectively. Cardiothoracic surgery was consulted and the patient underwent right thoracotomy and surgical cyst excision. Cyst pathology was consistent with severe inflammatory changes. Within 24–48 hours after the surgery, the resolution in the patient’s symptoms were noted in terms of decrease in need of pain and nausea medications. Repeated labs showed resolution of leukocytosis.
|
[[44.0, 'year']]
|
F
|
{'8020324': 1, '21515207': 1, '18064522': 1, '27263614': 1, '15337033': 1, '11058643': 1, '27070336': 1, '17670412': 1, '20616941': 2, '30345024': 2}
|
{'2893431-1': 1}
|
3,207 |
6171780-1
| 30,324,044 |
comm/PMC006xxxxxx/PMC6171780.xml
|
Drug-induced Thrombotic Microangiopathy Caused by Gemcitabine
|
A 66-year-old male with a past medical history of hypertension and pancreatic adenocarcinoma presented to our hospital with complaints of nausea, vomiting, and generalized weakness in the arms and legs. The patient was diagnosed with locally advanced, pancreatic cancer, T1 N0 M0 a year prior to presentation. Magnetic resonance cholangiopancreatography (MRCP) revealed a 1.7 cm mass at the head of his pancreas, locally invasive but without the involvement of lymph nodes, superior mesenteric artery, superior mesenteric vein or portal vein. Endoscopic biopsy revealed adenocarcinoma. The patient was a poor surgical candidate due to social issues, alcoholism, residence at a nursing home and was at a high-risk for post-surgical complications. The patient was treated palliatively with nine cycles of gemcitabine and paclitaxel. The initial dose of gemcitabine was 2000 mg. The tumor decreased in size and CA 19-9 level declined from an initial level of 2000 to 26 units/mL. Later the dose of gemcitabine was reduced to 1400 mg (20% reduction) after the sixth cycle due to pancytopenia.\nOn admission to our hospital, the patient reported abdominal pain that was sharp and located in the right lower quadrant (RLQ). He denied fevers or chills. The patients' vital signs were: temperature 99.3 °F, heart rate of 73 beats per minute, blood pressure 129/60 mmHg, respiratory rate of 17 breaths per minute and oxygen saturation 100% on room air. The physical examination was remarkable for RLQ tenderness. The laboratory data revealed hemoglobin (Hb) 6.5 g/dL, hematocrit (Hct) 19.8, mean corpuscular volume (MCV) 83.2fL /red cell, red cell distribution width (RDW) 19.1 %, white cell count of 9.44 x 109/L, platelets of 54 x 109/L, alanine transaminase (ALT) 133 IU/L, aspartate transaminase (AST) 222 IU/L, alkaline phosphatase (ALP) of 147 IU/L and a total bilirubin of 5 umol/L. BUN was 42 mg/dl, creatinine 2.12 mg/dl (baseline creatinine of 0.8), LDH was 1700 u/l, reticulocyte count was 7.8%. Peripheral smear showed microcytic anemia with frequent schistocytes consistent with a microangiopathic hemolytic process (Figures -). Urinalysis was positive for 1+ blood and 1+ albumin. Computed tomography (CT) scan of the abdomen without contrast showed a stable pancreatic mass and no signs of hydronephrosis (Figure ). ERCP revealed choledocholithiasis. Choledocholithotomy was performed and subsequently the bilirubin improved. Blood cultures grew Klebsiella. He was treated with piperacillin-tazobactam. The patient received intravenous (IV) fluids, blood and platelets when the Hb and platelets declined to Hb of 6.4 g/dl and platelet counts of 8 x 109. He was treated with methylprednisone 30 mg IV q24 and the platelet count increased to 20 x 109. His creatinine increased to 12 mg/dl and BUN to 112 mg/dl. ADAMTS13 activity was 34%. A diagnosis of GiHUS was made. The patient was offered plasmapheresis, but he opted for hospice.
|
[[66.0, 'year']]
|
M
|
{'19203505': 1, '9109218': 1, '2104558': 1, '8770981': 1, '7452889': 1, '9109216': 1, '1610985': 1, '32528969': 1, '14986082': 1, '16968717': 1, '11532079': 1, '7696109': 1, '8260241': 1, '16006690': 1, '9414181': 1, '17989688': 1, '9117804': 1, '3923162': 1, '8613975': 1, '33717763': 2, '12324937': 1, '152058': 1, '30324044': 2}
|
{'7954088-1': 1}
|
3,208 |
6172139-1
| 30,333,943 |
comm/PMC006xxxxxx/PMC6172139.xml
|
Abscopal Effect after Palliative Radiation Therapy for Metastatic Adenocarcinoma of the \nEsophagus
|
A 74-year-old male presented in February 2016 with increasing dysphagia. There was no history of prior abdominal infection or surgery. On esophagogastroscopy, a necrotic and circumferential friable tumor was seen at 33 to 40 cm from the incisors, with an endoscopic appearance of involvement of gastroesophageal (GE) junction and the proximal 2 cm of the stomach. Biopsies of the distal esophageal tumor confirmed poorly differentiated adenocarcinoma. The patient was anemic with a hemoglobin of 89 g/L. Staging endoscopic ultrasound suggested a breach of muscularis propria and four enlarged paraesophageal nodes. Neoadjuvant chemoradiotherapy followed by esophagectomy was initially considered; however, a staging positron emission tomography (PET) scan demonstrated 18-fluorodeoxyglocose (FDG) uptake not only in the primary tumor, but also in the paraesophageal region near the GE junction and upper abdominal lymph nodes extending as far inferiorly as the right renal vessels, in a retrocaval location (Figure ).\nA radiation oncology consultation was sought regarding treatment options of such extensive lymphadenopathy. Palliative radiation therapy (RT) was recommended. The patient was also evaluated by a medical oncologist who advised that chemotherapy may be considered after assessing the response to palliative radiotherapy.\nFrom March 21, 2016 to April 5, 2016, the patient received palliative RT to the symptomatic primary tumor and closest adjacent nodes using a pair of anterior and posterior fields. A total dose of 30 Gray (Gy) was prescribed over 10 daily fractions. As the lymphadenopathy in the lower abdomen was not symptomatic, and would have contributed to increased toxicity, this region was deliberately excluded from the high dose RT volume (Figure ). Other than very mild odynophagia, the patient had no other RT-related side effects. On the first follow-up visit, one month following treatment completion, he had improved swallowing function and a weight gain of six pounds.\nFollow-up computed tomography (CT) scan was obtained on May 24, 2016 to evaluate for the suitability of chemotherapy and to serve as a baseline during systemic therapy. This demonstrated persistent thickening of the lower esophagus, with lymphadenopathy reported to have decreased in size and no significant retroperitoneal adenopathy. When given the option of receiving palliative chemotherapy, the patient declined and chose to continue on observation only. Further CT scans in August and October 2016 showed a complete response in the irradiated primary tumor and nodes, with a stable 10 mm lymph node at the right renal vein.\nIn January 2017, due to symptoms of increasing dysphagia, the patient was assessed by a thoracic surgeon for consideration of esophageal stent placement. Endoscopy on January 12, 2017 noted that there was a possible small amount of residual tumor at the GE junction, but there was no significant narrowing or stricture, and no biopsies were taken. A further CT scan on April 10, 2017 showed minor circumferential thickening of the distal esophagus, but unchanged from previous. Paraesophageal lymphadenopathy was reported to be unchanged. The PET-positive lymph node at the renal vein decreased from 10 mm to 5 mm.\nThe patient’s symptom of dysphagia resolved spontaneously, and an evaluation was made with a further PET scan on May 19, 2017 (Figure ). This demonstrated mild residual FDG activity within the distal esophagus, more likely inflammatory change rather than malignancy. The FDG activity within all the lymph nodes, both treated and untreated, had unexpectedly resolved.
|
[[74.0, 'year']]
|
M
|
{'15197201': 1, '24039351': 1, '25651787': 1, '6185172': 1, '26582738': 1, '19573801': 1, '32545427': 1, '13042090': 1, '25872878': 1, '26950826': 1, '31475117': 1, '33297519': 1, '31119136': 1, '30649679': 1, '34768644': 1, '20555101': 1, '30333943': 2}
|
{}
|
3,209 |
6172140-1
| 30,333,944 |
comm/PMC006xxxxxx/PMC6172140.xml
|
Anomalous Aortic Origin of Coronary Arteries from the Opposite Sinus: A Case Report
|
A 64-year-old male with a history of urothelial bladder cancer, who was a former smoker of a packet of cigarettes a day for 15 years, presented at his private medical doctor’s (PMD) practice with complaints of exertional chest pain. This chest pain was located in the middle of his chest, was pressure-like in nature, and was exacerbated with exertion and relieved with rest. The patient denied any associated diaphoresis or palpitations. An exercise stress test was performed, which showed inferior wall ischemic changes, and the patient was subsequently presented at our hospital for an elective angiogram. Upon admission, he was afebrile with a blood pressure of 147/85 mm/Hg and a regular heart rate of 79 beats/minute. The electrocardiogram (ECG) showed a sinus rhythm with a right bundle branch block and no ST segment or T wave changes indicative of ischemia (Figure ). The lab analyses, such as troponin, lipid profiles, and fasting blood glucose, were within normal limits. The patient was referred to the catheterization lab for a coronary angiogram (CAG) through the right femoral artery. Cannulation of the right coronary ostia revealed the anomalous origin of the left circumflex artery (LCx) and the right coronary artery (RCA) from a shared ostium. The RCA was found to have 80% stenosis in the middle and distal segments with the right posterior descending artery (RPDA) having a 70% stenosis in the proximal segment (Figure ). The LCx showed no significant stenosis. In the pursuit to locate the left coronary ostia, the discovery of the anomalous origin of the left anterior descending artery (LAD) from the right coronary cusp was made. It arose just anterior to the shared ostium of the RCA and LCx. The LAD had no stenosis. The procedure was thus aborted to perform a cardiac multidetector computed tomography (MDCT) to further study the anatomy of the patient in order to decide whether he would benefit from a surgical intervention or a percutaneous coronary intervention (PCI) of his obstructive coronary artery disease (CAD) (Figure ). The MDCT confirmed the findings of the CAG. Considering the favorable anatomy of the LAD with no intramural course, a separate ostium, and no significant stenosis, the patient was referred back to the catheterization lab for a PCI. He received two drug-eluting stents in his RCA and one stent in his RPDA with excellent angiographic results. During the patient’s four-week follow-up appointment, he admitted to having better exercise tolerance and was free of exertional chest pain.
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[[64.0, 'year']]
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M
|
{'29755631': 2, '4547578': 1, '22056684': 1, '15227247': 1, '2208265': 1, '18021878': 1, '6693648': 1, '17404407': 1, '19038677': 1, '21184546': 1, '24886614': 1, '26563852': 1, '28335843': 1, '20186982': 1, '17620686': 1, '30333944': 2}
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{'5942243-1': 1}
|
3,210 |
6172416-1
| 30,305,895 |
comm/PMC006xxxxxx/PMC6172416.xml
|
Atypical angiofibroma in a patient with compromised general health: A case report
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In March 2016, a 47-year-old male patient was admitted to the Oral and Maxillofacial Surgery and Traumatology service of a public hospital, referred by the medical team with the chief complaint of respiratory difficulty after the appearance of a soft palate lesion. On anamnesis, the patient reported rapid weight loss, drug use for more than 10 years, and the development of a hard palate lesion three years earlier, which was left untreated. In addition, the patient reported the development of a soft palate lesion one month earlier. Intraorally, an extensive mass of mucosa-like color was present in the palate region, which obstructed the oropharynx and consequently caused dyspnea.\nThe sagittal computed tomography (CT) image reveals a soft tissue mass in the nasal cavity extending to the posterior portion of the nasopharynx and the lower part of the sphenoid sinus, with lowering of the entire musculature of the soft palate (A). The coronal CT image shows density loss of the septum in the nasal cavity and nasal conchae, maxillary sinus opacification, and lesion extending to the sphenoid cavity floor (B). The axial CT image reveals the soft tissue mass observed in the nasal cavity with opacification of the maxillary sinuses (C).\nAfter the initial examinations, the patient was submitted to tracheostomy (A) and intraoral incisional biopsy under general anesthesia (B). Intraoperatively, the tumor had a fibrous consistency and showed normal bleeding. The specimen was sent for histopathological analysis (A). Microscopically, the presence of a densely collagenated connective tissue was observed, with numerous blood vessels that were usually of small caliber and sometimes congestive; also, foci of hemosiderosis were visible (B). Based on the microscopic reports, clinical-radiological characteristics and physical examination, the diagnosis of NA was established.\nThe patient was referred for excision of the lesion. However, due to the extension of the lesion and the patient's systemic conditions, the teams of different specialties decided not to perform surgical resection or radiotherapy, opting for embolization. However, as a technology procedure was not available at the time, the patient remained hospitalized awaiting treatment availability. Approximately one month after the incisional biopsy, bilateral swelling in the submandibular region and parapharyngeal regions was noted (A and B). In addition, the patient presented severe headache, difficulty in closing the eyes, dysphagia and dyspnea, trismus, left facial paralysis and episodes of fainting. The patient was under palliative care and died after a few weeks.
|
[[47.0, 'year']]
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M
|
{'27752379': 2, '12220215': 1, '23087366': 1, '22584751': 1, '25722603': 2, '25328316': 2, '8630204': 1, '20549087': 1, '27613565': 1, '22164185': 1, '33854926': 2, '23332298': 1, '27957369': 2, '21274578': 1, '23483486': 1, '23998026': 1, '25991988': 1, '28508272': 1, '25437676': 1, '30305895': 2}
|
{'7721473-1': 1, '4338468-1': 1, '5124446-1': 1, '4196304-1': 1, '5056289-1': 1}
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3,211 |
6172567-1
| 30,305,896 |
comm/PMC006xxxxxx/PMC6172567.xml
|
Primary acinic cell carcinoma of the breast: A case report with a clinicopathological and immunohistochemical study of a rare breast cancer subtype
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A 41-year-old female presented with a 7 months history of a palpable breast lump in right upper outer quadrant. No abnormalities were discovered on physical examination. Results of laboratory tests were all within the reference range. Sonography and mammographic findings showed no evidence of abnormality in either breast or axillae. The Fine Needle Aspiration (FNA) was atypical cytology, and showed scattered or rarely clustered, uniformly round cells with small nuclei and a moderate amount of cytoplasm, suggesting a benign or low grade malignant tumor. Core needle biopsy (CNB) of the mass was diagnosed as Infiltrating Ductal carcinoma-NOS. Modified radical mastectomy was done and sent for histopathological examination.\nOn gross examination, the tumor was a 2.5 × 2.0 × 1.0 cm, gray white with a rubbery consistency, with a well-defined border and a slightly lobulated appearance (). Microscopically, the tumor showed a diffuse infiltrative growth patterns with small acinar or glandular structures mixed with solid nests (, ). Most of the tumor was comprised of monotonous round cells with a finely granular, weakly eosinophilic, or clear vacuolated cytoplasm resembling acinar cells of the salivary glands. Some neoplastic cells had a clear cytoplasm. The nuclear grade of the tumor cells was determined to be grade 2. Foci of vascular invasion were also present. Lymphatic permeation was occasionally seen, but the sentinel lymph node was free of metastasis. The mitotic count was up to 0–3/high power field. The Final surgical margins were negative. Cells with eosinophilic granules and globules were strongly periodic acid–Schiff (PAS) (diastase resistant) positive.\nImmunohistochemically, tumor cell populations were strongly positive for lysozyme (A and D) and were negative for estrogen receptor, progesterone receptor and human epidermal growth factor receptor-2 (HER2/neu). Because the patient was diagnosed as having invasive breast cancer with a triple-negative phenotype, postoperative radiotherapy (50Gy-/25 fractions) followed by adjuvant chemotherapy (TC: docetaxel 75mg/m2 and cyclophosphamide 600 mg/m2 administered intravenously every 3 weeks for 4 cycles) was administered. Although the followup period to date has been short (1 year), there have thus far been no signs of recurrence.
|
[[41.0, 'year']]
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F
|
{'34830849': 1, '11494007': 1, '19207954': 1, '15880955': 1, '21847414': 2, '8865856': 1, '12835294': 1, '17387718': 1, '20410810': 1, '27613565': 1, '10963383': 1, '11091630': 1, '15569060': 1, '23600952': 1, '21163678': 1, '17199742': 1, '20306833': 1, '19901010': 1, '34663287': 2, '23374397': 2, '30305896': 2}
|
{'8522227-1': 1, '3148534-1': 1, '3636039-1': 1}
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3,212 |
6172666-1
| 30,564,642 |
comm/PMC006xxxxxx/PMC6172666.xml
|
Intussusception following rotavirus vaccination: a reminder for practitioners
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A 2-month-old male infant was admitted under the paediatric team with a 1-day history of non-bilious vomiting, pyrexia, and irritability a day after receiving his first-dose rotavirus vaccination. On examination he was haemodynamically stable and had no focal signs of sepsis. His abdominal examination revealed a soft, non-distended abdomen with no palpable masses. He had passed normal stool within the preceding 24 hours. Following initial assessment, he underwent a full septic screen including lumbar puncture, the results of which were all within normal range.\nAfter developing bilious vomiting overnight a paediatric surgical review was obtained and an upper gastrointestinal contrast study was performed. This revealed no evidence of malrotation. An abdominal X-ray was subsequently performed which revealed a soft tissue mass in the right hypochondrium, dilated proximal small bowel loops, and a paucity of distal bowel gas, in keeping with small bowel obstruction (). An urgent ultrasound scan was obtained which showed dilated proximal small bowel loops and the characteristic target sign typically seen in intussusception (). The child received full resuscitation before an air enema reduction was performed under fluoroscopic guidance. This was successful at first attempt.\nThe following day the patient was well, tolerating feeds, and passing normal stools. He was subsequently discharged home. Following discussion with Public Health England the child’s parents were advised to decline the second-dose rotavirus vaccination.
|
[[2.0, 'month']]
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M
|
{'19418060': 1, '16394298': 1, '23871447': 1, '25066368': 1, '26719697': 1, '22695189': 1, '30564642': 2}
|
{}
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3,213 |
6172667-1
| 30,564,644 |
comm/PMC006xxxxxx/PMC6172667.xml
|
Frey’s syndrome as a differential diagnosis for food allergy: a case report
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A 5-year-old girl presented to her GP with a history of an erythematous rash that appeared on her left cheek associated with eating certain foods including strawberries, apples, and sweets. The rash would appear immediately on mastication and would entirely disappear within 30 minutes of ingestion.\nHer medical history was unremarkable apart from a road traffic accident at 3 years of age when she suffered facial and chest trauma leading to a mandibular fracture and right lower lobe collapse. The patient required intubation and ventilation for 9 days on the paediatric intensive care unit and underwent maxillofacial surgery for the mandibular fracture.\nPhysical examination revealed a well-grown child with no systemic abnormalities or eczema. Within a few seconds of eating candy a facial flushing appeared on her left cheek, stretching from her the temporal region to the corner of her mouth. This faded within a few minutes as demonstrated in. There was no associated lip or tongue swelling or difficulty in breathing.\nThe patient was referred for skin prick testing which was performed on an extended panel and was negative. She was reviewed by a consultant paediatrician who made a diagnosis of Frey’s syndrome and counselled the family with regard to the non-allergic pathogenesis of this condition.
|
[[5.0, 'year']]
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F
|
{'12269544': 1, '18619076': 1, '7607824': 1, '14616110': 1, '34568264': 1, '10792802': 1, '20065342': 1, '19900355': 1, '30564644': 2}
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{}
|
3,214 |
6172805-1
| 30,286,730 |
comm/PMC006xxxxxx/PMC6172805.xml
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High cut-off membrane for in-vivo dialysis of free plasma hemoglobin in a patient with massive hemolysis
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A 51-year-old man presented to the emergency department with fever, abdominal pain and jaundice. Past and recent medical history were unremarkable and the patient did not report any recent trip, risky sexual behaviour, parenteral drug intake or ingestion of potentially contaminated food. The physical examination revealed right hypochondrium and epigastric tenderness and no signs of peritonitis. Lab tests showed Aspartate AminoTransferase (AST) 3560 UI/L, Alanine AminoTransferase (ALT) 4513 UI/L, hyperbilirubinemia (total 16 mg/dL), alkaline phosphatase, GGT 90/418 UI/L, PT 50%, normal pancreatic enzymes and normal renal function. Abdominal ultrasound showed no alterations.\nTwenty-four hours after the admission, liver function rapidly declined, with PT 40% and maximum total bilirubin of 47 mg/dL. In parallel, blood test showed an elevation of LDH, haptoglobin consumption, reticulocytosis and AKI stage 3 with creatinine of 4 mg/dL and a peripheral blood smear suggestive of hemolysis. Urinalysis was positive for bilirubin and hemoglobin, while the urinary sediment discarded the presence of red blood cells. Serological tests were positive for IgM Hepatitis A Virus (HAV). In addition, a previously unknown complete glucose-6-phosphate dehydrogenase deficiency was detected.\nOn the basis of these findings a diagnosis of acute hepatitis A infection complicated with massive hemolysis due to glucose-6-phosfate dehydrogenase deficiency was done. Hemolysis was probably triggered by fitomenadione administration and its diagnosis was partially masked by high bilirubin levels due to the severe hepatitis. AKI was interpreted as the result of pigmented-cast nephropathy. The haemolytic crisis was initially managed with 2 sessions of plasma exchange. However, considering the need of dialysis and the presence of CPH, continuous renal replacement treatment with a HCO filter (Septex™, 1.1m2, Gambro-Baxter, Hechingen, Germany; Fig. ) in CVVHD modality was started. In order to measure the CPH clearance, plasma was collected in EDTA tubes from arterial, venous and dialysate ports of the CRRT circuit and CPH was measured with Drabkin-based spectrophotometric analysis at 540 nm. The Sieving coefficient (SC) was calculated as CD/[CIn + COut)/2] where CD, CIn and COut represent CPH concentration at the dialysate, blood inlet and blood outlet side. CPH clearance was calculated as {CD/[CIn + COut)/(2)]}Qe, where Qe is the effluent flow. This filter was used for 48 h, observing a CPH value of 4,24 g/L at the beginning and of 3,72 g/L at the end of the treatment. The calculated SC for CPH was 0.08 at treatment start, later decreasing to 0.02 after 24 h. The calculated clearance of CPH declined as well, from 2,87 ml/min on the first day to 0,76 ml/min after 24 h (Table for treatment data and CPH clearance profile, Table for common laboratory data before and after CVVHD treatment).\nAfter this treatment, as the patient was still oliguric, seven sessions more of intermittent hemodialysis were performed. Eventually, 4 weeks after admission urine output ensued and the patient’s renal function started to recover. At the time of discharge, total bilirubin was 3.4 mg/dL and creatinine 2.8 mg/dL. Finally, 3 months after discharge the patient presented normal renal and hepatic function.
|
[[51.0, 'year']]
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M
|
{'5778789': 1, '23691780': 1, '17660031': 1, '12808174': 1, '10321668': 1, '22800762': 1, '26553708': 1, '22515814': 1, '16763508': 1, '9872677': 1, '14605279': 1, '30286730': 2}
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{}
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3,215 |
6172811-1
| 30,286,805 |
comm/PMC006xxxxxx/PMC6172811.xml
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Burkitt lymphoma of the ovaries mimicking sepsis: a case report and review of the literature
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We present the case of a 21-year-old Greek woman who presented to the Emergencies Department of our hospital with breast pain, abdominal distension, and weakness of approximately 1 week’s duration. Her individual, gynecological, and family history were unremarkable.\nShe had a high breathing rate (~ 22 breaths/minute), tachycardia (~ 110 beats/minute), hypotension with mean arterial pressure (MAP) of 55 mmHg, lethargy, swollen and painful breasts, abdominal dilatation with diffuse sensitivity to palpation and dullness on percussion, and low grade fever (~ 37.5 °C).\nShe was directly subjected to ultrasound (U/S) of her upper and lower abdomen that showed enlarged ovaries as well as a large amount of free ascitic fluid. Complete laboratory testing and blood gases were obtained and an urgent computed tomography (CT) scan of her upper and lower abdomen was performed, confirming the findings of the U/S: enlarged and inflammatory ovaries, pleural effusions, and large amount of free ascitic fluid (Fig. ). Laboratory tests showed neutrophilic leukocytosis with white blood cells (WBC) 30,000/μL, polymorphonucleocytes (PMN) 95%, and thrombocytopenia with platelets (PLT) 90,000/μL with signs of disseminated intravascular coagulation (DIC), increased urea (U) and creatinine (Cr) levels, increased bilirubin (Bil), increased serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT), and severe lactic and metabolic acidosis. Control for viral and human immunodeficincy virus (HIV) infection was negative. With these data and due to further deterioration of our patient’s clinical condition, it was decided to conduct a research laparotomy.\nIntraoperatively there were found enlarged and inflamed ovaries, a large amount of ascitic fluid, and an inflamed appendix, which was removed and sent for biopsy. The peritoneum was clear and free of any visible implants. A biopsy was also obtained from both her ovaries and cytology and ascitic fluid cultures were sent, a suprapubic fluid drainage tube was placed and due to the reproductive age of our patient it was decided not to remove her ovaries. After surgery, she was transported to the Intensive Care Unit (ICU), intubated, and mechanically ventilated; she was hemodynamically unstable, presenting hypoxemia with partial pressure of oxygen in arterial blood/fraction of inspired oxygen (PaO2/FiO2) of 150 and severe metabolic and lactic acidosis.\nThe differential diagnosis included ovarian hyperstimulation syndrome (OHSS) and other ovarian tumors. OHSS is a systemic disorder attributed to the release of vasoactive agents released from the ovaries after overstimulation []. The pathophysiology of OHSS is characterized by increased capillary permeability leading to large fluid extravasation, accumulation in the third space, and intravascular dehydration []. The serious manifestations of the syndrome include thrombosis, renal and hepatic insufficiency, and acute respiratory distress syndrome (ARDS), which cause severe morbidity []. Mortality from the syndrome is fortunately rare, with only sporadic references in the literature []. Women should be aware that mild forms of OHSS are common and complicate 33% of in vitro fertilization (IVF) cycles, while moderate and severe forms occur in 3–8% of cases of OHSS []. The majority of serious OHSS cases occur after IVF cycles, but the syndrome may also occur after any form of ovulation induction, such as clomiphene and gonadotropins []. The incidence of the syndrome, particularly the complex form, is higher in young women, women with polycystic ovaries, and in gestational cycles. Laboratory tests may show high hematocrit levels (> 55%), hypoproteinemia, and leukocytosis []. The treatment of OHSS is initially supportive until the situation resolves [].\nShe was initially treated as severe septic shock; blood cultures were obtained and broad-spectrum antibiotic treatment was administered. Due to acute renal failure, she was placed in continuous venous-venous hemofiltration (CVVHDF).\nWhile she was in our ICU she showed progressive clinical, gasometric, and hemodynamic improvement, draining ~ 2000 ml of ascitic fluid/day; on the third day of admission an attempt was made to wean her from the ventilator, pending the results of the cultures and ovarian and appendix biopsies. She was febrile (~ 38.4 °C), hemodynamically stable with normal hourly diuresis, and improved laboratory testing, therefore CVVHDF was removed. Severe leukopenia (WBC 2000/μL) was evident, for which she received subcutaneous granulocyte growth factor. On the fourth day of admission, the results of blood and ascites fluid cultures were negative and biopsy results showed high-grade Burkitt lymphoma of the ovaries and the appendix. With these data our patient was transported to a specialized oncology center for immediate onset of chemotherapy and further treatment.\nShe was gradually weaned from mechanical ventilation and was successfully extubated on the 12th day of her hospitalization. On the sixth day she received a combined chemotherapy regimen intravenously. On the 15th day she left the ICU and on the 28th day she was discharged from hospital, presenting improved clinical and laboratory condition, waiting for further cycles of chemotherapy.
|
[[21.0, 'year']]
|
F
|
{'26887776': 1, '8253917': 1, '10923741': 1, '17197360': 1, '10431959': 1, '22086870': 1, '16614233': 1, '16282281': 1, '3746930': 1, '15265787': 1, '16502413': 1, '1709685': 1, '19480266': 1, '9221989': 1, '30286805': 2}
|
{}
|
3,216 |
6172832-1
| 30,323,715 |
comm/PMC006xxxxxx/PMC6172832.xml
|
Biphasic low-grade nasopharyngeal papillary adenocarcinoma: a case report and literature review
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A round tumor with a diameter of approximately 10 mm that involved the posterior end of the nasal septal mucosa at the midline of the epipharynx was discovered in a 58-year-old man while screening for laryngeal cancer (Fig. ). The patient was referred to our department for further evaluation, whereupon imaging analyses and a regional biopsy were performed under local anesthesia using a biopsy fiberscope. Pathological findings resembled an inverted ductal papilloma of the salivary glands, but did not produce a definitive diagnosis. The patient had a history of renal cancer for which he had undergone surgery 5 years prior.\nPlain computed tomography (CT) revealed a soft tissue shadow tumor approximately 10 mm in size in the vault of the nasopharynx at the junction of the nasal septum and roof (Fig. ). Magnetic resonance imaging (MRI) showed a 10 mm mass at the same location as that observed on CT. T1- and T2-weighted images showed the same intensities as that of the nasal concha, and a regular contrast effect was observed (Fig. ). These MRIs suggested a benign tumor. Furthermore, positron emission tomography did not show any abnormal uptake of 18F-fludeoxyglucose in the nasopharynx, thyroid gland, or elsewhere in the body.\nTo excise the tumor and obtain a definitive pathological diagnosis, surgery was performed under general anesthesia using an endoscopic endonasal approach. First, an electrocautery needle was used for electrocoagulation and excision. Next, a suction curette was used for exfoliation of the tumor. Finally, the suction probe of the electrocautery device was used for electrocoagulation to stanch the bleeding.\nHematoxylin-eosin staining showed that the tumor had a papillary structure lined by a columnar epithelium with a hyalinized fibrous core, and was additionally composed of sheets of spindle cells (Fig. ); these two types of structures merged imperceptibly. A negative tumor margin was confirmed after surgery, and immunohistochemical studies showed that both columnar and spindle cells were diffusely positive for CK7 (Fig. ), TTF-1 (Fig. ), CK19, and vimentin (data not shown); however, they were negative for CK20, p63, smooth muscle actin (SMA), S-100, Epstein-Barr-encoded RNA (EBER), p16, human papillomavirus (HPV), and thyroglobulin (data not shown). The Ki-67 index was approximately 2–3%. P53 was irregularly positive in a small number of cells, suggesting wild-type status.\nWe diagnosed the tumor as a biphasic LGNPPA with a prominent spindle cell component []. No postoperative adjuvant treatment was administered. The patient is well and free of disease 34 months after the surgery.
|
[[58.0, 'year']]
|
M
|
{'22531688': 1, '21424532': 1, '16844563': 1, '21393036': 1, '20398195': 1, '28601658': 1, '32438756': 1, '17001898': 1, '19757421': 1, '29381996': 1, '18084247': 1, '22524571': 1, '18492272': 2, '24893893': 1, '9064286': 1, '34922607': 1, '28105348': 1, '2462370': 1, '33330610': 2, '24969705': 1, '24018817': 1, '21285870': 1, '16787643': 1, '16084450': 1, '30323715': 2}
|
{'2426684-1': 1, '7710863-1': 1}
|
3,217 |
6172840-1
| 30,286,731 |
comm/PMC006xxxxxx/PMC6172840.xml
|
Development of membranoproliferative glomerulonephritis-like glomerulopathy in a patient with neutrophilia resulting from endogenous granulocyte-colony stimulating factor overproduction: a case report
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A 76-year-old Japanese woman presented with neutrophilia, mild renal dysfunction, and proteinuria and was referred to our Department in year X (Table ). Her neutrophilia was first discovered during a medical check-up when she was 74 years old (year X-2), and thereafter, her neutrophil count progressively increased. Her serum G-CSF was 161 pg/mL (Table ), which was far beyond the normal range (< 39.0 pg/mL).\nHer 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG-PET/CT) scan showed intense uptake in the bone marrow but did not show any evidence of a malignant solid tumor or an occult abscess related to bacterial infection. Fluorescence in situ hybridization was performed on peripheral blood smears, and there was no clonality in the patient’s neutrophils. Her urine had tested positive for urinary occult blood since she was 50 years old, and she developed proteinuria after her neutrophil count increased above 20.0 × 103/μL in year X-1.\nHer blood pressure was 118/59 mmHg; other vital signs were also normal. Physical examinations were unremarkable. When she was admitted in year X, the results of laboratory tests were as follows: white blood cell (WBC) count, 35.9 × 103/μL (neutrophil count, 31.3 × 103/μL; 87.2% of the WBC count); hemoglobin level, 11.5 g/dL; platelet count, 27.3 × 104/μL; serum creatinine, 0.85 mg/dL; estimated glomerular filtration rate, 49.4 mL/min/1.73 m2; blood urea nitrogen, 16 mg/dL; lactate dehydrogenase, 170 U/L; total protein/albumin, 8.0/3.6 g/dL; and immunoglobulin G (IgG), 2901 mg/dL. Serum immunoelectrophoresis revealed a monoclonal IgG λ peak; however, the levels of other immunoglobulins were normal, and bone marrow aspiration showed less than 10% clonal plasma cells, thereby yielding the diagnosis of monoclonal gammopathy of undetermined significance (MGUS). Tumor markers including carcinoembryonic antigen, squamous cell carcinoma antigen, and cytokeratin fragment were all within normal range. Both the levels of C-reactive protein and complements were normal, and both antinuclear antibody and rheumatoid factor were negative. Tests for hepatitis B virus and hepatitis C virus were negative. Her urinary protein excretion was 2.55 g per gram urinary creatinine, and the proteinuria selectivity index was 0.17. We found hematuria (20–29 red blood cells/high-power field) and granular casts in her urinary sediment.\nA renal biopsy was performed, and sections evaluated by light microscopy showed many lobulated glomeruli. Mesangial proliferation and focal double contouring of the glomerular capillary walls were also present (Fig. ). Additionally, endocapillary proliferation was observed in the glomeruli (Figs. ). Immunoperoxidase staining for neutrophil elastase revealed some neutrophils infiltrating the glomeruli (Fig. ). Double immunofluorescence staining for neutrophils and macrophages showed that the infiltration of macrophages was mainly around the glomeruli, and the glomeruli contained more neutrophils than macrophages (data not shown). We identified intratubular cellular casts and interstitial expansion in the tubulointerstitial area (Fig. ). Immunoperoxidase staining for G-CSF did not show a specific staining pattern (data not shown). Immunofluorescent staining showed no deposition of immunoglobulins or complements (data not shown). Expansion of the subendothelial space suggesting injury of glomerular endothelial cells and effacement of the podocyte foot processes were seen in sections evaluated by electron microscopy (Fig. ). There were no electron dense deposits. Based on these biopsy findings, we diagnosed the patient with MPGN-like glomerulopathy.\nThe patient was conservatively treated with an angiotensin II type 1 receptor blocker, but her proteinuria did not resolve. On the contrary, her proteinuria fluctuated in accord with the changes in her blood neutrophil count. Finally, the neutrophil count decreased without any medication, and the proteinuria diminished considerably (Table ).
|
[[76.0, 'year']]
|
F
|
{'27941791': 1, '15747404': 1, '25722669': 2, '28287111': 1, '25915812': 1, '29703839': 1, '7529539': 1, '7981231': 1, '21120643': 1, '12042897': 1, '17136696': 1, '18756367': 1, '27147425': 1, '16980970': 1, '11805162': 1, '8652892': 1, '21654720': 1, '10931006': 1, '24707907': 1, '30286731': 2}
|
{'4322689-1': 1}
|
3,218 |
6172932-1
| 30,302,346 |
comm/PMC006xxxxxx/PMC6172932.xml
|
An Esophagogram or Tracheobronchogram? A Review of Barium Sulfate Aspiration
|
An 84-year-old male with multiple comorbidities including prior ischemic stroke without any residual deficits was admitted to the hospital for worsening lethargy and weakness due to progressive dysphagia to solids and liquids and weight loss of 15 pounds in the past 6 to 8 months. According to the family, he had a long-standing history of coughing and choking while eating and complained about food getting stuck in his chest. His vitals were stable in the emergency department and was breathing on ambient air. Esophagogram was ordered for the workup of his chronic dysphagia. During esophagogram, he started coughing and choking after which the study was terminated. After 5 hours of study, he started becoming hypoxic with oxygen saturation of 86% on room air requiring a non-rebreather mask, fever of 101°F, tachycardia 112/min, and hypotension to 90s mm Hg systolic blood pressure. Aggressive intravenous (IV) resuscitation was done, IV antibiotics including vancomycin and piperacillin-tazobactam were started, and he was upgraded to intensive care unit for a higher level of care.\nEsophagogram showed early laryngeal penetration of contrast and subsequent presence of contrast in the trachea and bronchial tree with minimal contrast in the esophagus ().\nChest X-ray showed contrast highlighting the tracheobronchial tree and bilateral upper lungs (). He was managed conservatively with IV fluids and IV antibiotics. He started to improve within 6 hours of aspiration event with stabilization of vital signs including resolution of hypotension and tachycardia. Oxygen requirement also improved to 2 L through nasal cannula within 24 hours. Repeat chest X-ray showed the advancement of contrast into bilateral bronchioles and alveoli with left-sided predominance (). His respiratory status remained stable; however, later on, due to his other comorbidities, family opted for hospice care.
|
[[84.0, 'year']]
|
M
|
{'16227934': 1, '12928969': 1, '15900382': 1, '2758750': 1, '28233902': 1, '29798458': 1, '7502332': 1, '28670162': 1, '27767330': 1, '31236468': 1, '21865311': 1, '8772987': 1, '8320526': 1, '23739762': 1, '12815152': 1, '14752188': 1, '24818122': 1, '8470567': 1, '8054001': 1, '20303622': 1, '20607457': 1, '22417257': 1, '9033535': 1, '33235777': 1, '23757166': 1, '9973698': 1, '9759469': 1, '29381987': 1, '24262956': 1, '28323271': 1, '1008348': 1, '25309769': 2, '23657894': 1, '15763294': 1, '10525777': 1, '15610809': 1, '12637611': 1, '19399489': 1, '26284743': 1, '9292908': 1, '30302346': 2}
|
{'4189518-1': 1}
|
3,219 |
6173321-1
| 30,294,454 |
comm/PMC006xxxxxx/PMC6173321.xml
|
Malignant Pleural Mesothelioma presenting with Cardiac Tamponade- A Rare Case report and Review of the literature
|
A 71 year-old-male with past medical history of hypertension, hyperlipidemia, diabetes, chronic obstructive pulmonary disease and marijuana abuse presented with intermittent retrosternal pleuritic chest pain for two weeks, sharp in nature, 7/10 in intensity, non-radiating, and aggravated by sitting up from a lying position, deep breathing, and exertion. The patient reported intermittent nonproductive cough, fatigue, decreased appetite and a 10-pound weight loss in the past eight months. Chest radiography and physical exam findings were all noted as normal one year prior to presentation. He had a 40 pack year’s history of smoking; he quit 25 years ago.\nOn examination, he was afebrile, pulse rate 88 beats per minute, blood pressure of 133/70 mmHg, with an oxygen saturation of 98% on room air. An electrocardiogram revealed diffuse ST-segment elevation. A chest radiograph revealed cardiomegaly, congestion, and a pleural-based opacity in the left upper lung field. Transthoracic echocardiography showed a left ventricular ejection fraction of 30%, grade 1 diastolic dysfunction, inferior vena cava dilation with blunting of respirophasic changes (less than 50% variation), and a large circumferential pericardial effusion with “swinging” of the heart, suggestive of cardiac tamponade physiology. Laboratory investigations revealed a hemoglobin of 9.3 g/dL, glycosylated hemoglobin at 9.4 g%, troponin I obtained 8 hours apart were in normal range (0.014 ng/mL and 0.024 ng/mL). Computed tomography of the chest with contrast revealed a 4.5 cm left upper lobe mass, left hilar and mediastinal lymphadenopathy, and a large pericardial effusion. A pericardial window was placed and 750 ml of serosanguinous pericardial fluid was drained. Pericardial fluid cytology was negative for malignant cells and bacteria. Elevated lactate dehydrogenase (7157 units per liter) and glucose level (266 milligrams per deciliter), reactive mesothelial cells and numerous white blood cells were noted. A computed tomography-guided biopsy of the left lung mass was performed; hematoxylin and eosin stains showed poorly differentiated malignant neoplasm. Immunohistochemical analysis revealed malignant pleural mesothelioma. The pericardial biopsy did not show any mesothelioma cells or fibrous plaques. The patient has been lost to follow-up since the diagnosis.
|
[[71.0, 'year']]
|
M
|
{'948545': 1, '6202538': 1, '10049665': 1, '7091938': 1, '8299643': 1, '14571437': 1, '15451223': 1, '2666592': 1, '17090323': 1, '8771014': 1, '11501711': 1, '10027347': 1, '13782506': 1, '9381428': 1, '11172613': 1, '186091': 1, '7448712': 1, '7067523': 1, '9227715': 1, '17965072': 1, '15070023': 1, '9237066': 1, '15805256': 1, '3335886': 1, '25852564': 1, '30294454': 2}
|
{}
|
3,220 |
6173349-1
| 30,379,262 |
comm/PMC006xxxxxx/PMC6173349.xml
|
Partial Papillary Muscle Rupture after Myocardial Infarction and\nEarly Severe Obstructive Bioprosthetic Valve Thrombosis: an Unusual\nCombination
|
We report a case of a 70 year-old male, with a history of dyslipidaemia and\nsmoking habits, who suffered an inferior ST elevation myocardial infarction\n(STEMI). Given the impossibility to achieve a timely percutaneous coronary\nartery intervention, thrombolysis was performed within 4 hours of symptoms\nonset. Advanced atrioventricular block requiring a transcutaneous pacemaker\noccurred soon after, followed by cardiorespiratory arrest in ventricular\nfibrillation, which was reversed after one cycle of advanced life support. The\npatient was transported by airplane to a percutaneous coronary intervention\n(PCI)-capable centre. Coronary angiography showed a 50-60% stenosis in the\nproximal segment of the right coronary artery, which was treated with a bare\nmetal stent. Echocardiography showed a moderate left ventricular systolic\ndysfunction (estimated ejection fraction of 35%), with inferior, inferolateral\nand inferoseptal akinesia and moderate mitral regurgitation. On the fifth day,\nthe patient was transferred to our centre, after a 10-hour flight. On admission\nto intensive care unit, the patient was in cardiogenic shock with inotropes and\nnon-invasive ventilation. A bedside transthoracic echocardiography revealed a\nsevere mitral valve regurgitation of uncertain mechanism, along with moderate\nleft ventricle systolic dysfunction and right ventricle systolic compromise.\nAdditional characterisation by transoesophageal echocardiography revealed a 9 mm\ndisruption of the posteromedial papillary muscle consistent with a contained,\nalbeit morphologically imminent, rupture. The instability of the sub-valvular\napparatus, leading to a broad posterior leaflet prolapse, caused severe mitral\nregurgitation with an eccentric jet with Coanda effect, reaching the left atria\nroof (). The patient underwent\nurgent mitral valve replacement with a biological prosthetic valve (St. Jude\n#29), with preservation of anterior and posterior leaflets. The patient\nexperienced a favourable post-operative recovery and was discharged 12 days\nafter surgery with anticoagulant therapy for three months, in addition to dual\nantiplatelet therapy. On the fourth month after surgery, the patient initiated\nprogressive heart failure symptoms (NYHA class III) without any further\ncomplaints. Additional transthoracic and transoesophageal evaluations were\nperformed, revealing a significant restriction of the prosthetic mitral valve\nleaflets mobility due to thrombotic material deposition, leading to severe\nobstruction, with a mean gradient of 19 mmHg and an effective orifice area\nestimated by PISA method of 0.4 cm. Additionally, in continuity with the prosthesis, a large\nmural thrombus was present covering the left atrial posteroseptal wall (). Urgent surgery, within twenty-four\nhours after diagnosis, was performed involving mitral bioprosthesis replacement\nwith another biologic prosthesis with significant improvement in clinical\nstatus. After an extensive study, no evidence was found of atrial fibrillation\nor thrombotic disorders. Pathology examination of the excised prosthetic\nmaterial confirmed prosthetic thrombosis, with no signs of endocarditis.
|
[[70.0, 'year']]
|
M
|
{'23488568': 1, '9362411': 1, '9347271': 1, '8887873': 1, '2035450': 1, '26610876': 1, '8881874': 1, '25622516': 1, '19064683': 1, '18205938': 2, '30379262': 2}
|
{'2248568-1': 1}
|
3,221 |
6173734-1
| 30,220,707 |
comm/PMC006xxxxxx/PMC6173734.xml
|
Brief Report: Potent clinical and radiological response to larotrectinib in TRK fusion-driven high-grade glioma
|
The patient is a 3-year-old girl who was diagnosed with a brain tumour at 5 months of age. She presented initially with vomiting and seizures and an MRI showed a heterogeneous mass measuring 6 × 3 × 2 cm in the right lateral ventricle. Following gross total resection pathology showed predominance of large epithelioid and spindle-shaped cells with mild pleomorphism, mitotic index of 14 per 10 high power fields and a Ki67 proliferative index of 40%. The tumour showed patchy positivity for GFAP, strong nuclear staining for p53, and was negative for synaptophysin, chromogranin, NeuN, BRAF V600E, H3K27M and ATRX. She was diagnosed with a HGG and was treated with an infant brain tumour protocol with 13 cycles of chemotherapy.\nFour months after completing treatment, she had disease progression in the tumour bed with multiple nodules in the lateral and third ventricles. Further tumour debulking confirmed recurrent HGG. After 6 months, a new mass in the tumour bed was subtotally resected and she received focal radiotherapy of 54 Gy to the tumour bed. The resected tumour was profiled on a pilot personalised medicine study. Three months following completion of radiation therapy, she represented with difficulty walking, drowsiness, vomiting and irritability. MRI showed widespread progressive disease with increased enhancement at the resection site, and enlarging suprasellar and subependymal nodules in the lateral and third ventricles. Dexamethasone was continued at 1.5 mg daily. The parents were told that she was incurable, and she was referred to palliative care for symptom management.
|
[[3.0, 'year']]
|
F
|
{'31256325': 1, '32906676': 1, '23917401': 1, '32923892': 2, '32087611': 1, '33353026': 1, '31075511': 1, '34651095': 1, '31738426': 1, '32665022': 1, '34429303': 2, '28719467': 1, '31450696': 1, '32734509': 1, '27332770': 1, '31749132': 1, '32238360': 1, '26565381': 1, '24705251': 1, '31882734': 1, '29606586': 1, '26216294': 1, '34064757': 1, '26784937': 1, '16234523': 1, '33738452': 1, '15758009': 1, '31838007': 1, '29466156': 1, '34885207': 1, '33749791': 1, '30715603': 1, '31738425': 1, '34277419': 1, '31554817': 1, '33020650': 1, '33921960': 1, '33330081': 1, '34604027': 1, '27282398': 1, '33400240': 1, '32914009': 2, '33257674': 1, '8832466': 1, '30220707': 2}
|
{'7446323-1': 1, '7446323-2': 1, '7446437-1': 1, '8559620-1': 1}
|
3,222 |
6173833-1
| 30,290,813 |
comm/PMC006xxxxxx/PMC6173833.xml
|
Does it take three to tango? An unsuspected multimorbidity of CD8+ T cell lymphoproliferative disorder, malaria, and EBV infection
|
A 43-year-old Sudanese male was admitted to Acibadem University Hospital in Istanbul, Turkey with hyperpigmented painful skin rashes on his whole body. He was experiencing these symptoms intermittently for a year and self-medicated himself with non-steroid anti-inflammatory drugs with no fever or other health problems. He had recently experienced joint pains. A complete blood count during admission showed normal erythrocyte counts (5.1 × 106/µL) and Hb levels (13.9 g/dL) with a high white blood cell levels (23.710/µL, of which 85% were lymphocytes) and low neutrophil (10.500/µL) and platelet (128.000/µL) levels. Investigation of a peripheral blood smear revealed 29% large granular lymphocytes (LGLs). Flow cytometric analysis of peripheral blood confirmed that 95% of lymphocytes (CD3+/TCRαβ+ population) were positive for pan-T antigens (CD2, CD5, and CD7) and CD8, but negative for CD4 and CD56. Ultrasonography and FDG-PET-CT evaluation of the abdominal area found hepatomegaly, splenomegaly, and hypermetabolic supra-infradiaphragmatic lymph nodes as well as a hypermetabolic spleen. He had a history of malaria, but HCV and HIV tests were negative. These results were compatible with CD8+ T cell lymphoproliferative disorder with skin involvement. Therefore, a 0.5-cm-deep skin punch biopsy was performed in an inner part of the leg showing lesions.\nLGL leukaemia is a rare lymphoproliferative disease and presents with anaemia, neutropenia, and an increase in the number of LGLs []. About 85% of LGL leukaemias are derived from a T cell lineage (T-LGL leukaemic cells express CD3, CD8, CD16, and CD57), while the rest are derived from the natural killer (NK) cell lineage (NK-LGL leukaemic cells express CD2, CD16, CD56, and CD57) [, ]. Furthermore, CD8+ T cell lymphoproliferative disorder is a very rare form of T-LGL with poorly defined clinical, aetiological, immunophenotypic, molecular and pathological features []. Although T-LGL is an indolent disease, it may chronically affect the immune system and cause recurrent infections, symptomatic anaemia, and autoimmune conditions such as rheumatoid arthritis. Prednisone, methotrexate, and cyclosporine have been used for T-LGL treatment. Therefore, the patient with this pre-diagnosis was prescribed methotrexate (20 mg/week) and Prednol® (80 mg) for 6 weeks, and further immunopathological parameters were evaluated in skin lesions.\nMicroscopic evaluation of skin sections by haematoxylin–eosin (HE) staining showed that the epidermis was minimally spongy and the upper dermis was oedematous with mild perivascular lymphocyte infiltration. However, the deep dermis was infiltrated by intra- and peri-vascular small lymphocytes (Fig. a). Standard analysis of paraffin-embedded sections by Benchmark-XT (Ventana Medical Systems) with its inner controls showed that 99% of the total lymphoid population was CD3+, CD2+, and CD5+, among which 90–95% were positive for CD8 (Fig. b, red arrow shows a histiocyte with no CD8 staining), while only 5–10% were positive for CD4. Notably, Granzyme B showed a similar staining pattern as CD8 (data not shown). In contrast, CD20 (B cells) and CD56 (NK cells) were negative. At the bottom of the tissue, a few giant multinuclear histiocytic cells were noticed (Fig. a, red arrow). Notably, these cells contained small intra-cytoplasmic microorganism-like structures that were not discernibly stained with any dye specific for fungi or bacteria (PAS, Alcian Blue, Grocott’s methenamine silver stain, and Ziehl–Neelsen stain) (Fig. a, white arrows). Overall, the patient was finally diagnosed with CD8+ T cell lymphoproliferative disorder involving both the periphery and skin.\nAfter this final diagnosis, methotrexate and Prednol were administered for 6 weeks. Six weeks later, blood values had normalized, skin and arthritis symptoms subsided, and the patient was discharged. No other follow-up could be performed because the patient returned to his country. However, because the patient was from Sudan, a malaria endemic region, and the unusual presence of small intra-cytoplasmic microorganism-like structures in histiocytic cells, the pathologist, who had no experience with malaria cases, consulted a malaria specialist at Osaka University, Japan.\nCareful evaluation of skin biopsy samples by polarized microscopy revealed birefringent crystalloid structures resembling malarial haemozoin (Fig. a, arrows show representative shiny crystalloid structures) []. Haemozoin is a by-product of haemoglobin metabolism in Plasmodium parasites and readily captured by macrophages and the reticuloendothelial system of the host, which can be easily recognized as birefringent crystals under polarized light [, ]. Haemozoin-like structures were mainly loaded in macrophages and giant histiocytes. To further investigate the possibility of asymptomatic submicroscopic chronic malaria infection, we performed nested PCR to detect Plasmodium parasites []. After purification of DNA from the skin biopsy samples by a tissue DNA extraction kit (NucleoSpin, Macherey–Nagel), P. falciparum DNA was amplified (Fig. b).\nThe co-presence of EBV infection with malaria is a well-known aetiology of lymphoma. Hence, EBV-early RNA (EBER) transcripts were investigated in paraffin-embedded tissue samples and found to be positive in macrophage-like histiocytes (Fig. ).
|
[[43.0, 'year']]
|
M
|
{'20414048': 1, '29300968': 1, '28369146': 1, '26121587': 1, '20056487': 1, '8479452': 1, '11722988': 1, '29332936': 1, '19131945': 1, '17045649': 1, '25613730': 1, '23175378': 1, '26794909': 1, '21351121': 1, '25059949': 1, '25163591': 2, '20676828': 1, '23316401': 2, '30290813': 2}
|
{'3535817-1': 1, '4150421-1': 1}
|
3,223 |
6173835-1
| 30,290,778 |
comm/PMC006xxxxxx/PMC6173835.xml
|
Long-term desensitization for ABO-incompatible living related kidney transplantation recipients with high refractory and rebound anti-blood type antibody: case report
|
A 60-year-old man was referred to our hospital for kidney transplantation. His wife, a 59-year-old woman, volunteered to donate her kidney to him when he started hemodialysis at age 59. The proposed transplant was ABO incompatible, from a donor with blood-type A to a recipient with blood-type O, and the recipient’s anti-A blood-type IgG antibody titer was measured at 4096-fold dilution.\nPreoperative testing included HLA-DNA typing, which revealed a mismatch in 6 antigens. Initial flow cytometric crossmatch testing (FCXM) was negative. Moreover, the flow cytometric panel reactive antibody (Flow PRA) screening test was negative for human leukocyte antigen (HLA) class I and class II. Single antigen testing was also negative.\nThree months prior to surgery, mycophenolate mofetil (MMF) 750 mg/day was initiated and the anti-CD20 monoclonal antibody Rituximab (200 mg) was administered according to our pre-transplantation regimen (Fig. ). Following 3 months of desensitization therapy, the patient underwent two sessions of double filtration plasmapheresis (DFPP).\nAnti-blood type antibody titers (IgG/IgM) were then assayed using the column agglutination technology (gel microcolumn) method (Bio-Rad®, Japan). Our target antibody titer level was < 128-fold dilution; however, the anti-A blood-type IgG antibody titer decreased to only 512-fold dilution (Table ). In addition, serum IgG before the induction of DFPP was 1428 mg/dl. The high titer state following plasmapheresis was considered “refractory rebound”, and the planned transplant was postponed in order to resume desensitization therapy (MMF 750 mg/day). Four months following the initial start of desensitization therapy (MMF), the anti-A blood-type antibody level rebounded to 1024-fold dilution.\nShortly after the re-initiation of desensitization therapy (150 days from the initial start of therapy), the patient developed herpes zoster infection. He was treated with anti-viral medication and the MMF dose was reduced from 750 mg/day to 500 mg/day. After 1 month, the MMF dose was increased back to 750 mg/day.\nTransplantation was rescheduled to occur 210 days from the initiation of MMF. The pre-transplantation regimen was as follows. Rituximab was administered at 200 mg and 100 mg at 21 days and 1 day before transplant, respectively. Twelve days prior to surgery, the dose of MMF was increased to 1000 mg/day (At 11 days prior to surgery, serum MMF Area Under the Curve (AUC)0–12 was 35.6 ng/ml.). The initial dose of extended-release tacrolimus (TacER) (0.15 mg/kg/day) was administered 13 days prior to transplantation and the dose was adjusted based on serum concentration. Because the initial DFPP sessions did not decrease the anti-A blood-type antibody titers, 4 sessions of selective plasma exchange (PE) were used to remove the anti-blood type antibody. With these interventions, the anti-A blood-type IgG antibody decreased to 128-fold dilution and the serum IgG level decreased to 357 mg/dl on the day of transplant (Table ).\nThe renal graft was transplanted into the right iliac fossa without incident. Subsequently, the graft became pink and urine was produced immediately. The post-transplant induction immunosuppression protocol consisted of TacER, MMF 2000 mg/day, basiliximab 20 mg administered on postoperative day (POD) 0 and 4, and systemic steroids starting on POD 0. A graft biopsy performed 1 h after reperfusion demonstrated no evidence of hyperacute rejection (Fig. ). The serum creatinine (s-Cr) level began to decrease immediately. On POD 6, the s-Cr level was 1.5 mg/dl, and anti-A blood-type IgG and IgM antibodies were measured at 16-fold and 4-fold dilutions, respectively. The antibody titer levels remained at these levels throughout the post-operative course. However, serum IgG increased to 957 mg/dl. On POD 12, cytomegalovirus (CMV) antigenemia was diagnosed. The antiviral medication baragancyclovir was initiated and the dose of MMF was decreased to 1000 mg/day. No further post-operative complications were observed.\nThe sCr fluctuated between 1.29 and 1.42 mg/dl during the 1.5 months after ABO-iLKT. A protocol biopsy was performed on POD 50. The histopathological examination revealed i) acute T cell-mediated rejection IB, and ii) no evidence of acute antibody-mediated rejection (Fig. ). Steroid pulse therapy (500 mg for 3 consecutive days) was administered.\nAt the time of 18 months after ABO-iLKT, the sCr level was between 1.30 and 1.49 mg/dl (estimated glomerular filtration rate (eGFR)-calculation of 38.0–40.8 ml/min/1.73m2). Urinalysis showed urine albumin of 30–80 mg/L, urine red blood cells of 0–1 /high power field, urine white blood cells 0–1 /high power field and no granular casts. His blood pressure was maintained as 132/80–138/88 mmHg on Amlodipine 5 mg once daily. Anti-A blood-type IgG and IgM antibody titers were stable at 16-fold and 8-fold dilutions, respectively. Serum IgG was preserved within the normal range. The patient was maintained on triple immunosuppression therapy consisting of TacER, MMF 1000 mg/day, and steroid 5 mg/day.
|
[[60.0, 'year']]
|
M
|
{'25050471': 1, '23195021': 1, '31522462': 1, '17908276': 1, '25890338': 1, '22310615': 1, '19906036': 1, '22755421': 1, '10567309': 1, '17767439': 1, '19384174': 1, '18498916': 1, '25894122': 1, '27819033': 1, '23746202': 1, '21873529': 1, '17593512': 1, '20590688': 1, '25807854': 1, '11532188': 1, '25363583': 1, '15196066': 1, '24860855': 1, '26484043': 1, '28403566': 1, '10580071': 1, '21449947': 1, '30290778': 2}
|
{}
|
3,224 |
6173840-1
| 30,290,835 |
comm/PMC006xxxxxx/PMC6173840.xml
|
A rare case of large pyosalpinx in an elderly patient with well-controlled type 2 diabetes mellitus: a case report
|
A 72-year-old Japanese woman with a 10-year history of T2DM had symptoms of diarrhea and persistent pain in left lower abdomen for 2 days and visited the emergency room in Kawasaki Medical School. She had an approximately 10-year history of hypertension and dyslipidemia. At that time, she was taking 4 mg/day of benidipine hydrochloride and 20 mg/day of azilsartan for the treatment of hypertension, and 25 mg/day of alogliptin and 500 mg/day of metformin for T2DM, and 2.5 mg/day of rosuvastatin for dyslipidemia. She had no remarkable family history. She was a housewife and she did not smoke tobacco or drink alcohol. She had no past history of digestive disease or obstetrics and gynecology disease. She had mild tenderness to palpation in her abdomen. Her height and body weight were 150.0 cm and 69.5 kg, respectively. Her vital signs were as follows: blood pressure 150/87 mmHg, heart rate 110 beats/minute, and temperature 36.4 °C. Inflammation markers were markedly elevated: white blood cell (WBC), 20,110/μL (neutrophil, 89.0%); C-reactive protein (CRP), 16.12 mg/dL. Anemia and mild hypoalbuminemia were observed although their causes remained unknown: red blood cell, 304 × 104/μL; hemoglobin (Hb), 9.3 g/dL; total protein (TP), 6.8 g/dL; and albumin (Alb), 3.2 g/dL. Her liver and renal function were within normal range as follows: aspartate aminotransferase (AST), 14 U/L; alanine aminotransferase (ALT), 9 U/L; gamma-glutamyl transpeptidase (γ-GTP), 8 U/L; lactate dehydrogenase (LDH), 202 U/L; creatinine (Cre), 0.81 mg/dL; blood urea nitrogen (BUN), 7 mg/dL; Na, 134 mEq/L; K, 3.8 mEq/L; Cl, 99 mEq/L; Cre clearance, 66.9 mL/minute; and urinary Alb, 15.1 mg/g·Cr. As shown in Fig. , her abdominal computed tomography (CT) on admission revealed a large tumor with calcification in left side of intrapelvis (upper middle panel) which was not observed in abdominal CT 1 year before (upper left panel). She had abdominal CT 1 year before by a urologist because bladder diverticulum was suspected at an annual medical checkup with abdominal ultrasonography. The tumor size was as large as 65 mm in diameter. In addition, as shown in Fig. , MRI showed a large tumor in left side of intrapelvis at the same lesion site observed in CT. An axial T1-weighted (T1W) image through the pelvis showed a markedly dilated fallopian tube posterior to the left ovary (upper left panel). Axial T2-weighted (T2W) image showed a slightly higher intensity (upper right panel). Axial diffusion-weighted (DW) image and contrast-enhanced T1W image showed a high intensity lesion at the same place (lower left and right panels). Based on these findings, we finally diagnosed her as having pyosalpinx.\nOn admission, she had symptoms of diarrhea and persistent pain in left lower abdomen, but there were no findings in physical and neurological examinations. Her glycemic control was relatively good: HbA1c, 6.6%; glycoalbumin, 23.6%. In addition, her HbA1c levels were around 6% for over 1 year with the medication (metformin 500 mg, alogliptin 25 mg). However, during the acute phase of infection, we treated her with intensive insulin therapy using insulin aspart and insulin glargine. Tumor makers were within normal range: carcinoembryonic antigen (CEA), < 1.0 ng/mL; cancer antigen (CA) 19-9, 6.0 U/mL; and CA-125, 11.0 U/mL. Pathogenic bacteria were not detected. Her Treponema pallidum hemagglutination (TPHA) was positive but rapid plasma reagin (RPR) for Treponema pallidum was negative. Candida antigen and β-D-glucan were negative. Neisseria gonorrhoeae deoxyribonucleic acid (DNA) and Chlamydia trachomatis DNA in the urine were negative. Although pathogenic bacteria were not detected, we started antibiotics therapy for pyosalpinx (13.5 g/day of tazobactam/piperacillin and 500 mg/day of levofloxacin) (Fig. ). We discussed the necessity of surgery such as laparoscopy with gynecologists, but finally we selected antibiotics therapy without laparoscopy because her symptoms and laboratory data were very much improved. Her laboratory data 14 days after starting the antibiotics were improved and became within normal range (WBC, 5500/μL (neutrophil 47.4%); CRP, 0.04 mg/dl); we stopped antibiotics (Fig. ). Laboratory data were within normal range even after stopping antibiotics. T2DM was well controlled with orally administered anti-diabetes drugs (metformin 500 mg, alogliptin 25 mg, and gliclazide 10 mg): HbA1c, 6.0%; glycoalbumin, 16.5%. The tumor gradually reduced in size: 25 days later (upper right panel, Fig. ), 3 months later (lower left panel, Fig. ), and 6 months later (lower middle panel, Fig. ) compared to that on admission (upper middle panel, Fig. ); however, the tumor did not disappear completely even 6 months later. Finally she was discharged without any symptoms and/or problems. After discharge, she had no symptoms and/or problems, and her inflammation markers remained within normal levels for at least 6 months.
|
[[72.0, 'year']]
|
F
|
{'16901918': 1, '17187246': 1, '26042815': 1, '7008604': 1, '27933478': 1, '33794866': 2, '12547890': 1, '30290835': 2}
|
{'8017632-1': 1}
|
3,225 |
6173903-1
| 30,324,081 |
comm/PMC006xxxxxx/PMC6173903.xml
|
Corynebacteria as a cause of pulmonary infection: a case series and literature review
|
A 75-year-old man on hemodialysis for end-stage renal disease was hospitalized for cough, fever, and altered mental status. His temperature was 103 °F, pulse 68, blood pressure 124/69, respiratory rate 22, and O2 saturation 96% on 2 L of O2 by nasal cannula. He was lethargic, with bibasilar crackles and a normal cardiac examination. His white blood cell (WBC) count was 20,100 cells/mm3 and his plasma procalcitonin was 1.1 ng/mL. Chest X-ray showed bibasilar infiltrates. Microscopic examination of Gram-stained sputum showed profuse polymorphonuclear leukocytes (PMNs) and Gram-positive rods, many of which appeared to be intracellular (Fig. ). Sputum culture yielded overwhelmingly predominant Corynebacteria, with rare P. aeruginosa. The Corynebacteria was identified as C. propinquum by MALDI-TOF. Blood cultures and viral PCR were negative. The patient was initially treated with vancomycin, cefepime, and metronidazole. Based on the predominance of Corynebacteria with the absence of other bacteria on Gram stain and a negative PCR for respiratory viruses, his pneumonia was attributed to C. propinquum, and only vancomycin was continued. He responded and was discharged to complete a 10-day course of linezolid.
|
[[75.0, 'year']]
|
M
|
{'34548923': 1, '9650969': 1, '6605104': 1, '239258': 1, '33287847': 1, '3513286': 1, '7803665': 1, '22361761': 1, '8075298': 1, '9011218': 1, '32944501': 1, '11075494': 1, '2439888': 1, '32178586': 1, '18660996': 1, '30794625': 1, '23955623': 1, '4746580': 1, '33513871': 1, '26380345': 1, '463927': 1, '16737433': 1, '29221301': 1, '26252066': 1, '7727668': 1, '4049053': 1, '23523447': 1, '432687': 1, '2116939': 1, '26744687': 1, '29028977': 1, '21162757': 2, '12420632': 1, '8136430': 1, '22337985': 1, '20171132': 1, '32722535': 1, '32185636': 1, '10610204': 1, '26944378': 1, '28866114': 1, '1450504': 1, '10546474': 1, '2718963': 1, '21477896': 1, '10212746': 1, '27836329': 1, '34218811': 1, '25828766': 1, '23271676': 1, '8505572': 1, '15314974': 1, '7727667': 1, '28621102': 1, '32968689': 1, '20678316': 1, '6302181': 1, '8993861': 1, '12791076': 1, '1351980': 1, '15108836': 1, '3488878': 1, '26650159': 1, '19228291': 1, '34599245': 1, '25356355': 1, '3183010': 1, '3956138': 1, '30324081': 2}
|
{'6173903-2': 2, '6173903-3': 2, '3009641-1': 1}
|
3,226 |
6173903-2
| 30,324,081 |
comm/PMC006xxxxxx/PMC6173903.xml
|
Corynebacteria as a cause of pulmonary infection: a case series and literature review
|
A 61-year-old man was found unresponsive post laryngectomy and tracheostomy for laryngeal squamous cell carcinoma. His temperature was 97.8 °F, pulse 99, blood pressure 114/86, and respiratory rate 22. Breath sounds were decreased bilaterally. WBC count was 7200 cells/mm3, lactate 1.2 mg/dL. Chest X-ray showed a new left-sided infiltrate. Sputum Gram stain revealed many Gram-positive rods, including those found within PMNs. Sputum yielded many Corynebacteria, identified by MALDI-TOF as C. propinquum, and few S. aureus. Sputum was liquefied with 2% N-acetyl cysteine and diluted serially; aliquots were cultured on blood agar and the number of colony forming units (CFU) was calculated []. The specimen contained 2 × 109 CFU of Corynebacteria and < 105 CFU of S. aureus per mL. Blood cultures and viral PCR were negative. The patient was initially given vancomycin, cefepime, and ampicillin; treatment was switched to ampicillin/sulbactam after the Corynebacterium was reported susceptible. His mental status rapidly improved, and he was subsequently discharged to complete a 10-day course of amoxicillin/clavulanate.
|
[[61.0, 'year']]
|
M
|
{'34548923': 1, '9650969': 1, '6605104': 1, '239258': 1, '33287847': 1, '3513286': 1, '7803665': 1, '22361761': 1, '8075298': 1, '9011218': 1, '32944501': 1, '11075494': 1, '2439888': 1, '32178586': 1, '18660996': 1, '30794625': 1, '23955623': 1, '4746580': 1, '33513871': 1, '26380345': 1, '463927': 1, '16737433': 1, '29221301': 1, '26252066': 1, '7727668': 1, '4049053': 1, '23523447': 1, '432687': 1, '2116939': 1, '26744687': 1, '29028977': 1, '21162757': 2, '12420632': 1, '8136430': 1, '22337985': 1, '20171132': 1, '32722535': 1, '32185636': 1, '10610204': 1, '26944378': 1, '28866114': 1, '1450504': 1, '10546474': 1, '2718963': 1, '21477896': 1, '10212746': 1, '27836329': 1, '34218811': 1, '25828766': 1, '23271676': 1, '8505572': 1, '15314974': 1, '7727667': 1, '28621102': 1, '32968689': 1, '20678316': 1, '6302181': 1, '8993861': 1, '12791076': 1, '1351980': 1, '15108836': 1, '3488878': 1, '26650159': 1, '19228291': 1, '34599245': 1, '25356355': 1, '3183010': 1, '3956138': 1, '30324081': 2}
|
{'6173903-1': 2, '6173903-3': 2, '3009641-1': 1}
|
3,227 |
6173903-3
| 30,324,081 |
comm/PMC006xxxxxx/PMC6173903.xml
|
Corynebacteria as a cause of pulmonary infection: a case series and literature review
|
A 59-year-old male with widely metastatic squamous cell carcinoma of the tongue was admitted for bleeding from his tracheostomy site. His temperature was 99 °F, blood pressure 108/84, pulse 119, respiratory rate 24, and oxygen saturation 82% on room air. He had blood at the tracheostomy site and bibasilar rhonchi. WBC count was 22,000 cells/mm3, hemoglobin 11.1 g/dL, and lactate 1.8 mg/dL. Chest X-ray revealed a left upper-lobe infiltrate. Sputum sample showed profuse PMNs and Gram-positive rods. Culture yielded C. striatum (confirmed by MALDI-TOF) and few Escherichia coli. The patient was placed on comfort care and died 8 days later.
|
[[59.0, 'year']]
|
M
|
{'34548923': 1, '9650969': 1, '6605104': 1, '239258': 1, '33287847': 1, '3513286': 1, '7803665': 1, '22361761': 1, '8075298': 1, '9011218': 1, '32944501': 1, '11075494': 1, '2439888': 1, '32178586': 1, '18660996': 1, '30794625': 1, '23955623': 1, '4746580': 1, '33513871': 1, '26380345': 1, '463927': 1, '16737433': 1, '29221301': 1, '26252066': 1, '7727668': 1, '4049053': 1, '23523447': 1, '432687': 1, '2116939': 1, '26744687': 1, '29028977': 1, '21162757': 2, '12420632': 1, '8136430': 1, '22337985': 1, '20171132': 1, '32722535': 1, '32185636': 1, '10610204': 1, '26944378': 1, '28866114': 1, '1450504': 1, '10546474': 1, '2718963': 1, '21477896': 1, '10212746': 1, '27836329': 1, '34218811': 1, '25828766': 1, '23271676': 1, '8505572': 1, '15314974': 1, '7727667': 1, '28621102': 1, '32968689': 1, '20678316': 1, '6302181': 1, '8993861': 1, '12791076': 1, '1351980': 1, '15108836': 1, '3488878': 1, '26650159': 1, '19228291': 1, '34599245': 1, '25356355': 1, '3183010': 1, '3956138': 1, '30324081': 2}
|
{'6173903-1': 2, '6173903-2': 2, '3009641-1': 1}
|
3,228 |
6173919-1
| 30,323,860 |
comm/PMC006xxxxxx/PMC6173919.xml
|
Neuroschistosomiasis mimicking lower back pain: case report of a rare differential diagnosis in a pediatric patient
|
A 13-year-old male adolescent, with no history of any medical illnesses, presented to the emergency room complaining of severe continuous backache and fatigability for 3 days. He had recently traveled to the southern region of Saudi Arabia. No bowel or bladder symptoms were present. Written informed consent was obtained from the patient by King Fahd Hospital of the University, Imam Abdulrahman Bin Faisal University.\nClinical examination revealed tenderness of the lower back region on palpation and a reduction in the strength of both knees and hip during extension and flexion (grade 3/5), with sensory loss in both lower limbs on pinprick examination. Other parameters on neurological examination were intact. Laboratory results revealed anemia with mild leukocytosis and peripheral eosinophilia. All other results of routine laboratory tests were within the reference range.\nAn X-ray examination of the lumbar spine showed no gross abnormality. Emergent magnetic resonance imaging (MRI) revealed cord edema with an abnormal signal intensity in the thoracic and lumbar regions (Figs. , ). The clinical and laboratory findings of the radiological features indicated acute transverse myelitis secondary to infectious or inflammatory changes. However, the possibility of other differentials remained. A lumbar puncture was performed using standard procedures. Gram staining and culture of the cerebrospinal fluid yielded negative results. No isolated parasitic eggs were present in the urine or stool specimens. Brain MRI findings were unremarkable. However, the Schistosoma serology titer showed a marked elevation.\nTherefore, a presumptive diagnosis of neuroschistosomiasis was made, and an experimental oral treatment for schistosomiasis was prescribed without any spinal intervention. The patient’s symptoms and signs rapidly subsided, with a regression of the spinal myelitis pattern on follow-up MRI examination (Figs. , ). Subsequently, he was discharged from the hospital within 1 week in dependable health and continued his anti-microbial regimen for 1 month. Follow-up examinations at the neurology clinic revealed a gradual improvement in the patient’s clinical condition. The patient was referred for further follow-up in the infection clinic. The patient was followed for 1 year and showed a complete long-term resolution of symptoms.
|
[[13.0, 'year']]
|
M
|
{'24596501': 1, '18978535': 1, '23829918': 1, '33324527': 2, '34950274': 1, '20737799': 1, '18499080': 1, '27288782': 1, '3351523': 1, '15088799': 1, '21216199': 1, '7917101': 1, '15486636': 1, '23765531': 1, '30323860': 2}
|
{'7732780-1': 1}
|
3,229 |
6174051-1
| 30,320,018 |
comm/PMC006xxxxxx/PMC6174051.xml
|
Nasal Myiasis: A Case Report
|
The patient was a 35-yr-old man with gastric cancer history for one year referred to Golestan Hospital, Ahvaz southwest of Iran in 2015 due to clinical signs including vomiting, loss of consciousness, food intolerances, impotence, icterus and paleness for 1 year. He had undergone chemotherapy bytaxotel (50mg), cisplatin (35mg) and flucytosine (500mg) according to his practitioner recommendation for four days. The chemotherapy schedule was repeated 4 times. The vital sign and biochemical parameters were: BP: 100/60 mm/Hg, PR: 110/min, RR= 28 /min, OT: 38.5C. The other biochemical parameters were:\nALT = 166, AST= 250, WBC: 23.80x 10 3, HB: 7.4, PLT: 56x10 3, FBS: 93, Na: 130, K: 5.9, Ca: 8.1, P: 3.9, bilirubin (T): 33.6, bilirubin (D): 30.1BUN= 149, Cr= 5.3 and in urinalysis: PRO 2+, Hb: 3+.\nThe patient was transferred to ICU due to respiratory distress. After few days, several larvae and pupa stage were seen in nasal and oral cavity (). The larvae and pupa were removed by forceps and transferred to parasitology department for precise diagnosis (, ). Nasal myiasis was recognized by infectious department consulting.\nThe patient was treated with turpentine, meropenem, vancomycin, and fluconazole for myiasis, pneumonia and candidiasis infection. The patient died after 5 d. The identification of third stages of larvae was performed according to internal and external morphological characteristics. Anterior and posterior air spiracles were removed from the body of maggots and examined microscopically (–). The pupa was cultured in room temperature for recognizing adult fly (). According to larvae, pupa and adult characters, Lucilia spp. was identified ().
|
[[35.0, 'year']]
|
M
|
{'23669173': 1, '24382372': 1, '23133480': 2, '23524903': 1, '21874753': 1, '29018832': 2, '31976109': 1, '34332474': 1, '22232372': 1, '23125939': 2, '23179955': 1, '18485982': 1, '18613876': 1, '28096867': 1, '30320018': 2}
|
{'5629300-1': 1, '3485497-1': 1, '3488829-1': 1}
|
3,230 |
6174053-1
| 30,320,017 |
comm/PMC006xxxxxx/PMC6174053.xml
|
Sudden Death of a Teenager Caused by Actinomyces israelii: A Case Report
|
We present a male case of a 14 yr old 2016 met at Legal Medicine Bihor County Service, Romania who bought an energy drink and while he was consuming it, he was feeling sick and felt down on the ground. He was resuscitated for about 1 hour, but unfortunately, he was declared dead. After we discussed with his family, he felt ill for two weeks, accusing chest pain, drowsiness, fatigue, productive cough and low-grade fever treated withtylenol and aspirin. He was at attending physician the day before his death and he was given tylenol and aspirin because he was diagnosed as having flu. No complementary examination like complete blood count or imaging exams (computed tomography) was made.\nWe followed the human subjects’ procedure, established by our institution. The research was conducted with the rules of good conduct in scientific research. The identity of the participant in the research is confidential when the results of this study are published. Informed consent was taken from the relatives of the patient.\nExternal exam of the corpse did not reveal any violent lesions neither pathological.\nExamination of the oral cavity showed normal dentition, but the gums corresponding to the teeth 1, 1, 1, 2.1, 3, 2.1, 2.2 were red and swollen, specific for gingivitis. There was no visible sign of illness at the level of head and neck so we could exclude the orocervicofacial form of this disease.\nMacroscopic the lungs were described as pneumonia, emphysema and pulmonary edema; the entire myocardium looked like myocarditis () and on the posterior wall of the left ventricle was an area with cardiosclerosis () which made us think that it could be a scar from a myocardial infarction.\nInside the bronchi from the lungs inflammatory granulomas with A. israelii (not stained periodic acid Schiff-PAS negatively) were visible (). In myocardium bacterial colonies, microabscesses, diffuse cardiosclerosis, myocytes with necrosis and polymorphonuclear cells were visible (). Therefore microscopic exam revealed acute myocardial infarction, heart failure, myocardosclerosis, chronic myocarditis and into the lungs infection with A. israelii.\nCorroborating the clinical features, autopsy findings and complementary examinations it was established that this sudden death was caused by an acute myocardial infarction as a result of chronic myocarditis and pulmonary pneumonia with A. israelii.
|
[[14.0, 'year']]
|
M
|
{'27311002': 1, '32904293': 1, '28828332': 1, '25045274': 2, '21990282': 1, '18164641': 1, '23672372': 1, '30320017': 2}
|
{'4094581-1': 1, '4094581-2': 1, '4094581-3': 1, '4094581-4': 1, '4094581-5': 1, '4094581-6': 1, '4094581-7': 1, '4094581-8': 1, '4094581-9': 1}
|
3,231 |
6174063-1
| 30,292,243 |
comm/PMC006xxxxxx/PMC6174063.xml
|
Massive hemothorax due to two bleeding sources with minor injury mechanism: a case report
|
An 83-year-old Japanese man awoke from sleeping and fell out of a bed that was approximately 40 cm high. He called an ambulance 3 hours later because of persistent left-sided chest and back pain and was transferred to our hospital. He had also fallen 3 days before presenting at our hospital and had hit his left arm and the occipital region of his head, for which he had received treatment elsewhere. He had a medical history of cerebral infarction, atrial fibrillation, and prostate cancer, and he had been prescribed apixaban 2.5 mg twice daily and bicalutamide 80 mg/day. His habitual history and familial history were unremarkable. He was a retired medical doctor and lived with his wife’s sister. On arrival at the emergency room, his vital signs were as follows: temperature, 36.2 °C; pulse, 68 beats per minute with an irregular rhythm; respiratory rate, 24 breaths per minute; blood pressure, 143/64 mmHg; and oxygen saturation, 100% on 6 L/minute with a simple oxygen mask. His status on the Glasgow Coma Scale was 13 (E3V4M6), indicating slightly affected consciousness due to mild brain injury. On examination, he was found to be drowsy, pale, and restless. His heart sounds were unremarkable. Cardiac apex was not palpable. His trachea was central and left-sided chest expansion was reduced. There was significant left-sided chest tenderness. Coarse crackles were heard with decreased breath sounds over the left side of his chest. His abdomen was not distended. There was no hepatosplenomegaly. His cranial examination was normal. His limbs examination was normal except for his left arm which had a bruise. Arterial blood gas (ABG) analysis revealed the following: pH, 7.38; partial pressure of carbon dioxide (PCO2), 30 mmHg; partial pressure of oxygen (PO2), 211 mmHg; bicarbonate (HCO3−), 17.5 mmol/L; base excess, − 6.5 mmol/L; hemoglobin, 12.2 g/dL; and lactate, 6.0 mmol/L. Chest radiography and computed tomography (CT) revealed left hemothorax with fractures of the 9th to 12th ribs, which we suspected was associated with the injury sustained during his first fall 3 days before admission (Fig. –). His blood pressure gradually decreased to 93/45 mmHg after CT assessment, and intensive fluid resuscitation was then initiated. Contrast-enhanced CT (CECT) 4 hours later showed worsening hemothorax with contrast extravasation in the region supplied by the tenth intercostal artery (Fig. –). A tube thoracostomy at the fifth intercostal space initially drained 950 mL of hemothorax. TAE resulted in hemodynamic stabilization (Fig. ). He was admitted to the intensive care unit (ICU) after TAE, but experienced persistent chest tube drainage at a rate of > 200 mL/hour, eventually reaching a total volume of 1820 mL. Measurements of ABG revealed that his hemoglobin had fallen to 7.6 g/dL despite a transfusion with 4 units of red blood cells (RBC).\nA thoracotomy at 4 hours after TAE revealed active bleeding from a partial-thickness wound at a peripheral site of his left diaphragm, corresponding to the edge of the broken tenth rib (Fig. ). A crushed bleeding lesion was removed from his diaphragm and the site was directly sutured. His fractured ribs were fixed, hemodynamic stabilization was confirmed, and further hemothorax did not arise (Fig. ). He required 6 units each of RBC and fresh frozen plasma during surgery. He was discharged from the ICU on hospital day 4 and the chest tube was removed on the following day. His postoperative course was uneventful and he was transferred to another hospital for rehabilitation without complications on day 29. He stayed at a nursing home and received no follow-up visit after discharge. He was managed at the hospital where he used to work and no adverse events were observed at 6 months after discharge.
|
[[83.0, 'year']]
|
M
|
{'17495287': 1, '25952278': 1, '27051252': 2, '31065358': 2, '23694863': 1, '23289630': 2, '19497514': 1, '24200663': 1, '29766084': 1, '24176006': 2, '34321811': 2, '26604982': 2, '27802875': 1, '30292243': 2}
|
{'4657199-1': 1, '3826551-1': 1, '6487754-1': 1, '4810351-1': 1, '3641980-1': 1, '8312918-1': 1, '8312918-2': 1}
|
3,232 |
6174068-1
| 30,323,983 |
comm/PMC006xxxxxx/PMC6174068.xml
|
Early detection of transformation to BPDCN in a patient with MDS
|
A 76-year-old man presented initially for evaluation of refractory anemia. His history included a diagnosis of Felty syndrome at the age of 64 years, after he was found to have rheumatoid arthritis, neutropenia, and an enlarged spleen. A diagnosis of anemia of chronic disease was made after complete workup including a BM examination was negative for malignancy. He received multiple therapeutic agents over time to control his rheumatoid arthritis, including adalimumab, methotrexate, abatacept, infliximab, azathioprine, rituximab, and prednisone. He underwent splenectomy at 67 years.\nHis anemia progressed and he became transfusion dependent at the age of 68 years. He was diagnosed with myelodysplastic syndrome (MDS) after a repeat BM examination revealed minimal morphologic dysplasia with a diploid karyotype. He received erythropoietin support for 1 year with worsening of his anemia. He was next treated with adjusted-dose lenalidomide (5 mg every other day) and rapidly achieved transfusion independence and a hemoglobin level of 13 g/dL. He progressively lost his response and became transfusion dependent. After 5 years, lenalidomide was discontinued and he received one cycle of azacitidine. Azacitidine was discontinued after BM examination at that time showed no morphologic support for residual MDS, and he continued to receive transfusions for nearly one year before presenting to our institution.\nA BM core biopsy and aspiration on initial evaluation demonstrated hypercellular marrow with trilineage dysplasia, moderate reticulin fibrosis, and 2% blasts (Fig. a, b). Flow cytometry demonstrated changes consistent with MDS, including markedly decreased side scatter in granulocytes (cytoplasmic hypogranularity), absence of hematogones, and a small number of aberrant myeloid blasts that had expression pattern of increased CD13 and CD34 and decreased CD38. Dendritic cells with a CD123bright, CD4+, HLA-DR+, CD56− immunophenotype were 0.2% of all analyzed cells (Fig. , top panel). Cytogenetic studies showed a normal diploid karyotype, and no mutations were identified on next-generation sequencing of 28 leukemia-associated genes. He was treated on clinical protocol with oral decitabine and had decreased transfusion requirements. Repeat BM aspirations showed persistence of dysplastic features and no significant increase in blasts.\nFlow cytometry of a surveillance BM aspirate sample approximately 8 months after decitabine initiation showed the emergence of a minimal population of aberrant plasmacytoid dendritic cells (CD123bright, CD4+, HLA-DR+, CD56+), comprising 0.79% of cells (Fig. , middle panel). This represented an immunophenotypic shift from CD56− plasmacytoid dendritic cells cells at presentation. After 1 year of decitabine treatment, he experienced increasing fatigue and developed scattered violaceous plaques on his abdomen, upper chest, and forearms (Fig. c) in addition to bilateral discoloration of the inferior conjunctiva. BM aspiration and biopsy revealed 70% immature appearing cells with finely dispersed nuclear chromatin, conspicuous nucleoli, and scant, eccentrically placed cytoplasm imparting a “hand-mirror” appearance. Immunohistochemical studies showed the immature cells were positive for CD4, CD56, CD123, and TCL1, and negative for CD34, MPO, and lysozyme. Flow cytometry showed a distinct population of CD45dim cells with CD123bright expression. These cells were CD4+, HLA-DR+, CD56+, CD34−, CD117−, CD64−, CD14−, and made up 35% of analyzed events (Fig. , bottom panel). This constellation of findings was diagnostic for BPDCN with extensive BM involvement. Cytogenetic studies showed a normal diploid karyotype and next-generation sequencing studies identified mutations in KRAS, NOTCH1, and RUNX1. Biopsy of an abdominal wall lesion showed BPDCN skin involvement (Fig. d, e). He was enrolled in a clinical trial (NCT02113982) of single-agent SL-401, a recombinant human IL-3 conjugated to truncated diphtheria alpha-toxin, which targets CD123. After 1 cycle, he experienced a decrease in BM blasts to 22%, resolution of skin lesions (Fig. f) and ophthalmic lesions, and marked improvement in performance status. After the second cycle, his BM aspirate showed 2.5% residual aberrant blastic plasmacytoid dendritic cells.
|
[[76.0, 'year']]
|
M
|
{'19066330': 1, '7736391': 1, '19851130': 1, '34884997': 1, '24859366': 1, '21275969': 1, '33027528': 1, '17068154': 1, '23203822': 1, '27264021': 1, '23065521': 1, '24441662': 1, '11861268': 1, '19388928': 1, '17439829': 1, '31811114': 1, '31530159': 2, '29200419': 1, '30323983': 2}
|
{'6833378-1': 1}
|
3,233 |
6174197-1
| 30,327,639 |
comm/PMC006xxxxxx/PMC6174197.xml
|
Primary Epithelioid Angiosarcoma of the Thyroid in a Patient Occupationally Exposed to Radiations
|
A 63-year-old man came to the clinical observation because of a rapid onset of dyspnea and dysphonia along with the development of a bulky node in the left side of the neck. He had been working as an interventional cardiologist in an angiographic room for 15 years at the local Hospital. Family history was negative with regard to malignancies and thyroid disease.\nThe relevant medical history included hypertension treated with valsartan and hydrochlorothiazide and non-insulin-dependent diabetes mellitus treated with metformin. There was no previous history of thyroid disease. Two years before the admission, he was treated with warfarin because of a deep venous thrombosis of the left leg occurred after a short bed rest for prostatitis. He was a heavy smoker.\nThe iodine status of the patient was not known; however, he was from a non-Alpine region and he was still living in the same area which is considered as a mildly iodine insufficient [].\nOn physical examination, the patient had a 8 × 10-cm firm left-sided neck mass with a right-sided shift of the larynx. On ultrasound examination, a nodule of the left thyroid lobe was found measuring 5 and 6-cm in its antero-posterior (AP) and transverse (T) diameters, respectively. The nodule was hypoechoic but inhomogeneous, with no vascularization; at the strain elastography, the nodule ranged from a medium elasticity to a hard pattern. The volume of the right thyroid lobe was reduced with a small hypoechoic nodule. No enlarged lymphnodes were found at the neck ultrasound. Computed tomography (CT) of the neck confirmed a 7 × 5 × 13-cm (T × AP × Long diameters) large, inhomogeneous neck mass originating from the left lobe that caused displacement of the trachea, the left common carotid artery and the left internal jugular vein. No evidence of primary malignancies or suspicious for secondary lesions was found at the CT of the head, abdomen, and pelvis. The chest CT showed a 6-mm round-shaped nodule not suspicious for malignancy close to the parietal pleura at the lower lobe of the right lung.\nA fine needle aspiration cytology (FNAC) of the mass was performed which yielded hemorrhagic smears with few groups of large, epithelioid cells, with vesicular, severely atypical nuclei and eosinophilic dense cytoplasms. A diagnosis of malignancy was given (Category 6 according to Bethesda 2010) with a suggestion for an anaplastic carcinoma (Figure ).\nThe patient underwent a total thyroidectomy and lymphadenectomy of central and left lateral cervical nodes. At the gross pathology examination, the tumor measured 6 × 6 × 12 cm (T × AP × Long diameters) and was partially circumscribed by a fibrous pseudocapsule. The mass had a gray, tan and red cut surface, with areas of hemorrhagic necrosis. Histology showed a vasoformative high grade neoplasia characterized by large epithelioid cells growing in sheets and lining abnormal vascular spaces; some cells showed intracytoplasmic lumina. There were areas of spontaneous necrosis and hemorrhage and a brisk mitotic activity; angioinvasion was noted. The tumor immunostained for vascular markers (CD31, ERG, CD34, factor VIII and vimentin), whereas epithelial differentiation markers were negative (cytokeratins, thyroid transcription factor 1, thyroglobulin, and EMA). The final histologic diagnosis was primary epithelioid angiosarcoma of the thyroid, grade 3 according to FFCCS (Figures ). This diagnosis was confirmed at a second opinion from a different institution. The tumor was restricted to the thyroid with free surgical margins. The mass had substernal extension and displaced the surrounding structures but it did not infiltrate the thyroid capsule, the strap muscles, or other neck tissues. The remaining thyroid tissue had nodular colloid goiter. No lymphnode metastases were detected.\nFifteen days after the thyroidectomy, the patient was operated to prevent rupture of an aneurysm of the abdominal aorta. One month after thyroidectomy, the chest CT showed multiple pulmonary nodular lesions some of them with a solid pattern surrounded by a ground-glass halo, 12 mm in maximum diameter. There was no consensus as to the oncologic relevance of these lesions, therefore, no biopsy was performed. A bone scintigraphy yielded negative results.\nChemotherapy with Epirubicin, Ifosfamide, and Mesna was administered but it was discontinued after 4 cycles because of pancytopenia and infection by Klebsiella Pneumoniae, treated with piperacillin/tazobactam, and by Clostridium difficile, treated with vancomycin. The patient recovered from the infections and, at a 6-month follow-up, the chest CT showed a reduction of the number and volume of the lung lesions with only three of them remaining in the medial lobe of the right lung.\nAt a further 18-month control, the chest CT was unchanged. The 6 mm round-shaped nodule close to the parietal pleura at the lower lobe of the right lung was also found to be stable. One year later, the patient developed pneumonitis and recovered after antibiotic therapy. At that time, he was investigated by neck, chest, abdomen and pelvis CT as well as with FDG-PET without any evidence of disease recurrence.\nAfterward, a 6-month CT follow-up program was started which is still ongoing. At present, the patient is alive with no evidence of disease after 62 months from initial diagnosis.
|
[[63.0, 'year']]
|
M
|
{'28810922': 2, '29895127': 1, '28351565': 1, '6895108': 1, '33489155': 1, '22648906': 1, '23794134': 1, '25935446': 1, '33633996': 1, '26741273': 1, '18766472': 1, '24349811': 2, '9630175': 1, '23608996': 1, '32747921': 2, '33717519': 2, '20485168': 1, '32292620': 2, '27150873': 1, '27229516': 1, '8917714': 1, '24652086': 1, '26868891': 1, '14717668': 1, '25745482': 2, '23570682': 1, '2294782': 1, '15380572': 1, '12562256': 1, '29909901': 1, '19913279': 1, '3099463': 1, '6363269': 1, '18941766': 1, '34754933': 2, '22517468': 1, '20537949': 1, '18019649': 1, '3297296': 1, '30327639': 2}
|
{'7728125-1': 1, '5558755-1': 1, '3855954-1': 1, '7150700-1': 1, '7948022-1': 1, '8565704-1': 1, '4338647-1': 1}
|
3,234 |
6174357-1
| 30,327,760 |
comm/PMC006xxxxxx/PMC6174357.xml
|
Heterozygous Mutation in Adenosine Deaminase Gene in a Patient With Severe Lymphopenia Following Corticosteroid Treatment of Autoimmune Hemolytic Anemia
|
A 14-years-old girl came to our attention because of severe and persistent lymphopenia during an episode of autoimmune hemolytic anemia. Her familiar history was negative for invasive infections and autoimmune diseases. Patient medical history was unremarkable for infections. In addition, previous blood counts were normal. The study conformed to all the protocols of Asst Spedali Civili of Brescia. Informed consent for blood tests and genetic studies was obtained from her parents.\nShe presented with acute onset anemia (hemoglobin 5.5 g/dl) with positive direct antiglobulin test (Coombs test, IgG 2+), normal platelets (299.000/μL), and white cell count (total leucocytes 5.760/μL, neutrophils 4.160/μL, lymphocytes 1.330/μL). At the beginning she was treated with oral prednisone (2 mg/kg/day), but poor response to the treatment was observed. Therefore, she was switched to four intravenous pulses of methylprednisolone each one at 2 mg/kg within 72 h, followed by intravenous immunoglobulins (1 g/kg).\nThe laboratory tests showed normal white cell counts, except for marked lymphopenia (Figure ), reduction of CD4+ cells (ranging from 50 to 300 cells/μL), increase of fetal hemoglobin, (6.4–13.9% during follow-up), supposedly related to reticulocytosis. While autoantibodies, including Anti-Nuclear Antibodies, Extractable Nuclear Antigen, Anti-DNA antibodies, Anti-Smooth Muscle Antibodies, Anti-phospholipid Antibodies, complement factors, and serum immunoglobulins were within the normal ranges. Immunological screening for celiac and thyroid disease were also negative. Serologic tests for Parvovirus B19, EBV, CMV, and Waaler-Rose test, were consistent with prior infection or non-immunized state. The fecal occult blood test was negative; chest radiograph, echocardiography and abdomen ultrasound were all unremarkable.\nShe underwent also bone marrow aspirate, that showed normal proportion of myeloid cells, presence of megakaryocytes, and mild dyserythropoiesis, without evidence of cytogenetic abnormalities.\nDuring corticosteroid therapy, hemoglobin levels slowly increased and Coombs test became negative within 3 months. Prednisone (1 mg/kg/bid) was continued for 10 months with progressive tapering. However, this therapy was associated with multiple side effects, such as alopecia, weight gain, moon face, stretch marks, including lymphopenia. This was also associated with reduction of IgG concentrations (IgG 520, n.v. 640–1909 mg/dl; IgM 115, n.v. 59–297 mg/dl, IgA 121, n.v. 61–301 mg/dl) which prompted us to start IVIG every 4 weeks for 3 months. In addition, because of the risks related to lymphopenia and to prolonged immunosuppressive therapy with corticosteroids, prophylaxis with cotrimoxazole and acyclovir was prescribed.\nIn order to exclude an underling immunodeficiency, we examined lymphocyte subsets. Flow cytometric immunophenotyping showed marked alterations in the distributions of the T-lymphocytes (Table ): reduction of the CD3+CD4+ T cells (19.7%), especially the Recent Thymus Emigrants (RTE) CD4+ T Cells (2.9%), and increase of the TCR γ/δ T cells (24.7%). Transitional B cells (0.4%), and terminal differentiated B cell subsets (0.06%) were reduced, while Switched Memory B cells (34.2%) were increased. T-cell Receptor Excision Circles (TRECs) and Kappa-deleting Recombination Excision Circles (KRECs) were below normal range, while analysis of the T-cell receptor repertoire showed a marked monoclonal expansion of TCRBV6 expressing cells. Increase of TCR γ/δ T cells could be related to many conditions, including infections. CD3+/CD4−/CD8− (double negative T cells) subset were in the normal range, thus ruling out the hypothesis of Autoimmune lymphoproliferative syndrome.\nNext, we analyzed by next generation sequencing (Ion Torrent pgm, Thermo Fischer) a panel of genes that are associated with SCID or CID/lymphopenia. Genetic analysis revealed an heterozygous mutation in exon 10 of the gene encoding for adenosine deaminase (ADA, p.S291L c.561C>T), while other genes that are associated with autoimmune diseases, including LRBA and CTLA4 were negative for mutations. Sanger sequencing of ADA gene coding and non-coding flanking regions revealed the same mutation. The assessment of adenosine and deoxyadenosine nucleotides levels in the patient at the time of lymphopenia revealed a moderate increase of both metabolites: adenosine was 3.6 μMol/ml RBC (n.v. 0.8–1.6) while deoxyadenosine was 0.006 uMol/ml RBC (n.v. < 0.005), respectively. Total AXP and dAXP in RBC were quantified by high performance liquid chromatography measuring the levels of Ado and dAdo formed by treating neutralized acid extracts with alkaline phosphatase and venom phosphodiesterase ().\nAnalysis of ADA activity in red blood cells lysates, as measured by spectrophotometric analysis of the absorbance change at 265 nm (), was reduced but within the normal range (0.8 U/g Hb; n.v. 0.8–2.5) while PNP activity in red blood cells lysates was normal (200 μ/g Hb; n.v >330). Analysis of ADA activity, of total AXP and dAXP in RBC in her parents were normal; unfortunately, their genetic status has not been investigated for parental decision.\nAfter corticosteroid tapering the patient's total numbers of lymphocytes gradually increased and reached normal levels (Figure ). One year after stopping corticosteroid therapy lymphocyte count was 1.410 cells/μL, with 550 CD4+cells/uL. Thus, she interrupted the prophylactic therapy with acyclovir and cotrimoxazole.
|
[[14.0, 'year']]
|
F
|
{'11445793': 1, '6115830': 1, '22184407': 1, '22447032': 1, '17614781': 1, '17765813': 1, '1284479': 1, '19633200': 1, '4795850': 1, '25875700': 1, '22350222': 1, '17274740': 1, '14760277': 1, '15498720': 1, '26376800': 1, '22969765': 1, '9758612': 1, '11807006': 1, '1468454': 1, '23335557': 1, '19638621': 1, '2596574': 1, '4117384': 1, '498598': 1, '8614422': 1, '9108404': 1, '30327760': 2}
|
{}
|
3,235 |
6174561-1
| 30,293,532 |
comm/PMC006xxxxxx/PMC6174561.xml
|
The first case of thrombocytopenia, anasarca, fever, renal impairment or reticulin fibrosis, and organomegaly (TAFRO) syndrome with unilateral adrenal necrosis: a case report
|
A 46-year-old Asian man without any significant past medical history presented to an out-patient clinic complaining of fever, epigastric pain, and back pain. He was diagnosed as having gastric ulcer by upper gastrointestinal endoscopy and prescribed a proton pomp inhibitor; however, his fever of approximately 38 °C and his back pain remained. Two weeks later, his back pain had worsened, and the laboratory data of the out-patient clinic showed an elevated C-reactive protein level (17.2 mg/dL); thus, he came to our hospital for further evaluation. His medication included only orally administered azelnidipine for hypertension. There was no significant family medical history. He denied smoking tobacco, alcohol consumption, and exposure to toxins. He worked at a ceremonial hall without any ill contacts. He had a fever of 37.9 °C, heart rate of 90 beats per minute (bpm), respiratory rate of 20 breaths/minute, blood pressure of 126/78 mmHg, and oxygen saturation of 97% on room air. A physical examination including a neurological examination showed a well man without any specific abnormal findings. Blood tests at the first encounter revealed a white blood cell count of 10,300/μL with 70% neutrophils, 14% lymphocytes, and 16% monocytes, and the platelet count was 275,000/μL. His lactate dehydrogenase level was 299 IU/L (normal range, 119–229 IU/L), his alkaline phosphatase level was 983 U/L (normal range, 103–335 U/L), and his gamma-glutamyl transpeptidase level was 256 IU/L (normal range, 0–73 IU/L). His C-reactive protein level was 23.47 mg/dL (normal range, 0–0.29 mg/dL). Other results are shown in Table . A contrasted computed tomography (CT) scan showed edema around his gallbladder without gallstones or bile duct dilation, along with left adrenal enlargement without contrast, suggesting necrosis and slight pleural effusion (Fig. ). His right adrenal gland was contrasted normally. Contrasted magnetic resonance imaging (MRI) of his adrenal glands was also performed, and the results showed necrosis of his left adrenal gland with a slight possibility of infarction and no specific evidence of hemorrhage. He was hospitalized for further investigation into the cause of the unilateral adrenal necrosis.\nLupus anticoagulant and don't break the value complex antibody were measured, and both were negative, which suggested a low possibility of antiphospholipid syndrome. He did not meet the criteria for diagnosis of systemic lupus erythematosus. We considered the possibility of adrenal insufficiency or pheochromocytoma and measured several types of adrenal hormones, such as serum cortisol, adrenocorticotropic hormone, plasma renin activity, plasma aldosterone activity, and urinary metanephrine and normetanephrine, but none of them explained our patient’s condition. The culture results from blood drawn at the first encounter were all negative. We performed CT-guided needle biopsy of his left adrenal gland, which revealed necrosis and the formation of fibrotic granulomatous tissue (Fig. ). There was no epithelioid granuloma, malignant lymphoma cells, or hemosiderin deposition, suggesting a low possibility of the involvement of a hemorrhagic etiology. The bacterial culture of this biopsy tissue was also negative. After the biopsy was finished, he was discharged. However, 1 week later, severe thrombocytopenia (5000/μL) appeared, and he was rehospitalized. His creatinine level had increased to 1.03 mg/dL from the initial value of 0.85 mg/dL. Bone marrow aspiration first resulted in a dry tap, but subsequent results showed increased megakaryocytes and hypercellular marrow with fibrosis classified as MF-1 according to the European consensus on bone marrow fibrosis staging (Fig. ). A contrasted CT scan showed new left axillary lymphadenopathy with a size of 15 mm, right pleural effusion, and increased ascites (Fig. ). Because our patient’s condition was worsening, we needed to start immediate treatment for any possible underlying causes, including bacterial infection and autoimmune disease, before obtaining the exact diagnosis. The laboratory data from the second hospitalization are shown in Table . The clinical course of this case is shown in Fig. . The initial treatment included ampicillin/sulbactam and a methylprednisolone pulse followed by orally administered prednisolone and intravenous immunoglobulin therapy (400 mg/kg for 5 days), considering the underlying causes mentioned above, such as severe bacterial infection or autoimmune diseases including antiphospholipid syndrome and immune thrombocytopenia; however, all of these treatments seemed to be ineffective. We also used recombinant thrombomodulin (380 U/kg) for 7 days to cope with the possibility of a thrombotic event or disseminated intravascular coagulation. Because the blood and adrenal gland biopsy culture results were both negative, we stopped the antibiotic treatment. On hospital day 9, we performed a left axillary lymph node needle biopsy, which showed no evidence of malignant lymphoma. With the edema, severe thrombocytopenia, fever above 37.5 °C, reticulin myelofibrosis (MF), mild lymphadenopathy, and progressive renal insufficiency and with other diseases excluded, we diagnosed this patient as having TAFRO syndrome according to the diagnostic criteria []. The administration of intravenously administered tocilizumab (8 mg/kg) was begun on the same day with tapering prednisolone dose; his C-reactive protein and alkaline phosphatase levels gradually improved, along with his renal function and fever (Fig. ). For the anasarca, furosemide and potassium canrenoate were used and were highly effective.\nBecause the thrombocytopenia remained, we added eltrombopag, a thrombopoietin receptor agonist, on hospital day 14, followed by tocilizumab administered on hospital day 16. Then, his platelet count began to increase. Under the strong immunosuppressive treatment, he contracted methicillin-resistant Staphylococcus epidermidis bacteremia on hospital day 20 and cytomegalovirus viremia on hospital day 31, which were successfully treated with vancomycin and ganciclovir, respectively. Tocilizumab was administered a third time on hospital day 47, and our patient was discharged on hospital day 48. After discharge, he remained afebrile and with an alkaline phosphate level within normal limits, and tocilizumab administration was no longer necessary. Eltrombopag administration was stopped because his platelet count increased and remained stable within normal limits. Nine months after the first treatment, this patient continues to do well. He is only being treated with low-dose prednisolone at approximately 5 mg per day and is still tapering carefully because of the presence of unilateral adrenal necrosis, considering the possibility of adrenal insufficiency.
|
[[46.0, 'year']]
|
M
|
{'27084250': 1, '29018798': 1, '26133054': 1, '33191324': 1, '10651763': 1, '28578446': 2, '30182658': 1, '28087540': 1, '20534952': 1, '29157613': 1, '28502946': 1, '27063975': 1, '26805758': 1, '30293532': 2}
|
{'5541190-1': 1}
|
3,236 |
6174575-1
| 30,344,840 |
comm/PMC006xxxxxx/PMC6174575.xml
|
Contraceptive Implant–Related Acute Ulnar Neuropathy: Prompt Diagnosis, Early Referral, and Management Are Key
|
A 22-year-old, right-hand-dominant woman was referred to our Plastic Surgery Department from her sexual health clinic 1 day postinsertion of a contraceptive implant (Implanon) in her left arm. It was explained that the implant was inserted by a nurse at the clinic who felt that the implant went in at “a slight angle, rather than superficial,” after the patient had flinched on insertion of the trochar. The subject experienced pain and paresthesia along her arm that had then subsided; however, she returned later that same day with worsening symptoms. On examination in the clinic, the implant was not palpable. The patient described paresthesia along the ulnar distribution of her hand and the forearm, as well as shooting pain on palpating the course of the ulnar nerve. Ultrasonography found the implant to be lying in the subfascial plane. On exploration in the operation theater, the implant was found lying in the perineurium, with the nerve itself intact (). The medial intermuscular septum was released and the implant was removed in one piece without the need to repair any structures. She recovered well postoperatively. On review in the clinic 4 weeks later, she had persistent hypersensitivity of the dorsoulnar aspect of the distal forearm and reduced sensation in the ulnar digital and radial digital nerves of the little finger. The power of the intrinsic muscles in the hand was normal. Three months after removal of the implant, all her ulnar nerve functions apart from a slight residual sensory alteration had returned to normal.
|
[[22.0, 'year']]
|
F
|
{'25288703': 1, '34201123': 1, '22770789': 1, '16121626': 1, '32555102': 2, '22003483': 1, '26252457': 1, '9743065': 1, '30344840': 2}
|
{'7944845-1': 1}
|
3,237 |
6174731-1
| 30,345,127 |
comm/PMC006xxxxxx/PMC6174731.xml
|
An Evaluation of Rapidly Progressive Dementia Culminating in a Diagnosis of Creutzfeldt–Jakob Disease
|
A 76-year-old male linguistics professor was referred to the general internal medicine service by emergency medicine for a 2-week history of worsening confusion. He was independent for his activities of daily living (ADLs) and his instrumental activities of daily living (IADLs) at his baseline 6 months ago. The family endorsed a cognitive decline that started with memory issues, word-finding difficulty, and unsteady gait. They also endorsed a history of agitation and hallucinations at night. In the 2 weeks prior to his emergency room visit, his symptoms progressed at an even more rapid pace, with him being too weak to ambulate, and experiencing new incontinence of urine and stool. Until the worsening of his cognitive deficits, he was still working as a linguistics professor at the postsecondary level.\nHis past medical history was significant for coronary artery disease, hypertension, type 2 diabetes, asthma, and benign prostatic hyperplasia. There was no personal or family history of malignancy or dementia. He had never been screened for malignancy. There was no history of hunting or consuming game meat. His medications included ASA, candesartan, hydrochlorothiazide, metformin, glimepiride, iron supplements, multivitamins, and timolol eye drops. There were no over-the-counter medications, illicit drugs, or alcohol. On exam, his vitals were stable. His mucous membranes were dry, and his JVP was flat. His cardiac, respiratory, and abdominal exams were unremarkable. His neurological exam revealed a slight upward gaze palsy and velocity-dependent hypertonia in the upper extremities. There were no fasciculations or myoclonus. Reflexes and sensation were intact.\nHis white blood cell count was 2.7 × 109 (normal 3.5–10.5), his hemoglobin was 134 g/L, and his platelets were 196 × 109. The electrolytes and extended electrolytes were within normal limits aside from sodium of 125 mmol/L (normal 136–145). LTFs and bilirubin were within normal limits, and TSH was 2.35 (normal), and B12 level was 278 pmol/L (normal). Syphilis and HIV serologies were both negative, as was the antinuclear antibody (ANA). A diffusion-weighted MRI demonstrated diffuse parenchymal volume loss that was prominent for age and mild microangiopathic changes. His EEG was abnormal but nonspecific with irregular periods of 6–7 Hz theta activity, intermingled with short 2–4 Hz delta rhythms most prominent in the frontal regions. There was no alpha activity or obvious epileptiform, focal, or lateralizing features. CSF showed a nucleated cell count of 6 (normal 0–5), normal glucose, and slightly elevated protein at 0.55 g/L (normal 0.15–0.45 g/L). Oligoclonal bands were not detected in the CSF. CSF was negative for tau and 14-3-3 protein but positive for end-point quaking-induced conversion (EP-QuIC) at the National Microbiology Laboratory in Winnipeg. The paraneoplastic (anti-hu, ri, yo, ma2, cv2, and amphiphysin) antibody panel (mitogen) was negative.\nHe developed myoclonus and mutism, and he was discharged to a palliative care facility. He passed away 8 weeks after his initial emergency room presentation. The postmortem autopsy of the brain demonstrated microspongiosis, neuronal loss, and gliosis in the cortex, hippocampus, basal ganglia, and cerebellum, consistent with sCJD.
|
[[76.0, 'year']]
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M
|
{'27249661': 1, '27042906': 1, '21364356': 1, '27076662': 1, '27235341': 1, '28028861': 1, '24640978': 1, '26089671': 2, '26646926': 1, '21091283': 1, '28360562': 1, '25998112': 1, '26413241': 2, '23795314': 1, '24934543': 1, '23634367': 1, '27656779': 1, '23229042': 1, '26754777': 1, '29346380': 1, '21674591': 1, '30345127': 2}
|
{'4572664-1': 1, '4572664-2': 1, '4572664-3': 1, '4468995-1': 1}
|
3,238 |
6174732-1
| 30,345,128 |
comm/PMC006xxxxxx/PMC6174732.xml
|
Acute Brucellosis Presenting with Bleeding Tendency due to Isolated Severe Thrombocytopenia
|
A 20-year-old male patient with no past medical history presented to the emergency room (at Jahra Hospital, Kuwait) with history of fever associated with malaise and arthralgia for 7 days. On arrival in the causality, he was febrile (39°C). Rest of the physical examination was normal. A history of ingesting unpasteurized camel's milk was reported, and a serological test for brucellosis was positive. A complete blood count (CBC) showed hemoglobin 145 g/L, WBCs 7.6 × 109/L with 45.6% lymphocytes and 49.2% neutrophils, and platelets 4 × 10/L. Other laboratory tests showed urea 3.6 mmol/L, creatinine 75.25 µmol/L, total bilirubin 16.1 µmol/L, ALT 48 IU/L, and AST 52 IU/L. There was severe isolated thrombocytopenia (4000), but no evidence of skin or mucous membranes bleeding. He denied use of any over-the-counter drugs, painkillers, or NSAIDs. The ER physician advised for hospital admission but he refused. Therapy with doxycycline and rifampicin was prescribed, but then he left against medical advice. Two days later, he returned to the emergency room with complaints of epistaxis, gingival bleeding, and hematuria. No hematemesis or melena was reported. He was febrile with a body temperature of 38.7°C, an arterial blood pressure of 110/75 mmHg, and a heart rate of 72 beats/min. There was nonitchy flat purpuric rash, particularly on his lower extremities. His physical examinations of the cardiovascular, respiratory, abdominal, and central nervous systems were normal. Repeat CBC showed hemoglobin 128 g/L, WBCs 4.9 × 109/L with 51.8% lymphocytes and 41.1% neutrophils, and platelets 2 × 109/L. A peripheral blood smear examination showed normal RBCs, WBCs morphology, and marked thrombocytopenia with occasional giant platelets and no platelet clumps. When true thrombocytopenia was confirmed and to exclude other causes of thrombocytopenia, malaria blood film, coagulation profile, fibrinogen level, antinuclear antibody (ANA), double-stranded DNA antibody (anti-ds DNA), and serological tests for HbsAg, anti-HCV, HIV, cytomegalovirus, and Ebstein–Barr virus all were unremarkable. Brucella agglutination test was positive (titer 1 : 1280). We considered a diagnosis of brucellosis with immune thrombocytopenic purpura. Due to the very low platelet count and the mucous membrane hemorrhage, 12 units of platelets were infused. Treatment with intravenous immunoglobulin (IVIg) was initiated at a dose of 500 mg/kg/day, combined with prednisolone (1 mg/kg/day), doxycycline (100 mg/12 hours), and rifampicin (600 mg/day). Fever resolved on the second day of treatment, platelet count started to rise, and bleeding manifestations improved. On the 6th day, his platelet count was 66000, and he was discharged from hospital on tablet prednisolone of 25 mg daily with gradual tapering, tablet rifampin of 600 mg daily, and capsule doxycycline of 100 mg twice a day for total six weeks. Blood cultures performed on specimens obtained at the time of admission showed no growth. He was planned for follow-up one month after discharge from the hospital, but he did not show up. A follow-up phone call confirmed that all his symptoms resolved and he finished his treatment course.
|
[[20.0, 'year']]
|
M
|
{'11049768': 1, '28459811': 1, '10762113': 1, '17988299': 1, '3353631': 1, '16439329': 1, '19910232': 1, '19846889': 1, '6481187': 1, '12949890': 1, '30345128': 2}
|
{}
|
3,239 |
6174736-1
| 30,345,125 |
comm/PMC006xxxxxx/PMC6174736.xml
|
Chronic Myeloid Leukemia Relapsing 25 Years after Allogenic Stem Cell Transplantation
|
A previously healthy 41-year-old woman was diagnosed with CML, after presentation of symptoms caused by hypersplenism with gravity sensation under the right costal margin. Initial blood tests demonstrated severe leukocytosis 227 × 109/L (normal range 4–11 × 109/L) together with increased serum concentration of lactate dehydrogenase (LDH) 969 U/L (200–450 U/l) and cobalamin 2834 pmol/L (150–840 pmol/L). A blood smear demonstrated dominance of myeloid precursor with increased metamyelocytes and rods. CML was confirmed by identification of the Philadelphia chromosome t(9; 22) by using conventional G-banding analyses.\nTreatment was initiated with hydroxyurea combined with interferon, and the patient reached morphological remission, then proceeded to allo-SCT for consolidation treatment. The transplantation was performed by a myeloablative condition (MAC) regime with busulphan 1 mg/kg for four days followed by cyclophosphamide 60 mg/kg for two days, followed by bone marrow-derived stem cell from her human leukocyte antigen- (HLA-) matched sister. Standard graft versus host disease (GVHD) prophylaxis by using cyclosporine A and methotrexate on day 1, 3, 6, and 11 after transplant was given []. No severe complications were observed after transplant, and especially, she did not develop any signs of acute or chronic GVHD.\nAfter the development of polymerase chain reaction (PCR) analysis for BCR-ABL1 transcripts [], this test has been regarded as mandatory in the follow-up of CML patients []. Six years after the allo-SCT, an e13a2 transcript of BCR-ABL1 was detected by nested PCR. She was therefore controlled twice yearly, without signs of progression judged from karyotyping and interphase fluorescence in situ hybridization (FISH) of 200 interphases with probes against BCR and ABL1 in the bone marrow. By standardization of quantitative real-time (RT) PCR, yearly analyses were performed [], and low but detectable transcript levels were still observed, although molecular remission (MR) levels were below MR3.\nHer transcript levels then suddenly increased rapidly, and she lost her MR (). This was confirmed by analysis at two different laboratories. The patient proceeded to bone marrow examination showing normal metaphases by G-banding and only one cell with BCR-ABL1 of 245 interphases by FISH using dual fusion probes, and this was regarded as insignificant. The bone marrow smear was hypercellular with increased myeloid precursors and megakaryocytes, although without evidence of increased myeloblasts. Hence, we maintained the diagnosis of CML with molecular relapse appearing 25 years after initial allo-SCT. The patient was screened for other mutations commonly occurring in myeloid malignancies, including mutations in BCR-ABL1, but no additional mutations were detected. Donor chimerism status revealed that the majority of myeloid cells (99%) were of donor origin. We thought that her relapsed disease was likely to be sensitive to treatment with first-generation TKI, and she was given imatinib 400 mg daily. She tolerated the treatment well without major side effects; after three months, she obtained MR4 status (), and imatinib treatment was continued with regular monitoring of BCR-ABL1 quantitative RT-PCR.
|
[[41.0, 'year']]
|
F
|
{'11238091': 1, '27793879': 1, '16449534': 1, '11287972': 1, '24252361': 1, '25387087': 1, '19344950': 1, '17875506': 1, '23823695': 1, '28522574': 1, '8259165': 1, '12970768': 1, '23803709': 1, '27552202': 1, '19811825': 1, '10231146': 1, '12176876': 1, '4126434': 1, '27297665': 1, '27252811': 2, '3510388': 1, '25581405': 1, '9053463': 1, '23892326': 1, '28421151': 2, '28159740': 1, '8114834': 1, '23486457': 1, '25348512': 1, '15297408': 1, '24712979': 1, '19194468': 1, '21354617': 1, '30345125': 2}
|
{'4888147-1': 1, '5379078-1': 1}
|
3,240 |
6174737-1
| 30,345,131 |
comm/PMC006xxxxxx/PMC6174737.xml
|
Long-Lasting Symptomatic Cerebral Hyperperfusion Syndrome following Superficial Temporal Artery-Middle Cerebral Artery Bypass in a Patient with Stenosis of Middle Cerebral Artery
|
A 39-year-old woman, who had been taking medication of quetiapine as an antipsychotics for depression, experienced mild dysarthria and visited the department of neurology in our hospital. Her symptom was diagnosed as drug-induced lip dyskinesia, which disappeared in a week. Screening head magnetic resonance imaging (MRI) at this time revealed stenosis of the left MCA with no brain parenchymal lesions (), why she was consulted to our department. We performed angiography, confirming moderate M1 portion stenosis (Figures and ). SPECT showed no apparent laterality in CBF, thereby we decided to observe her with no treatment.\nSeven months later, the patient experienced mild weakness and numbness in her right hand and visited our department. Although MRI showed no apparent ischemic change in her brain, arterial spin labelling (ASL) of MRI detected the decrease of CBF in the left cerebrum (), which was thought to well correspond for her symptoms. She was admitted and treated with an antiplatelet agent. Two weeks later, she still complained of numbness in her right hand; thereby, we decided to perform left STA-MCA anastomosis to prevent deterioration of her symptoms. Preoperative SPECT showed no apparent laterality in CBF (). On operation, left temporal craniotomy was performed, and the parietal branch of the STA was anastomosed with the M4 portion on the temporal lobe (Figures and ). The intraoperative course was uneventful, and the patient recovered from anesthesia without any new neurological symptoms\nPostoperatively, her speech was normal until postoperative day 1 (POD1). On POD2, she exhibited mild speech disturbance, which worsened day by day finally resulting in complete motor aphasia on POD6. Her comprehension was kept normal. On POD3, generalized convulsion occurred, which ceased quickly by diazepam, and levetiracetam was initiated. On the same day, she presented with mild weakness of right upper extremity, which improved gradually and disappeared on POD7. MRI and CT showed no ischemic or hemorrhagic changes, but ASL and SPECT revealed remarkable increase of CBF in the left cerebrum (Figures and ), by which the symptoms were diagnosed as CHPS. Despite the treatment with strict blood pressure and the administration of edaravone and minocycline, complete motor aphasia remained unchanged on POD21. MRI showed no abnormality except slightly hypointense changes on T2 weighted images and FLAIR (). At this point, the patient was discharged partly because of the request from the patient, and we continued to follow her in outpatient visit. One month after the surgery, the patient started to utter words that were not fluent, when SPECT and MRI showed normalization (). Thereafter, the improvement of her speech was slow, and totally more than three months was taken for full recovery after the surgery.
|
[[39.0, 'year']]
|
F
|
{'25139421': 1, '25746308': 1, '15501694': 1, '23087822': 2, '9183345': 1, '12959438': 1, '21501047': 1, '3941347': 1, '25294058': 1, '18077950': 1, '15185765': 1, '28664022': 1, '27516025': 1, '17486352': 1, '24641716': 1, '17320638': 1, '27174526': 1, '23274781': 1, '24176958': 1, '16297845': 1, '3351580': 1, '22850406': 1, '21221039': 1, '20361293': 1, '30345131': 2}
|
{'3475882-1': 1}
|
3,241 |
6174740-1
| 30,345,123 |
comm/PMC006xxxxxx/PMC6174740.xml
|
Focal Intramucosal Adenocarcinoma Occurring in Gastric Hyperplastic Polyps Treated with Endoscopic Mucosal Resection
|
A 59-year-old woman with epigastralgia was evaluated in gastroenterology and an upper digestive endoscopy was indicated. During the endoscopic examination a gastric polyp was found and the patient was referred to our hospital for treatment.\nEndoscopic examination of the upper digestive tract revealed extensive atrophic gastritis and a sessile lesion of 15 mm of reddish coloration in the distal gastric body (). Magnifying endoscopy with Fuji Intelligent Color Enhancement (FICE) of the polyp showed an irregular microsurface pattern at the apex, noticing a demarcating line, highly suggestive changes of malignancy (). Endoscopic mucosal resection (EMR) was performed with lateral safety margins (Figures and ).\nThe histopathological evaluation of the resected polyp revealed that the base corresponded to a hyperplastic polyp, in which a tubular adenoma with high-grade dysplasia was established with focal well-differentiated intramucosal tubular adenocarcinoma (). The lesion was resected completely with a lateral margin greater than 2 mm. No evidence of lymphovascular invasion was noticed. For this reason, it was concluded that the EMR was successfully performed fulfilling the criteria of histological cure []. The polyp with focal adenocarcinoma was classified as early gastric cancer, type 0-Is according to the Paris classification, and T1a according to the TNM classification []. Histopathological evaluation of the surrounding mucosa revealed atrophic gastritis in the body and antrum, with no evidence of Helicobacter pylori infection.
|
[[59.0, 'year']]
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F
|
{'24929480': 1, '17334711': 1, '24765156': 1, '23583466': 1, '28975540': 1, '26345287': 2, '16189701': 1, '20458557': 1, '25361760': 2, '29851815': 1, '28842047': 1, '29607431': 1, '27833379': 1, '34306396': 1, '22912909': 1, '30345123': 2}
|
{'4863182-1': 1, '4539450-1': 1, '4539450-2': 1}
|
3,242 |
6174746-1
| 30,345,136 |
comm/PMC006xxxxxx/PMC6174746.xml
|
Generalized Anxiety Disorder in Very Young Children: First Case Reports on Stability and Developmental Considerations
|
Case 1. Dustin, a five-year-old White male, was brought to the clinic by his mother for her chief concern of defiance and emotional dysregulation. During the first diagnostic interview, Dustin's worries included any social situations that included scrutiny from others (e.g., he refused to stand in front of the church for his baptism), death, feeling anxious in places where he does not have control, and intense fear of bugs. Worries occurred almost daily and appeared somewhat uncontrollable. At the second interview, two weeks later, his worries remained the same but now included getting lost. At school, his negative emotionality could escalate into tantrums of screaming and trying to bang his head on a wall, which could last two hours. At home, getting him to take a bath could involve an hour of crying and protesting. Symptoms first appeared at one-and-a-half years but because he was preverbal at that age his mother could not give examples that clearly met GAD criteria.\nPhysical symptoms present during Dustin's periods of worry included feeling restless, on edge, difficulty concentrating, and irritability. Functional impairment included a slight impact on parental relationships, a moderate impact on the relationship with his daycare provider, and a severe impact on the child's ability to go out in public. His mother almost always accommodated him by rarely taking him outside of the home.\nDustin met all of the criteria for GAD, ODD, and SAD. His treatment involved helping learn ways to calm himself and help his parents manage his behavior. He improved markedly by the end of the school year and treatment terminated over the summer. But his behavior flared up when school resumed and treatment had to be restarted.
|
[[5.0, 'year']]
|
M
|
{'16492262': 1, '15167092': 1, '28554154': 1, '24062146': 1, '27072682': 1, '16601400': 1, '29081005': 1, '22018968': 1, '20052532': 1, '15968234': 1, '27942997': 1, '20658807': 1, '25359313': 1, '9886222': 1, '28449199': 1, '19212972': 1, '30345136': 2}
|
{'6174746-2': 2, '6174746-3': 2}
|
3,243 |
6174746-2
| 30,345,136 |
comm/PMC006xxxxxx/PMC6174746.xml
|
Generalized Anxiety Disorder in Very Young Children: First Case Reports on Stability and Developmental Considerations
|
Case 2. Ivan, a five-year-old white male, was brought to the clinic by his mother for her chief concern of his worries about death. During the first diagnostic interview, Ivan was described as having excessive worries related to something happening to his family, death, Earth being sucked into a black hole, criminals harming someone in the family, and separating from parents when going to school. He worried that other children did not like him and that he would not do a good job on tasks. Symptoms first appeared at age four years.\nHis worries appeared clearly uncontrollable to his mother. Physical symptoms present during Ivan's periods of worry included difficulty concentrating. Functional impairment was endorsed in the parental relationship.\nNo excessive worries were endorsed during the second diagnostic interview even though those interviews were only two weeks apart. However, when his medical record was reviewed for this paper, it was clear that he had the same worries consistently for two years following those interviews up to the present time.\nIvan met all of the criteria for GAD plus SAD. He had not yet improved markedly after two years of treatment.
|
[[5.0, 'year']]
|
M
|
{'16492262': 1, '15167092': 1, '28554154': 1, '24062146': 1, '27072682': 1, '16601400': 1, '29081005': 1, '22018968': 1, '20052532': 1, '15968234': 1, '27942997': 1, '20658807': 1, '25359313': 1, '9886222': 1, '28449199': 1, '19212972': 1, '30345136': 2}
|
{'6174746-1': 2, '6174746-3': 2}
|
3,244 |
6174746-3
| 30,345,136 |
comm/PMC006xxxxxx/PMC6174746.xml
|
Generalized Anxiety Disorder in Very Young Children: First Case Reports on Stability and Developmental Considerations
|
Case 3. Alani was a six-year-old Pacific Islander female who was brought to the clinic by her mother for her chief concern of fear of bad weather. No other excessive worries were endorsed during the first interview, so her fear of weather was conceptualized as PTSD initially. During the second interview however Alani was described as having excessive worries related to peers making fun of her, grades, sickness, and worries about the safety of other people. Her treating clinician had been unaware of these. Her worries appeared clearly uncontrollable to her mother. Her symptoms first appeared at age four years.\nPhysical symptoms present during Alani's worry episodes included restlessness, feeling on edge, irritability, and problems sleeping. No functional impairments or accommodations were endorsed by her mother. Alani's clinician reported however that Alani experienced marked impairment due to her worries and severe restrictions on her activities, as her impairment was a central focus of the therapy.\nAlani met all of the criteria for GAD, PTSD, and ODD. She improved markedly over thirteen sessions of psychotherapy.
|
[[6.0, 'year']]
|
F
|
{'16492262': 1, '15167092': 1, '28554154': 1, '24062146': 1, '27072682': 1, '16601400': 1, '29081005': 1, '22018968': 1, '20052532': 1, '15968234': 1, '27942997': 1, '20658807': 1, '25359313': 1, '9886222': 1, '28449199': 1, '19212972': 1, '30345136': 2}
|
{'6174746-1': 2, '6174746-2': 2}
|
3,245 |
6174749-1
| 30,345,121 |
comm/PMC006xxxxxx/PMC6174749.xml
|
An Unusual Presentation of Acute Weakness: Acute Inflammatory Demyelinating Polyneuropathy in a Patient with Psychiatric Illness
|
A 58-year-old male presented to the emergency department via private vehicle with multiple complaints. Complaints included “chest discomfort”, low back pain, shortness of breath, generalized weakness throughout all extremities, and “numbness” of bilateral lower extremities. These symptoms began acutely at around 10 hours prior to arrival when he awoke from a dream. The patient stated during the dream that he was in an earthquake and his legs were trapped and crushed in the earthquake; when he awoke both of his lower extremities were numb and weak. He states that all of his symptoms are progressively getting worse and now he “can't move my legs.”\nThe patient's past medical history is significant for chronic back pain, anxiety, bipolar disorder, schizophrenia, major depressive disorder, and an episode of previous “paralysis.” The patient states in 1997 that he had a lumbar fusion and while in rehab he “became paralyzed and couldn't move my legs or walk” and that episode of weakness gradually improved and paralysis resolved without any medical intervention. The patient takes a total of 23 for his medical conditions that include zolpidem, methocarbamol, hydrocodone, carisoprodol, alprazolam, and gabapentin.\nVital signs at time of presentation are benign and reveal a temperature of 99.20 F, HR 68, BP 156/84, and Sating 95% on RA. General exam reveals a nontoxic patient in no acute distress, with a disheveled appearance. Neurological exam reveals that patient is alert and orientated X 3, with a GCS of 15, CN 2-12 intact, and 5+ bilateral upper extremity strength, normal finger to nose movement. Decreased bilateral patellar DTRs and decreased bilateral lower extremity strength 4/5. Otherwise physical exam was within normal limits.\nA CBC, CMP, CK, sed rate, UA, UDS, Troponin-I, D-dimer, EKG, noncontrast CT's of head and C-spine, and CT of chest/abdomen/pelvis with IV contrast to evaluate aorta with spinal reconstruction were ordered. Pertinent labs results include normal Troponin and D-dimer, calcium 10, sed rate of 9, CK of 437, UDS positive for benzodiazepines and opiates (both of which are chronic medications prescribed to patient), and otherwise unremarkable labs and all imaging within normal limits.\nThe patient was now reevaluated. We discussed how his evaluation is unremarkable and cannot explain his symptoms. He responds with “Doc, it's getting worse and now I can't move my legs at all.” A repeat neurological exam revealed decreased sensation and bilateral lower extremity strength now 0/5. Pinprick sensation not detected and elicited no movement, despite pinprick drawing blood.\nAt this point, the evaluation had ruled out electrolyte abnormalities, acute myocardial infarction, pulmonary embolism, aortic dissection, acute CVA, spinal pathology, or tick paralysis as potential causes for the patient's acute weakness. The differential diagnosis continued to include Multiple Sclerosis, Myasthenia Gravis, medication reaction, conversion disorder, and Guillain-Barré syndrome. In light of the patient's psychiatric history, atypical complaints, disheveled appearance, medication list, and history of onset related to a dream in which his lower extremities were crushed, the overall clinical picture suggests a psychosomatic conversion disorder. However, this is a diagnosis of exclusion after CNS, peripheral nervous syndrome, infections, vascular, cardiopulmonary, and other potentially life threatening etiologies are excluded and therefore, the medical decision was made to proceed with lumbar puncture and CSF analysis, as well as MRI to fully rule out neurological pathology.\nThe procedure was complicated secondary to patient's history of lumbar fusion surgery from L4-S1 twenty years previously. Scar tissue at the L3-L4 spinal space made the procedure difficult and failed three times. Pt was informed of the difficulty and he states “please Doc, try one more time.” At the insistence of the patient, a fourth attempt at lumbar puncture was made and successfully returned CSF that revealed RBC 0, WBC 2, glucose 66, and protein 73.\nFurthermore, an MRI was performed that revealed enhancement of bilateral nerve roots throughout entire thoracic and lumbar spine consistent with Acute Inflammatory Demyelinating Polyneuropathy (AIDP), a form of Guillain-Barré syndrome.\nThe patient was admitted to ICU, underwent 5 rounds of plasmapheresis, physical, and occupational therapy, improved, and was able to ambulate out of the hospital less than 2 weeks later. He never required intubation.
|
[[58.0, 'year']]
|
M
|
{'7600081': 1, '10402024': 1, '23642721': 1, '18848313': 1, '9746040': 1, '8995165': 1, '25072194': 1, '11871407': 1, '10526194': 1, '14975602': 1, '15958123': 1, '23983841': 1, '8437711': 1, '11844894': 1, '24163275': 1, '26351312': 1, '7477117': 1, '21631649': 1, '8797486': 1, '1514781': 1, '10959233': 1, '12429589': 1, '27596231': 2, '10599792': 1, '9989618': 1, '20837305': 1, '12694112': 1, '10716250': 1, '8968214': 1, '20600491': 1, '23826482': 2, '22470650': 1, '16000335': 1, '16271648': 1, '15102364': 1, '30345121': 2}
|
{'5011863-1': 1, '3698236-1': 1}
|
3,246 |
6174750-1
| 30,320,298 |
comm/PMC006xxxxxx/PMC6174750.xml
|
Cutaneous Angiosarcoma Postmastectomy (Stewart-Treves Syndrome)
|
A 70-year-old woman underwent a right-sided mastectomy and axillary lymph node excision because of invasive adenocarcinoma in 2007. She received additional radiotherapy on the mastectomy site and the right axilla. Extensive lymphedema of the right arm developed and formed ecchymosis, which persisted despite a microsurgical lymphovenous derivation in 2009. On clinical examination in 2017, a painful nodular and purpuric transformation of the skin was noted. Because of increasing pain in the upper arm, a biopsy of the skin was performed, revealing a cutaneous epitheloid angiosarcoma. The patient was referred for magnetic resonance imaging (MRI) of the right upper arm to evaluate local extent.\nAxial Tau Inversion Recovery (TIR) and T1-weighted images of the right upper arm (Figure and ) show a diffusely thickened cutis and subcutis with extensive lymphedema (arrowheads), as well as muscle edema (asterisk). There is an amorphous mass extending from the ventral cutis to the biceps muscle (arrows in Figure and ) with spicular infiltration reaching the neurovascular bundle. This mass has an intermediate signal on T1-weighted and a heterogeneous high signal on TIR images, and shows heterogeneous contrast enhancement (Figure ).\nThe patient was treated with an amputation of the affected arm. Follow-up CT examination revealed progressive disease with new subcutaneous and intramuscular metastases in the right hemithorax, and the additional follow up MRI revealed diffuse skeletal metastasis.
|
[[70.0, 'year']]
|
F
|
{'22682884': 1, '30320298': 2}
|
{}
|
3,247 |
6174754-1
| 30,320,299 |
comm/PMC006xxxxxx/PMC6174754.xml
|
Retro-Odontoid Pseudotumor in a Patient with Atlanto-Occipital Assimilation
|
A 67-year-old female, with a typical presentation of carpal tunnel syndrome in the right hand, presented initially with numbness in digit IV and V a year later. A few months later, she developed numbness in all five fingers on the left side. Furthermore, the patient mentioned that she had had a burning sensation in both feet for a few years. Another few months later she complained of weakness in all four limbs and was sent for a neurological consultation with electromyography. Clinical examination revealed a Hoffmann-Trömner reflex on the left side, mild loss of strength in both hands, loss of vibratory sense and hypoesthesia in the distal end of all four limbs and loss of proprioception in both legs. The electromyography showed disturbed sensorimotor signals in the left hand and mildly disturbed sensorimotor signals in the right hand. The disturbed electromyography was attributed to carpal tunnel syndrome, which was presumably less severe on the right side due to treatment with long acting corticosteroid injections. The paresthesia in digit IV, digit V and both feet, however, could not be explained with the diagnosis of carpal tunnel syndrome. Therefore, magnetic resonance imaging (MRI) of the cervical spine was performed. Imaging showed an extra-dural soft tissue mass posterior to the odontoid process of the axis. The mass extruded through the transverse ligament of the atlas with severe compression of the myelum and myelomalacia at the level of C1 (Figures , and ).\nA plain radiograph of the cervical spine was performed to check for atlanto-axial instability. The radiograph during flexion shows a slightly widened atlantodental interval, measuring 4 mm (normal value: <3 mm) (Figure and ).\nPre-operative imaging of the cervical spine also revealed an anatomical variant of the craniocervical junction, atlanto-occipital assimilation of the massa lateralis bilaterally (Figure ).\nThe patient was treated with laminectomy of C1 to decompress the spinal canal followed by posterior fixation of C1-C2 for stability.
|
[[67.0, 'year']]
|
F
|
{'16651215': 1, '1955901': 1, '33211944': 1, '3763907': 1, '33381556': 1, '10664422': 1, '33819944': 1, '27857933': 2, '18928224': 1, '30868232': 1, '23386281': 1, '24048650': 1, '27081234': 1, '25788812': 1, '10029181': 1, '19179910': 1, '30320299': 2}
|
{'5110914-1': 1}
|
3,248 |
6174758-1
| 30,345,132 |
comm/PMC006xxxxxx/PMC6174758.xml
|
A Malignant Squeeze: A Rare Cause of Cardiac Tamponade
|
An 85-year-old female with past medical history of recurrent deep venous thrombosis, pulmonary embolism on anticoagulation with a vena cava filter in place, rheumatoid arthritis, hypertension, hyperlipidemia, hypothyroidism, and type 2 diabetes mellitus presented to the emergency department with complaint of exertional dyspnea and chest pain. She denied fever, chills, or lower extremity edema and had no history of malignancy, weight loss, or night sweats. Initial vitals revealed BP of 86/62 mmHg that decreased to 79/60 mmHg with inspiration. Initial pulse was 95 bpm, and respiratory rate was 20. White blood cell count was mildly elevated at 11.5, troponins were normal, and electrocardiogram was unremarkable. D-dimer was elevated at 1290. Patient was sent for CT scan to evaluate for pulmonary embolism, and a moderate pericardial effusion was found (). Subsequently, an echocardiogram was done to further delineate the effusion which revealed a large circumferential effusion with mild respiratory variation concerning for impending cardiac tamponade (). She was admitted to the intensive care unit and underwent emergent pericardiocentesis. Flow cytometry of the pericardial fluid revealed a population of monoclonal B-cells with significant large cell component (). The overall morphologic and immunophenotypic features were consistent with high-grade B-cell lymphoma with t(8; 14) (). Bone marrow biopsy demonstrated monotypic B-cells compatible with the diagnosis of large B-cell lymphoma. The patient was started on rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) with an excellent initial response. She was transferred out of the ICU within days and discharged home for outpatient follow-up.
|
[[85.0, 'year']]
|
F
|
{'9338475': 1, '20605278': 1, '9134285': 1, '14989742': 1, '8697472': 1, '8980266': 1, '28287210': 1, '23324228': 1, '21892927': 2, '14565636': 1, '20306995': 1, '30345132': 2}
|
{'3180417-1': 1}
|
3,249 |
6174764-1
| 30,345,138 |
comm/PMC006xxxxxx/PMC6174764.xml
|
Yellow Nail Syndrome with Bilateral Pleural Plaques and Diffuse Pleural Thickening: A Mimic of Asbestos Related Disease
|
A 62 year-old male was diagnosed with yellow nail syndrome in 2000. He had a long history of recurrent sinusitis from 1983 and had developed numerous respiratory tract infections since 1996. Primary lower limb lymphoedema was diagnosed in 2000. Shortly thereafter he developed recurrent, initially right pleural effusions. Repeat thoracocenteses had revealed cloudy, thick fluid, exudative in nature. A right video-assisted thoracoscopic pleural biopsy was performed which showed chronic inflammation and reactive mesothelial changes but no malignancy. The diagnosis of yellow nail syndrome was made when xanthonychia developed in 2000. The clinical course continued with the development of bronchiectasis in 2003, complicated by recurrent chest infections and bilateral effusions.\nThe subject had a history of heavy prior tobacco smoking and had worked as a general manager, policeman, clothing design director, and dark room technician.\nHe died in 2010 following an infective exacerbation of his bronchiectasis.\nA CT scan performed shortly before his death showed extensive right pleuroparenchymal disease, including right diffuse pleural thickening, bronchiectasis and right airspace shadowing ().\nA postmortem examination was performed. External examination revealed the presence of yellow discolouration affecting the finger- and toenails (), along with bilateral lower leg oedema. Examination of the respiratory system showed extensive bilateral pleural adhesions, diffuse visceral pleural thickening and parietal pleural plaques (). Microscopical examination confirmed the presence of paucicellular hyaline collagenous plaques with ‘basket-weave' pattern, bilateral diffuse pleural fibrosis composed of similarly paucicellular collagen, and occasional lymphoid aggregates (). Septal lymphatics were noted to be markedly dilated (). A right-sided lobar pneumonia with organisation was present. Careful inspection of multiple lung sections by light microscopy failed to detect any asbestos body formation. There was a talc pleurodesis reaction in the right pleural space. Within the lung tissue bilaterally, remote from pleura, platy form polarisable material was seen consistent with talc particulates (). Other organ systems showed no significant abnormality.\nMineral analysis performed on tissue from the left lung by transmission electron microscopy and energy dispersive X-ray spectrometry detected: no commercial or noncommercial amphibole asbestos fibres or serpentine chrysotile asbestos. Fibrous mullite, a nonasbestos aluminium silicate, fibrous silica and muscovite were detected, confirming a technically successful analysis. Non-fibrous mineral analysis detected silicon, talc, aluminium, titanium, and iron.\nCause of death was recorded as yellow nail syndrome complicated by infection (lobar pneumonia) and diffuse pleural fibrosis (immediate cause).
|
[[62.0, 'year']]
|
M
|
{'25123563': 1, '14140738': 1, '26744684': 1, '3660310': 1, '28241848': 1, '30345138': 2}
|
{}
|
3,250 |
6174765-1
| 30,345,130 |
comm/PMC006xxxxxx/PMC6174765.xml
|
Uncommon Association of Two Anatomical Variants of Cerebral Circulation: A Fetal-Type Posterior Cerebral Artery and Inferred Artery of Percheron, Complicated with Paramedian Thalamomesencephalic Stroke—Case Presentation and Literature Review
|
This is a retrospective case study of a slim 37-year-old man exhibiting associated lifestyle risk factors (chronic marijuana and tobacco abuse, but neither alcohol excess, nor other illicit drugs) who suffered an acute thalamomesencephalic stroke, rapidly worsening to a comatose state.\nFamilial and personal medical history was negative for associated cardiocerebrovascular pathology or other specific risk factors.\nIn the evening that preceded the cerebral infarction, he submitted a large and elaborate tattoo over the left hypochondrium and abdominal (lumbar) flank and smoked a few cigarettes with cannabis.\nThe following morning, he experienced acute onset of dizziness, visual, speech, and gait disturbances.\nHe was admitted to the emergency room with walking difficulties, disturbed balance and coordination of movements, slurred speech, diplopia, confusion, and left palpebral ptosis. Neurological examination revealed right-sided severe ataxic hemiparesis, dysarthria, left palpebral ptosis and mydriasis, divergent strabismus, and fluctuating consciousness (Glasgow coma scale, GCS 10/15).\nBlood tests (white blood cells count, hemoglobin, electrolytes, liver, and renal function) revealed normal results. Urine toxicology at admission was positive only for tetrahydrocannabinol; no other illicit drugs were present on tox screen. Electrocardiogram (EKG) and chest X-ray findings were normal. Clotting tests were normal [antithrombin III was 108% (>80%), homocysteine was 7.5 μmol (≤ 12), lupus anticoagulant was negative, antinuclear antibodies were 0.3 UM (<0.7), C protein was 117% (70-130)].\nEmergent computed tomography (CT) scan on the day of admission showed no gross abnormality and no evidence of cerebral hemorrhage or encephalitis.\nIn a few hours he become comatose (GCS 7/15) and was transferred to the intensive therapy unit. Intubation and ventilation support were not necessary. EKG monitoring during admission in the intensive care unit did not revealed pathological aspects.\nAt about 20 hours after the onset of stroke, magnetic resonance imaging (MRI) of the brain and angiography (MRA) were also performed (). These revealed acute paramedian thalamic ischemic lesions extending to the rostral midbrain (asymmetrically, mainly on the left side). The imaging showed no evidence of cerebral venous occlusion, infiltrative neoplasm, severe infectious and inflammatory lesion, or a large embolus at the basilar tip, with stroke in the posterior circulation. MRA showed patency of the basilar and vertebral arteries, a normal appearance of the left P1 arterial segment and left PCA, and a right-sided full FPCA. Our 1.5-Tesla MRI device failed to visualize the TPAs; the left AOP was just presumed.\nHe recovered from a coma after 4 days and exhibited a slow, progressive evolution. Initially, he presented with severe alternating (superior) oculomotor hemiplegia (Weber syndrome), with left-sided oculomotor nerve palsy, a drooping eyelid and fixed-width pupil pointed down and out, diplopia, and dysarthria associated with contralateral severe ataxic hemiparesis.\nBased on clinical and neuroimaging findings, the positive diagnosis was acute ischemic stroke in the territory of the left AOP. The clinical spectrum of the AOP infarct was outlined in the frame of a “thalamopeduncular" syndrome, associated with the typical symptoms of bilateral paramedian thalamic infarcts (confusion and coma), accompanied by with oculomotor disturbances, contralateral hemiplegia, and cerebellar ataxia.\nAfter the acute episode, he was admitted on the neurorehabilitation department. He clinically manifested a paramedian midbrain syndrome, combining the previously described left-sided oculomotor impairment with moderate right-sided ataxic hemiparesis without hemianesthesia, tremor, dysmetria, dysarthria, and depression. Repeated EKG and blood tests and a transthoracic echocardiogram, respectively, did not reveal pathological aspects.\nThe diagnosis was established retrospectively, after a delay of 20 hours, too late for thrombolytic management. He initially received anticoagulant therapy (heparin for 3 weeks in the acute stroke department), followed by a novel oral anticoagulant for another 5 weeks during rehabilitation. He was discharged with small doses of aspirin, up to six months, as secondary prophylaxis. Statins were not administered, either in the acute or during the subacute stage.\nHe had a good evolutive trend and was discharged with a modified Rankin score (mRS) 3. Psychological evaluation emphasized a marked improvement of his masked depression and augmentation of the Mini-Mental State Examination (MMSE) score (from 23 to 29/30).\nHe completely changed his lifestyle, with abstinence from both tobacco and cannabis, and continued the rehabilitation program as an outpatient. He exhibited favorable outcomes, with no vascular recurrence.\nFour months after the acute stroke he achieved a mRS 2 and was slightly disabled and still unable to carry out all previous activities, especially professional ones (driver). Most symptoms abated, except for slight visual blurring, diplopia, and residual left third cranial nerve palsy.\nFavorable neurological results were consistent with repeated neuroimaging tests for control. Contrast-enhanced MR angiography remained unchanged. MRI showed no acute recurrences, but only small residual lacunae.
|
[[37.0, 'year']]
|
M
|
{'3529466': 1, '24436284': 1, '20673399': 1, '16401832': 1, '28198523': 1, '31920665': 1, '34609434': 1, '24526338': 1, '28265016': 1, '26755444': 1, '28707135': 1, '22715252': 1, '26029025': 2, '24144596': 1, '26413321': 1, '20006506': 1, '26066534': 1, '22261663': 1, '28800746': 2, '27003984': 2, '28154101': 1, '20671861': 1, '24392362': 1, '11153886': 1, '26566040': 1, '15749975': 1, '23271508': 1, '16788293': 1, '25700287': 1, '23834662': 1, '16220412': 1, '14625223': 1, '29246631': 1, '20610185': 1, '3950725': 1, '28028147': 1, '18274809': 1, '24778625': 1, '20299438': 1, '24566980': 1, '17113294': 1, '20300550': 2, '23139104': 1, '27833768': 2, '25680324': 1, '27660767': 1, '20157376': 1, '959702': 1, '23621712': 1, '21406535': 1, '4126735': 1, '30345130': 2}
|
{'5554405-1': 1, '5090067-1': 1, '2838368-1': 1, '4387990-1': 1, '4780158-1': 1}
|
3,251 |
6174767-1
| 30,345,135 |
comm/PMC006xxxxxx/PMC6174767.xml
|
Neuropsychiatric Disorder Associated with Group G Streptococcus Infection
|
An 11-year-old girl presenting with involuntary movements in the face and extremities, clumsiness, and slurred speech was admitted to our hospital. She had no family history of neuropsychiatric disorders. Early psychomotor development was normal, although mild mental retardation was suspected at school. At age 10 years, she developed transient vocal tics. About 3 months before admission, she had episodes of choreiform movements. There were no events preceding these symptoms. The symptoms gradually worsened to include dropping eating utensils, and her body weight decreased by 4 kg in 3 months because of difficulty in eating. About a week before admission, she could not walk without assistance and did not attend school, because of gait difficulties. These symptoms were not observed during sleep. There was no indication of recent infection, and she had no history of fever during the 3 months before admission.\nOn examination, she exhibited notable choreoathetoid movements of the face and extremities. She was unable to walk without assistance. Muscle cramping in the cheeks and palpebrae-like tics were observed. She was alert and cooperative with the examiners, and her orientation was maintained. However, she exhibited emotional lability, sudden loud vocalizations, and resistance to restraint by caregivers. She showed severe irritability, and rage attacks were circumscribed. Muscle tonus and deep tendon reflexes were normal.\nBlood testing showed no abnormalities. Antistreptolysin O titer (ASOT) (301.3 IU/ml; normal, 0–330 IU/ml) and thyroid studies on admission were normal, but ASOT was mildly elevated (414.6 IU/ml) at 8 days after admission (). GGS was isolated in a throat culture. Tests for rheumatoid factor, antinuclear antibody, and anticardiolipin antibody yielded negative results. Examination of cerebrospinal fluid (CSF) showed no pleocytosis or increase in protein level. Homovanillic acid (HVA) level in CSF was mildly elevated, at 80.9 ng/ml (normal, <50 ng/ml). Brain magnetic resonance imaging and electroencephalography findings were unremarkable. Serum IgM and IgG antibodies to lysoganglioside were positive. In SC and PANDAS, antilysoganglioside antibodies react with the neuronal cell surface because of a cross-reactive immune response with streptococcal antigen N-acetyl-beta-D-glucosamine (GlcNAc) [, ]. She was treated with oral ampicillin and intravenous immunoglobulin (IVIG) (400 mg/kg/day) for 5 days, and her symptoms eventually resolved. Her overall intelligence quotient on the Wechsler Intelligence Scale for Children, Third Edition was 50, which indicates mild intellectual disability.
|
[[11.0, 'year']]
|
F
|
{'18519489': 1, '24892819': 1, '23065479': 1, '26266339': 1, '16875742': 1, '23142103': 1, '18217553': 1, '11030302': 1, '19833781': 1, '14626438': 1, '30345135': 2}
|
{}
|
3,252 |
6174774-1
| 30,345,134 |
comm/PMC006xxxxxx/PMC6174774.xml
|
Sepsis and Pleural Empyema Caused by Streptococcus pyogenes after Influenza A Virus Infection
|
A 4-year-old boy was treated for fever, mild cough, and nasal discharge at another hospital. Thereafter, he was diagnosed with influenza A infection and was treated with oseltamivir (4 mg/kg/day, 5 days). However, his condition deteriorated and fatigue, low activity, and breathing difficulty progressed; he was admitted to our hospital 7 days after the diagnosis of influenza A infection. He had no medical history of recurrent bacterial infections or growth failure. Physical examination at admission revealed remarkable respiratory distress and consciousness disturbance (Glasgow Coma Scale, E4V3M4). His body temperature was 38.0°C, blood pressure was 126/77 mmHg, heart rate was 155 beats/min, respiratory rate was 60 breaths/min, and oxygen saturation was 90% at room air. Right breath sounds were reduced, and an end-inspiratory crackle was detected in the right upper lung. In addition, red, cracked lips, strawberry tongue, and trunk and bilateral feet erythema were observed. Neither bilateral conjunctival injection, cervical lymphadenopathy nor edema was detected. Laboratory examination revealed a white blood cell count (WBC) of 20,000/μL with 95.1% neutrophils, hemoglobin level of 14.0 g/dL, and platelet count of 22.7 × 104/μL. Inflammatory biomarkers were elevated; C-reactive protein level was 20.54 mg/dl, procalcitonin level was 45.23 ng/mL, lactate dehydrogenase (LDH) level was 512 U/L, ferritin level was 261 ng/mL, and soluble interleukin-2 receptor (sIL-2R) level was 6,176 U/mL. The levels of several cytokines were also increased: IL-1β was 1.3 pg/mL; IL-6 was 233 pg/mL; IL-10 was 67 mg/mL; and TNF-α was 2.6 pg/mL, whereas IL-2, IL-3, IL-4, IL-5, and IL-12 were all normal. A chest X-ray and chest computed tomography revealed consolidation and a large-right pleural effusion (Figures and ). Based on these findings, the patient was diagnosed with sepsis and pleural empyema due to GAS infection.\nThe clinical course of the patient is shown in . Initially, continuous chest-tube drainage, intravenous administration of antibiotics (CTRX) and immunoglobulin (150 mg/kg/day, 3 days), and prednisolone (1 mg/kg/day, 3 days) were prescribed for sepsis and pleural empyema. The aspirated pleural fluid was serological with a yellowish brown color and pH of 7.002, WBC of 33,900/µL, protein of 4.7 g/dL, LDH of 9,121 U/L, and adenosine deaminase of 173.7 U/L (). No bacteria were detected by blood culture, whereas GAS tests conducted on both pleural fluids and throat swab on day 1 after culture were positive. The genotype of GAS was found to be emm1/speA/speB/speF, which is known as a virulence factor gene. Based on this data, the antibiotics were changed from CTRX to ampicillin (ABPC) and clindamycin (CLDM). However, fever and tachypnea persisted. Alternatively, the chest tube was considered as being obstructed or failing to drain, and hence, the chest tube was replaced, and an additional fibrinolytic therapy (urokinase 40,000 units in 40 mL 0.9 percent saline, intrapleural) was included; however, the patient's clinical condition still did not improve. On day 9, video-assisted thoracoscopic surgery (VATS) was performed to remove the thick fibrous septations. Thoracoscopy of the thoracic cavity revealed an adhered pulmonary and parietal pleura with fibrin; the cavity was then peeled off and washed using saline (). The patient's clinical condition improved following VATS, and he was discharged on day 33. All inflammatory biomarkers and cytokines had reduced to normal levels. At the time of the final follow-up, the patient had been healthy without any symptoms.
|
[[4.0, 'year']]
|
M
|
{'27918954': 1, '30691434': 2, '23667113': 1, '8386517': 1, '32770825': 1, '20407400': 1, '26919911': 1, '15187140': 1, '27220813': 1, '19732082': 1, '10395857': 1, '28725562': 1, '24089191': 1, '16982840': 1, '1571429': 1, '25723597': 1, '30345134': 2}
|
{'6350381-1': 1}
|
3,253 |
6174775-1
| 30,345,126 |
comm/PMC006xxxxxx/PMC6174775.xml
|
Multiple Myeloma Masquerading as Ovarian Carcinosarcoma Metastases: A Case Report and Review of the Approach to Multiple Myeloma Screening and Diagnosis
|
A 67-year-old female with a history of ovarian carcinosarcoma presented to the hospital with one week of headache and neck pain.\nHer malignancy had been diagnosed one year prior to presentation after she had presented to her primary care physician with abdominal pain. Radiographic imaging at that time showed a large pelvic mass, and the patient subsequently underwent radical cytoreductive surgery which included total abdominal hysterectomy, bilateral salpingo-oophorectomy, and omentectomy. Pathology showed a focal left ovarian carcinosarcoma with metastases to the right ovary, omentum, and posterior cul-de-sac. The patient underwent six cycles of carboplatin and paclitaxel.\nEight months after completion of chemotherapy, the patient presented to her oncologist with new right pelvic pain. Pelvic imaging showed a new, deep right pelvic mass, and the patient underwent surgical resection which confirmed disease recurrence. The patient was set to begin localized radiation therapy and further chemotherapy when she developed headache and neck pain and presented to the hospital.\nUpon current presentation, she noted an intractable bandlike headache and neck pain. Physical examination revealed normal vital signs, a normal mental status assessment, and a nonfocal neurological examination. She had restricted range of motion at the neck and midline point tenderness in the upper thoracic spine.\nLaboratory testing demonstrated a normal complete blood count, normal renal function, and normal serum electrolyte levels. Magnetic resonance imaging (MRI) of the head and spine were obtained and showed a lytic mass centered in the left clivus and occipital condyle, as well as an expansile soft tissue lesion in the T4 spinous process (). A positron emission tomography-computed tomography (PET-CT) was also obtained (). In the setting of known ovarian recurrence, these findings were assumed to be metastases.\nHowever, a 1.83 g/dL M-spike (reference range: 0.80–1.70 g/dL) was detected on serum protein electrophoresis, and a monoclonal gammopathy with immunoglobulin G (IgG) lambda monoclonal immunoglobulin was seen on immunofixation. Lambda free light chains were elevated at 49.1 mg/L (reference range: 5.7–26.3 mg/L), and kappa free light chains were borderline decreased at 5.3 mg/L (reference range: 3.3–19.4 mg/L). The free kappa to free lambda ratio was abnormal at 0.12 (reference range: 0.26–1.65). No M-spike was detected on urine protein electrophoresis. A biopsy of the T4 lesion showed a plasma cell neoplasm, and a bone marrow biopsy showed a clonal population of >10%, confirming the diagnosis of multiple myeloma ().
|
[[67.0, 'year']]
|
F
|
{'20177023': 1, '16858075': 1, '19020545': 1, '16682511': 1, '23183428': 1, '23183429': 1, '33014234': 1, '21812699': 1, '17165636': 1, '25079172': 1, '12194945': 1, '16040291': 1, '25439696': 1, '30345126': 2}
|
{}
|
3,254 |
6174776-1
| 30,345,133 |
comm/PMC006xxxxxx/PMC6174776.xml
|
Late Presentation of an Iatrogenic Pseudoaneurysm of the Profunda Femoris Artery following Intramedullary Nailing
|
A 78-year old Caucasian male patient, without relevant medical history and in good health, presented to the emergency department with severe pain in the right hip after a high energy trauma due to a fall. On clinical examination, the right leg was shortened and externally rotated. There was no neurovascular deficit in the ipsilateral limb. A comminuted intertrochanteric hip fracture was diagnosed on a plain X-ray of the painful hip and pelvis (grade 31-A2 according to the AO classification) (). Intravenous pain medication was administered at the emergency department, and the patient was transferred to the operating room five hours after admission.\nClosed reduction and internal fixation with a 170 mm 125° intramedullary nail (proximal femoral nail antirotation (PFNA; Synthes®), 11 mm diameter) were performed. The patient was placed supine on a fracture table with traction and the hip in adduction and internal rotation. The nail could be introduced without any particular difficulty. A 115 mm blade and a 38 mm distal locking screw were inserted with the use of the aiming arm. For distal locking, a drill sleeve, a protection sleeve, and a 4.2 mm calibrated drill bit (340 mm) were used. Drilling was guided, however not guarded. There were no intraoperative or immediate postoperative complications. Postoperative radiographs were satisfactory. Postoperatively, three weeks nonweight bearing were instructed because of the high energy impact of the trauma. Also, low molecular weight heparin (Enoxaparin 40, 1 subcutaneous injection per day) was administered for six weeks.\nOn clinical and radiographic checkup six weeks after surgery, no particular difficulties were noticed. The patient was able to walk with one crutch, there was no obvious swelling of the limb, and radiographs showed a good position of the intramedullary nail ().\nEight months postoperatively, the patient presented to polyclinical consultation because of a progressive swelling of the right thigh. There was no recent trauma, episode of fever, or illness. Clinical examination revealed a nontender diffuse swelling over the proximal part of the right thigh without well-defined borders, redness, or fluctuation. Peripheral pulses of the lower limbs were palpable, although stronger in the left limb, and capillary refill was normal. Mobilisation of the hip was painless. Ultrasound revealed a calcified old muscular hematoma localised medial to the femoral diaphysis. Additional X-rays confirmed the presence of a medial mass centred over the distal locking screw with calcification of the peripheral borders, suggestive for an (infected) hematoma. Compression and severe osteolysis of the medial border of the femur were seen (). Contrast-enhanced computed tomography (CT) was performed, showing an active extravasation in the hematoma which led to the diagnosis of pseudoaneurysm (). Laboratory tests showed a haemoglobin value of 11 g/dL and an elevated CRP (42 mg/L). Other laboratory parameters were within normal range. On retrospective analysis of the X-rays six weeks postoperatively, the additional mass could have been already noticed. However, because of the very subtle signs, it was misdiagnosed.\nThe patient was referred to the department of vascular surgery for open drainage. Preoperative findings showed a PFA lesion facing the distal locking screw which was managed by direct arterial suture. The screw was not visible and therefore left in place. No weight-bearing limits were made within the context of the scalloping of the medial femoral cortex because of patient's compliance and a good consolidation of the fracture. The patient was followed up regularly, and further evolution was uneventful.
|
[[78.0, 'year']]
|
M
|
{'1959684': 1, '27134957': 1, '11818808': 1, '28178228': 1, '12111012': 1, '33954136': 2, '23271663': 1, '29419700': 1, '20808021': 1, '15067549': 1, '23910677': 1, '19595659': 1, '27266840': 1, '25213190': 1, '30345133': 2}
|
{'8051565-1': 1}
|
3,255 |
6174779-1
| 30,345,120 |
comm/PMC006xxxxxx/PMC6174779.xml
|
Head Down Deep Breathing for Cardioversion of Paroxysmal Supraventricular Tachycardia
|
Patient A was a 65-year-old female with history of dyslipidemia, anemia, and postural hypotension with syncope. She experienced palpitations once every three months, each lasting about six hours which spontaneously resolved. She was referred from her General Practitioner's clinic for fever with upper respiratory tract symptoms for two days and a few hours of palpitations. There was no chest pain or shortness of breath. Her physical examination was largely unremarkable apart from regular tachycardia and blood pressure 166/61 mmHg. Her arrival electrocardiograph (ECG) revealed regular narrow complex tachycardia (see ). She was placed in Trendelenburg position and instructed to take in deep breaths and subsequently hold her breath for five seconds before exhalation. She did this and converted to sinus rhythm (see ) within five breaths. She tolerated the HDDB maneuver well. The immediate postmaneuver BP was 171/64 and 30 minutes later it was 121/65. She did not have any complications and was later discharged from the emergency department (ED).
|
[[65.0, 'year']]
|
F
|
{'27484659': 1, '28740999': 1, '26314489': 1, '19104086': 1, '9437338': 1, '25316626': 1, '26209466': 1, '7418151': 1, '30345120': 2}
|
{'6174779-2': 2}
|
3,256 |
6174779-2
| 30,345,120 |
comm/PMC006xxxxxx/PMC6174779.xml
|
Head Down Deep Breathing for Cardioversion of Paroxysmal Supraventricular Tachycardia
|
Patient B was a 68-year-old female who had a history of hypertension and dyslipidemia. She felt sudden onset of palpitations associated with chest pain about 45 minutes before ED arrival. She had chest pain which radiated to her right shoulder and neck. She experienced some sweatiness but had no dyspnea or fever. At the ED, she was alert and not in pain or distress. On examination, she was tachycardic with normal blood pressure. Her lungs had clear air entry. Her ECG revealed SVT (see ). She was subjected to the similar head down deep breathing (HDDB) maneuver as described above and converted to sinus rhythm without any complications. Her postmaneuver BP was 131/73. Her initial serum Troponin T was 10 ng/L (normal lab range 0-29 ng/L). However, in view of the earlier presence of chest pain with cardiovascular risk factors, she was admitted to cardiology for observation. Her subsequent Troponin T levels remained normal, and an echocardiogram the next day showed normal left ventricular (LV) ejection fraction and diastolic function, with no structural heart disease. She was discharged thereafter.
|
[[68.0, 'year']]
|
F
|
{'27484659': 1, '28740999': 1, '26314489': 1, '19104086': 1, '9437338': 1, '25316626': 1, '26209466': 1, '7418151': 1, '30345120': 2}
|
{'6174779-1': 2}
|
3,257 |
6174791-1
| 30,345,137 |
comm/PMC006xxxxxx/PMC6174791.xml
|
Acute Hemoptysis Redefined: A Deadly Presentation
|
A ninety-year-old man with no significant medical history presented to the emergency department with abrupt onset of hemoptysis. The patient was hemodynamically stable. Lung exam revealed bilateral lung crackles. His chest X-ray showed left upper lobe opacity with widened mediastinum due to aortic dilatation (). CT of the chest revealed the aneurysmatic dilatation of the ascending arch and the descending aorta and pulmonary infiltrates in left upper lobe suspicious of aorto-bronchial fistula with bleeding in the lung (Figures , , and ). The patient was started on supportive care, including intubation and mechanical ventilation. Cardiology and Cardiothoracic Surgery were consulted. Cardiothoracic surgery agreed with the diagnosis of ascending aortic aneurysm and bronchopulmonary fistula; however due to his poor functional status and overall frailty the risk of surgery outweighed the benefits; hence surgical intervention was not pursued. During his second day of hospitalization the patient developed another episode of massive hemoptysis resulting in hypovolemic shock, and despite the best efforts of the medical personnel, the patient expired.
|
[[90.0, 'year']]
|
M
|
{'23916807': 1, '29457078': 2, '25365623': 1, '31894503': 1, '25323262': 1, '16429896': 1, '24560418': 1, '29279784': 2, '30345137': 2}
|
{'5723941-1': 1, '5804618-1': 1}
|
3,258 |
6174797-1
| 30,345,122 |
comm/PMC006xxxxxx/PMC6174797.xml
|
A Case Report and Literature Review of Clostridium difficile Negative Antibiotic Associated Hemorrhagic Colitis Caused by Klebsiella oxytoca
|
A 33-year-old Caucasian female with significant family history of inflammatory bowel disease (IBD) presents with profuse, bloody diarrhea for 5 days and associated tenesmus and urgency. One day prior to admission, she completed a one-week course of ampicillin for a urinary tract infection and noted that her symptoms began three days after she had initiated treatment. On presentation, patient was hemodynamically stable, afebrile, with mild lower abdominal pain, and a positive guaiac exam. Laboratory findings showed WBC 12.4 bil/L (normal values 3.3–10.7 bil/L), neutrophils 11.0 bil/L (normal values 1.6–7.2 bil/L), Hgb 13.1 g/dL (normal values 12.1–15.0 g/dL), platelets 275 bil/L (normal values 150–400 bil/L), lactic acid 1.4 mmol/L (normal values 0.5–2.2 mmol/L), and liver function tests within normal limits. Initial stool studies that included stool culture, ova and parasite, and Clostridium difficile toxin PCR were negative. A colonoscopy was planned as the patient had an extensive family history of IBD and presented with bloody diarrhea. Klebsiella oxytoca testing was requested on the stool culture after Clostridium difficile PCR came back negative, given her previous use of penicillins. Colonoscopy was notable for ulcerated mucosa with erythema and easy friability, suggestive of moderate colitis throughout the colon with rectosigmoid sparing (). Colonic biopsy was remarkable for mucosal congestion and ischemia suggestive of ischemic colitis (). Subsequently, requested stool culture was positive for many Klebsiella oxytoca. The patient's hematochezia resolved prior to discharge on day 3 of hospitalization, four days after cessation of ampicillin. She was advised to avoid future use of penicillins and minimize nonsteroidal anti-inflammatory drug (NSAID) use.\nThe patient has continued to follow with her gastroenterologist 10 months after her colonoscopy. She has had epigastric abdominal pain relieved by daily omeprazole. She no longer has documented hematochezia and there has been no repeat colonoscopy.
|
[[33.0, 'year']]
|
F
|
{'8034921': 1, '15017655': 1, '17963468': 1, '15229449': 1, '9870798': 1, '80635': 1, '28619975': 1, '34851134': 1, '28806959': 2, '17151365': 1, '19303568': 1, '31466981': 1, '25714160': 1, '22433794': 1, '23964038': 1, '10566543': 1, '19727105': 1, '1420669': 1, '30345122': 2}
|
{'5557549-1': 1}
|
3,259 |
6174802-1
| 30,345,139 |
comm/PMC006xxxxxx/PMC6174802.xml
|
Closed Loop Obstruction from Epiploic Appendage Adhesion Mimicking Pericecal Internal Hernia
|
A 58-year-old female presented to the emergency department with intermittent, crampy right-sided abdominal pain, nausea, and vomiting, which began approximately 18 hours previously. Her past medical history was significant for hypertension and her surgical history included a thyroidectomy for treatment of thyroid cancer and a Caesarean section. A contrast enhanced CT abdomen and pelvis was obtained, demonstrating multiple fluid-filled, dilated small bowel loops in the right abdomen, which were predominantly anterolateral to the ascending colon and cecum (). In addition, two transition points were identified in the right lower quadrant, with one transition point at the distal ileum just proximal to the cecum and a second transition point in the proximal ileum. The two transition points were in close proximity to each other, indicative of closed loop obstruction. Decreased wall enhancement of the dilated small bowel loops was concerning for ischemia. Mucosal hyperenhancement of the ileum at the proximal transition point was felt to relate to ischemia or decompressed state (). Given the patient's symptoms and findings of closed loop obstruction on CT, the patient was taken to operating room. In the operating room, an internal hernia with closed loop obstruction was confirmed and resulted from herniation of small bowel through an adhesion of a transverse colon epiploic appendage to the ascending colon mesentery. The herniated small bowel was nonviable and a total of 60 cm of small bowel was resected (). Retrospectively, kinking of the ascending and transverse colon could be seen on the initial abdominal CT and was felt to correspond with the site of adhesion ().\nAfter resection, the patient's small bowel was left in discontinuity and an abdominal wound-vac was placed. The following day, the patient returned to the operating room, at which time the terminal ileum was also found to be nonviable. An ileocecectomy with enterocolonic anastomosis was performed.\nThe patient had a complicated postoperative course, but was ultimately discharged approximately two weeks after the initial surgery.
|
[[58.0, 'year']]
|
F
|
{'26587890': 1, '28409048': 2, '34017578': 1, '24964406': 2, '28758042': 2, '26933000': 2, '30345139': 2}
|
{'5376451-1': 1, '5912703-1': 1, '4772000-1': 1, '5516733-1': 1}
|
3,260 |
6174808-1
| 30,345,124 |
comm/PMC006xxxxxx/PMC6174808.xml
|
Moderate Hypertriglyceridemia Causing Recurrent Pancreatitis: A Case Report and the Literature Review
|
A morbidly obese 43-year-old female with a history of hypertension, dyslipidemia, and diabetes mellitus presented with severe abdominal pain. She had an episode of acute pancreatitis one year ago. She complained of right upper quadrant pain radiating to the back over 6-hour duration alongside six episodes of vomitus. A review of systems was only notable for a headache and dizziness. She reported no family history of dyslipidemia or acute pancreatitis. She denied tobacco, alcohol, or illicit substance use. There was no history of gallstones, appendectomy, new medications, procedures (including ERCP), or any complications related to her diabetes.\nAdmission vitals revealed afebrile patient with a heart rate of 103/min, respiratory rate of 20/min, BP 116/62 mmHg, and oxygen saturation of 96% on a nasal cannula at 5 liter/min. The patient was alert and orientated but was in moderate distress. The abdomen was obese and soft and with tenderness in the epigastric region. There was no guarding, rigidity, or Murphy's sign. Her body mass index (BMI) was 47.1. Other systemic signs of elevated triglycerides including xanthelasma, corneal arcus, and tendon xanthoma were absent.\nInitial laboratory investigations showed an elevated white cell count of 16.9 μ/L (4.5 -11 μ/L), haemoglobin 12.2 g/dL (12-16 g/dL), platelet count 368000 mm3 (130,000-400,000mm3), sodium 129 mEq/L (136-144 mEq/L), potassium 3.8 mEq/L (3.5-5mEq/L), anion gap of 2 (8-16), BUN 45 mg/dL ( 7-20 mg/dL), creatinine 0.6 (0.4-1.3), glucose 206 mg/dL (74-117 mg/dL), and serum calcium 7.9 mg/dL (8.5-10.2 mg/dL). Liver function tests showed total bilirubin 0.5 mg/dL (0.1-1.2mg/dL), aspartate aminotransferase 16 IU/L (8-46 IU/L), alanine aminotransferase 11 U/L (7-55 IU/L), total protein 8.5 g/dL (6.1-7.9 g/dL), albumin 4 g/dL (3.5-5.5 g/dL), and PT 11.6 seconds (9.8-13.4 seconds). Initial arterial blood gas (ABG) analysis showed pH 7.5, pCO2 37.5, and pO2 67 at FiO2 of 40%.\nThe patient had an elevated lipase of 4143 U/L (reference 22-51 U/L), total cholesterol of 694 mg/dL (100-199 mg/dL), and a triglyceride level of 600 mg/dL (reference 0-149 mg/dL). Computed tomography (CT) of the abdomen showed diffuse enlargement of the pancreas consistent with pancreatitis (). There was no evidence of gallstones or biliary sludge which was also confirmed by an ultrasound abdomen. Other competing etiologies including alcohol, autoimmune pancreatitis, abdominal trauma, pancreatic divisum, sphincter of Oddi dysfunction (SOD), viral infection, drugs, and toxins were all ruled out, making the most likely diagnosis hypertriglyceridemia-induced AP (HTG AP).\nThe patient was treated with boluses of intravenous (IV) normal saline and supportive care. On the second day of admission, the patient developed hypotension and had persistent tachycardia. She likely developed acute respiratory distress syndrome (ARDS) from complications of acute pancreatitis. Fluid overload was ruled out with a sonogram of the inferior vena cava (diameter of 1.5 cm), a central venous pressure of 6 cm of H2O, and echocardiography indicating left ventricular ejection fraction of 55% with no left ventricular diastolic dysfunction. The patient was subsequently transferred to the intensive care unit for hypovolemic shock and respiratory distress requiring intubation and mechanical ventilation. As per revised Atlanta classification, she was categorized as severe acute pancreatitis based on Marshall scoring system for organ failure with a score of 3, with a score of 1 from respiratory failure (PaO2/FiO2 of 240) and two from cardiovascular (systolic BP <90, not fluid responsive). Patient's fasting blood glucose was 288 mg/dL (74-117 mg/dl), and diabetic ketoacidosis (DKA) was ruled out with the absence of serum or urine ketones, no elevated anion gap, and no acidosis. ABG analysis showed pH of 7.5, bicarbonate of 23, and an anion gap of 2.\nFollowing the patients decline into shock, an ABG indicated an acidic pH of 6.99, PCO2 9.4, PO2 134, and HCO3 of 5.4. The serum bicarbonate level was low at 15mmol/L and the calculated anion gap was elevated at 22 (normal 8–16). Lactic acid level was 3.8 mmol/L (0.5-1.9 mmol/L).\nRepeat abdominal contrast-enhanced CT on the third day showed marked pancreatic and peripancreatic infiltration consistent with AP and no signs of necrosis. Continuous insulin infusion was started for HTG from day 1, lowering her triglyceride levels down to 247 mg/dL over five days as shown in . She was also started on a liquid diet via nasogastric tube from day 5. After nine days in the ICU, the patient was successfully extubated and was switched to oral diet on day 11, which was gradually advanced as tolerated. She was downgraded to the floor on the same day and discharged on day 17. The patient required nasal oxygen to maintain saturation as she was recovering from ARDS. She was discharged on gemfibrozil 600mg twice daily to prevent further episodes of HTG AP. Patient has been followed upon discharge and remains compliant with gemfibrozil, leading to a controlled triglyceride level of 123 mg/dL and no further episodes of AP.
|
[[43.0, 'year']]
|
F
|
{'24172179': 1, '22885331': 1, '31901241': 1, '19322914': 1, '26323188': 1, '12460410': 1, '22962670': 1, '27785302': 2, '26228216': 1, '21723786': 1, '29362560': 1, '18983441': 1, '28217371': 1, '19293788': 1, '17484894': 1, '28225998': 1, '22049070': 1, '28697126': 1, '25960810': 1, '30345124': 2}
|
{'5040532-1': 1}
|
3,261 |
6175182-1
| 29,962,004 |
comm/PMC006xxxxxx/PMC6175182.xml
|
p63 and smooth muscle actin expression in low-grade spiradenocarcinomas in a case of CYLD cutaneous syndrome
|
A 50-year-old male presented with a rapidly enlarging lesion on his back. He had multiple skin lesions affecting most of his upper body, arms, and face (Figure A). The patient had first noticed skin tumors around the age of 18 years, and had multiple lesions removed, which were confirmed as cylindromas and spiradenomas. He was severely affected with multiple scalp tumors, such that he underwent total scalp excision with skin grafting. He had affected relatives, and sequencing of the CYLD gene in peripheral lymphocyte DNA revealed a novel pathogenic heterozygous truncating mutation (c.2476C>T; p.Gln823*) (Figure B), consistent with a diagnosis of CCS. The patient underwent surgical excision of the lesion on the back, which showed low-grade spiradenocarcinoma. Two years after this a further enlarging tumor was excised from his suprapubic skin and confirmed to be a primary spiradenocarcinoma. Five years since his first spiradenocarcinoma, neither lesion has recurred.\nHistopathology of the tumor from his back showed an ulcerated spiradenocarcinoma arising in a spiradenoma. The spiradenocarcinoma was characterized by increased cellularity and absence of the dual cell population seen in spiradenoma. The neoplastic cells were arranged in nodules and had minimal cytoplasm, and some showed a slightly spindled morphology (Figure A,B). The ductal structures (highlighted by carcinoma embryonic artigen staining; data not shown) appeared compressed and pushed to the periphery. There was loss of the diffuse infiltrate of small lymphocytes. Within the neoplastic nodules, the cells showed increased mitotic activity (15/10 hpf). The spiradenoma in comparison was characterized by a dual population of cells arranged in trabeculae. The cells were a mixture of small basaloid cells with small dark nuclei, and a second cell type with a larger more irregular vesicular nucleus and more cytoplasm. Mitotic activity was very low in the benign component (1/10 hpf).\nImmunohistochemistry for p63 and SMA was performed on spiradenoma and spiradenocarcinoma. p63 showed strongly positive cells closely associated with occasional weak p63 staining cells in spiradenoma and showed uniform but weak p63 staining in spiradenocarcinoma (Figure A,B). SMA showed a mixture of SMA positive cells and SMA negative cells diffusely throughout the lesion in spiradenoma, and nodules of SMA negative cells with SMA positive cells compressed at the periphery in spiradenocarcinoma (Figure A-C). These nodules were most easily recognized on low power magnification (Figure A). Similar features were seen in the spiradenocarcinoma arising in the suprapubic skin.
|
[[50.0, 'year']]
|
M
|
{'26969893': 1, '25857824': 1, '10770427': 1, '19194280': 1, '26370355': 1, '11958666': 1, '22077486': 1, '25782638': 1, '21618541': 1, '29962004': 2}
|
{}
|
3,262 |
6175201-1
| 30,338,179 |
comm/PMC006xxxxxx/PMC6175201.xml
|
Cerebral Sinus Venous Thrombosis in a Patient Using Etonogestrel/Ethinyl Estradiol Vaginal Ring
|
A 43-year-old female patient known to have a past medical history of depression, anxiety, and who used an etonogestrel/ethinyl estradiol vaginal ring for contraception, presented to the emergency department (ED) with new onset witnessed grand mal tonic-clonic seizure lasting at least two minutes with post-ictal confusion. The patient denied any previous seizure history. She did report drinking alcohol occasionally and had ingested two alcoholic drinks the previous evening. There was no associated trauma. Her vital signs on admission were: temperature 36.2ºC, pulse 119 beats per minute, respiratory rate 25 breaths per minute, blood pressure 140/105 mmHg, SpO2 99% on room air, and body mass index of 33.7 kg/m2. A thorough review of systems was negative other than nausea, diarrhea, and seizure. Physical examination, including a full neurological examination, was unremarkable. Laboratory data included: potassium 3.2 meq/L, bicarbonate 15 mmol/L, glucose 171 mg/dL, hemoglobin 11.5 g/dL, hematocrit 33.7%, platelet 134,000/mm3.\nComputed tomography (CT) head without intravenous contrast showed trace right parieto-occipital extra-axial collection and parenchymal hemorrhage of the right parieto-occipital and temporal regions, with an adjacent subarachnoid hemorrhage (SAH) (Figure ). The acute right parieto-occipital intraparenchymal hemorrhage with scattered adjacent SAH was secondary to an extensive acute thrombosis of the right venous sinuses (transverse, sigmoid, and jugular). The patient was admitted to the intensive care unit (ICU) for further evaluation of her brain hemorrhage. She was started on nicardipine drip for a target systolic blood pressure of <140 mmHg and kept on hemorrhagic stroke protocol.\nNeurology was consulted, and further evaluation included magnetic resonance angiogram (MRA) of the head without contrast. Findings were consistent with right transverse dural venous sinus thrombosis (Figure ). Brain magnetic resonance imaging (MRI) with and without contrast showed intraparenchymal hemorrhage of the right parieto-occipital and temporal regions secondary to venous thrombosis. Patchy meningeal enhancement is seen at the right parieto-occipital and temporal regions, likely related to venous stasis versus reactive changes secondary to thrombosis. Also, a small focus of hyperintense signal is seen on isotropic diffusion-weighted and fluid-attenuated inversion recovery (FLAIR) sequences in the left splenium of the corpus callosum without significant associated decreased signal on apparent diffusion coefficient (ADC) maps, this is likely due to subacute ischemia (Figure ).\nAdditionally, MRI venogram of the head without contrast showed a complete absence of flow-related enhancement in the right transverse and sigmoid sinuses and right internal jugular vein consistent with high-grade thrombosis of the right transverse sinus (Figure ). Neurosurgery service was also consulted and recommended no surgical intervention.\nOn the third day of admission, after starting heparin drip, the patient complained of right ear fullness and increasing headache. A repeat head CT scan without IV contrast showed enlargement of the intracranial hemorrhage (Figure ). Heparin infusion was held, with neurological assessments completed every hour. The patient was reassessed by neurosurgery and neurology teams, both of which recommended resumption of anticoagulation and starting warfarin for bridging with target international normalized ratio (INR) of 2-3. Once stable, the patient was transferred to a neurological center for further close follow-up and evaluation. The patient improved clinically over the following days and the cerebral hemorrhage improved on repeat CT imaging (Figure ).\nThe patient was discharged home on warfarin with a plan to continue for a minimum of six months. On follow-up, six months later, the patient reported complete resolution of symptoms and CT head without contrast revealed significant improvement in the size of intracranial hemorrhage (Figure ).
|
[[43.0, 'year']]
|
F
|
{'21293023': 1, '20402748': 1, '21151631': 1, '22315273': 1, '28583818': 1, '15858188': 1, '28833980': 1, '10066840': 1, '33833915': 2, '14976332': 1, '3975957': 1, '23251274': 1, '28041897': 1, '24264471': 1, '30338179': 2}
|
{'8019322-1': 1}
|
3,263 |
6175202-1
| 30,338,181 |
comm/PMC006xxxxxx/PMC6175202.xml
|
Acute Autonomic Symptoms with Anti-myelin-associated Glycoprotein Neuropathy as a Presentation of Small B Cell Lymphoma: A Case Report and Literature Review
|
A 68-year-old female presented with gradual onset of negative sensory symptoms like numbness, and weakness particularly on extremities bilaterally. She also had some balance problems for the same time duration. On neurological examination, there was diffusely reduced muscle strength of 4/5 on Medical Research Council (MRC) muscle power grading scale, along with the reduced perception to all modalities conducting either by dorsal column lemniscus or spinothalamic pathway. She also had some loss of sense of vibration and sense of proprioception peripherally. Moreover, there was a generalized hyporeflexia and gait examination showed a positive Romberg sign. On further inquiry, there was no previous history of similar symptoms or recent history of having any upper respiratory tract infection or diarrhea. There was no history of recent travel. Her current medications included losartan (50 mg) for her blood pressure control and the multi-vitamins. Her blood pressure was under control and lab results from the medical record of last year were normal. Initial workup for her unexplained neuropathy included serum TSH, vitamin B12, HbA1c along with routine baseline laboratory investigations, to rule out the more prevalent causes of these symptoms. These laboratory tests turned out to be normal. The patient then developed acute urinary incontinence and severe orthostatic hypotension. She also developed symptomatic bradycardia, severe enough to place a temporary pacemaker to relieve her symptoms.\nMeanwhile, further workup was ordered which showed M spike on serum electrophoresis with IgM kappa on immunofixation. IgM titers were surprisingly high; 568 mg/dl (normal 40–230 mg/dl). Initially, the probable diagnosis was monoclonal gammopathy of undetermined significance (MGUS) related neuropathy. Hematological workup was then extending, which revealed anti-MAG antibody titers >1:102400 (normal < 1:1600). Bone marrow biopsy showed small atypical lymphoid cells which stained positive for CD20, PAX-5, with rare CD138 positive plasma cells. These findings were consistent with a small B-cell lymphoproliferative disorder. She is currently being treated with rituximab with significant improvement in her neuropathic symptoms. Acute autonomic symptoms can be a rare [] and a confusing clinical manifestation of anti-MAG neuropathy.
|
[[68.0, 'year']]
|
F
|
{'6422066': 1, '26821540': 1, '8289086': 1, '25867460': 1, '2433641': 1, '28473042': 1, '25288371': 1, '21040140': 1, '11856795': 1, '850793': 1, '870771': 1, '497816': 1, '26065001': 1, '6982313': 1, '20842571': 1, '8618562': 1, '1656848': 1, '1379693': 1, '21826267': 1, '30338181': 2}
|
{}
|
3,264 |
6175203-1
| 30,338,195 |
comm/PMC006xxxxxx/PMC6175203.xml
|
Refractory Delusional Parasitosis in a 70-year-old Woman
|
A 70-year-old Caucasian female presented to an outpatient Partial Psychiatric Hospital Program (PPHP) after an episode where the patient was reported missing, and subsequently found by the police hiding under a tree with minimal clothing in freezing cold temperatures. The patient’s brother and sister-in-law, whom she resides with, were unable to locate her, and reported her missing to the police. Upon discovery by the police, the patient agreed to attend the outpatient PPHP. Upon admission, the patient explained that she ran away from her home due to feelings of guilt and “feeling like a burden to her family.” She then revealed that her feelings of guilt are primarily regarding her perceived parasite infestation, which she states has plagued her for decades. The patient states there are “little white bugs crawling in and out of my skin.” She further explained that they are difficult for her to capture because they dive deep into her skin. The patient expressed fear that her family members will also become infected, prompting her recent episode of escaping her home. She also mentioned feeling embarrassed about the issue, particularly because she is from a rural town and feels everyone will know.\nThe patient admits she has seen several healthcare providers including her primary care provider, parasitologists, and dermatologists, all reporting negative findings. When explaining this, the patient became very agitated and repeated, “I’m not crazy, but no one believes me.” Additional past medical history was benign other than the patient revealing she underwent an abortion at the age of 35. She does not link the parasite infestation with this event, but does express guilt over this decision.\nThe patient denied a history of physical or sexual abuse. She denied alcohol or drug abuse. She has never been married and has no children. Upon exam, the patient looked appropriate and stated her age. She maintained eye contact and spoke with coherence. The patient was anxious. Immediate retention and recall, recent memory, remote memory and fund of knowledge appeared to be fair. Insight and judgment were poor. The patient was not impulsive. The patient's current medications include Zyprexa 2.5 mg per os (PO) at bedtime and Zoloft 75 mg PO daily. A toxicology screening of the patient was negative.\nFrom reviewing the medical records, it was elucidated that the patient was admitted to the Behavioral Health Unit two times previously with the same complaint of parasite infestation. The patient could not pinpoint when the supposed infestation began, but does state that it had been many years, possibly 15 years.\nWhen questioned why the patient was at the PPHP, she states that after she was found by the police, she was taken to the Emergency Department (ED) and was medically cleared, but her family demanded she attend the outpatient PPHP because of her delusions. We were also able to ascertain that a computed tomography (CT) scan was taken in the ED, which demonstrated microvascular ischemic changes and cortical atrophy.\nOn completion of the interview, the patient was observed in group therapy, and a decision was made that the patient was not a good candidate for the PPHP, as her delusions were too severe and becoming disruptive to the group. At the request of her family, she was then transferred to a free-standing private psychiatric hospital for further evaluation and treatment. She currently remains there and is undergoing treatment.
|
[[70.0, 'year']]
|
F
|
{'6838775': 1, '10375340': 1, '1008566': 1, '8476732': 1, '12796218': 1, '7103678': 1, '7902366': 1, '17134847': 1, '3299633': 1, '9819949': 1, '31019855': 2, '11182606': 1, '30338195': 2}
|
{'6464987-1': 1}
|
3,265 |
6175253-1
| 30,338,183 |
comm/PMC006xxxxxx/PMC6175253.xml
|
Pulmonary Tuberculosis After Gastric Bypass: A Very Rare Complication
|
A 32-year-old female with history of diabetes mellitus type one and a successful RYGB for morbid obesity three years ago presented to our clinic with the complaints of cough, greenish yellow sputum production, chills and night sweats for the last three months. She was feeling more fatigued, generalized weakness and unintentionally lost 33 pounds during that time. She denied recent history of travel out of state. The patient was in the United States and had never been to a country with endemic tuberculosis. She denied recent remote history of incarceration. She also denied hemoptysis, shortness of breath, headache or fever. She had no history of being diagnosed with TB or history of recent sick contacts. On physical examination, her temperature was 36.9°C, blood pressure was 116/60 mm Hg, pulse was 84 per minute and respiratory rate was 16 per minute. On chest auscultation, few rhonchi were present in the right upper lung and the rest of the physical examination was unremarkable. The Initial blood work showed sodium of 134 mmol/L (136–145 mmol/L), potassium of 4.2 mmol/L (3.5–5.1 mmol/L), bicarbonate of 28 mEq/L (23–31 mEq/L), blood urea nitrogen (BUN) of 6 mg/dL (9–21 mg/dL), creatinine of 0.33 mg/dL (0.6–1.1 mg/dL), glucose of 150 mg/dL (80–115 mg/dL) and liver function tests were within normal range. Her white blood cell count was 14,500/µL (4500–11000/µL) with 81% neutrophils. Her chest X-ray showed multiple small nodular opacities throughout the right lung with a probable cavity in the right lung apex (Figure ). Suspicion was raised for possible active TB and she was admitted in airborne isolation. Two peripheral blood cultures, sputum culture along with acid-fast bacilli (AFB) were ordered. Computed tomography (CT) chest without contrast showed multiple thick-walled cavities in the right upper lobe. The largest cavity was 7 cm. There were innumerable centrilobular nodules and tree in bud opacities throughout the right lung (Figures , ). Mycobacterium tuberculosis bacillus was detected by sputum AFB staining and later confirmed by culture and polymerase chain reaction (PCR) assay. She also had a positive QuantiFERON test. She was started on anti-tuberculosis treatment (ATT) medications including Isoniazid 300 mg daily, Rifampin 300 mg twice daily, Ethambutol 800 mg daily, Pyrazinamide 1000 mg daily and Pyridoxine 50 mg daily for the first two months and then two drugs Isoniazid and Rifampin for the next four months. After three days of hospital stay, she started showing some improvement in her symptoms such as cough and night sweats. She understood the isolation precautions, especially respiratory precautions and use of mask in the presence of other individuals. She was later discharged in stable condition with the above-mentioned medications. She had complete resolution of her symptoms in two months and completed six months course of ATT.
|
[[32.0, 'year']]
|
F
|
{'6821188': 1, '23130251': 1, '4206095': 1, '6478910': 1, '921087': 1, '10998650': 1, '937642': 1, '4210271': 1, '77993': 1, '20727834': 1, '15014179': 1, '7291107': 1, '30338183': 2}
|
{}
|
3,266 |
6175255-1
| 30,338,180 |
comm/PMC006xxxxxx/PMC6175255.xml
|
Pneumocephalus as a Complication of Transsphenoidal Surgery for Pituitary Adenoma: A Case Report
|
A 49-year-old female with a history of acromegaly, status post-transsphenoidal pituitary resection three weeks prior, presented to the emergency room with a headache and clear nasal discharge present since the removal of a nasal splint. The patient described the cephalgia as severe, intermittent and throbbing, exacerbated by standing up and coughing and relieved by lying down and acetaminophen. On physical examination, her vital signs were normal and the results of neurological examination were normal, but a minimal clear nasal discharge was noted. A computed tomography (CT) scan of the head showed multiple air loculi in the basal cisterns, lateral, third and fourth ventricles and numerous air-filled spaces also scattered in the brain. No mass effect or midline shift was seen (Figure ).\nInitial management consisted of bed rest in the Fowler position at 30° and instructions to avoid Valsalva maneuver such as analgesia, coughing, and sneezing. Besides the supportive treatment, the headache worsened, and a repeat CT scan showed mild increased diffuse PNC with intracranial air loculi in the parafalcine region, anterior horn of the left ventricle, posterior fossa, and left middle fossa. There was also an increased amount of air in the posterior fossa causing a mass effect on the pons (Figure ).\nShe underwent a transsphenoidal endoscopic exploration of the sphenoid and sellar floor, with septoplasty and packing of the sphenoid sinus with abdominal fat graft, and with the insertion of a lumbar drain. After these procedures, she showed a significant improvement of her symptoms, the lumbar drain was removed after five days, and her headache and nasal leakage resolved. She was discharged on day 10 of hospitalization. At the time of follow up, the patient was free of symptoms, and repeat CT-scan revealed resolved PNC (Figure ).
|
[[49.0, 'year']]
|
F
|
{'9007854': 1, '26500801': 2, '20015750': 1, '25328392': 1, '9400638': 1, '28932993': 1, '24305016': 1, '24708096': 1, '31312549': 2, '8602677': 1, '18447708': 1, '30338180': 2}
|
{'6615587-1': 1, '4596054-1': 1}
|
3,267 |
6175263-1
| 30,338,196 |
comm/PMC006xxxxxx/PMC6175263.xml
|
An Unusual Case of Penile Spindle Cell Malignancy
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A 60-year-old male presented with growth over the glans penis for two months associated with pain. There was no history of contact bleeding. The patient was not circumcised. He had noticed a swelling on the scrotum for the past six months. On examination, there was a 2 x 3 cm ulceroproliferative growth over the glans extending over the corona onto the shaft of penis. The ulcer was fixed to the ventral aspect of glans penis with induration proximally extending up to mid shaft of penis (Figure ).\nBilateral inguinal lymph nodes were palpable, 3-4 on each side, 0.5 cm in size, firm and mobile in nature. The patient also had a right-sided primary vaginal hydrocele. A clinical diagnosis of SCC of penis was made and a wedge biopsy done. Histopathological analysis revealed an ulcerated stratified squamous epithelial lining with underlying lesion composed of fascicles of spindle cells with moderate pleomorphism. These were very few in number to proceed with IHC stains. A possibility of a primary sarcoma of penis was suggested.\nFine needle aspiration cytology (FNAC) was done from bilateral inguinal nodes which revealed reactive hyperplasia. All blood parameters, liver and renal function tests were normal. The chest X-ray and ultrasound abdomen were unremarkable.\nTotal penectomy with perineal urethrostomy was performed. The hydrocele was aspirated under aseptic precautions, three days before surgery. Post-operative course was uneventful. The patient was discharged on the eighth post-operative day and was advised to follow up with the regional cancer center for further management.\nThe final histopathological examination revealed moderate pleomorphic spindle cells arranged in sheets of fascicles, the overlying squamous epithelium was dysplastic. Focal areas of necrosis were seen. No definite feature of keratinization was seen (Figure ).\nThe tumor cells were strongly positive for pancytokeratin and vimentin, and negative for epithelial membrane antigen (EMA), neuron-specific enolase, CD 34, S100, Melan A and HMB 45 (Figure ).\nThe final report was sarcomatoid carcinoma (spindle cell carcinoma) of penis involving the glans. The urethra, proximal resected skin and shaft were free of tumor.
|
[[60.0, 'year']]
|
M
|
{'11484498': 1, '19468412': 2, '15311001': 1, '16096403': 1, '20730609': 1, '20598063': 1, '30338196': 2}
|
{'2684283-1': 1}
|
3,268 |
6175264-1
| 30,338,190 |
comm/PMC006xxxxxx/PMC6175264.xml
|
Intradural Extramedullary Thoracic Cavernoma in a Man with Familial Multiple Cavernomas
|
A 55-year-old male with a history of multiple cerebral cavernomas presented to the emergency department of an outside hospital for back pain radiating to the right chest region. He attributed his pain to muscle strain associated with fixing a popup camper. An extensive workup was done and was negative except for magnetic resonance imaging (MRI) of the spine. This showed evidence of an intradural extramedullary lesion at the T3-T4 level, located dorsally and directed rightward. The lesion appeared hyperintense on T1 and T2 with compression of the cord (Figure and Figure ).\nThe patient was referred to the neurosurgery clinic, where he had been seen one month prior for decreasing dexterity of the left hand of one year’s duration. The past medical history was significant for seizures beginning at age 15, for which the patient underwent separate partial resections of the right frontal and temporal lobes. Multiple new cavernomas had been found following a breakthrough seizure at age 50. When the patient first presented to the neurosurgery clinic at age 54, he reported a decrease in left-hand dexterity. The only interval change in the MRI at the time was an enlargement of a right porencephalic cyst in the context of the patient’s previous surgeries.\nNeurological exam revealed right-sided hyperreflexia but no weakness of the upper or lower extremities. He was diagnosed with thoracic myelopathy. Given the symptomatic presentation with severe radiculopathy and cord compression, the patient was offered surgery.\nUnder general anesthesia with neuromonitoring, a T3-T4 hinge laminotomy was performed. Ultrasound was used to confirm the location of the lesion within the dura. Under the magnification of the operating microscope, a curvilinear durotomy was performed. The lesion was hemorrhagic and highly friable. It appeared to be attached to the T3 dorsal nerve rootlets. Gross total resection was achieved in a piecemeal fashion using tumor forceps. After the tumor was mobilized off the spinal cord and the inner surface of the dura, it was seen to have left an impression on the thoracic spinal cord in the T3-T4 area. The durotomy was then closed in a water-tight fashion and the wound was closed in multiple layers. No complications were noted during the procedure and no changes were seen on neuromonitoring. Postoperative scans demonstrated no residual lesion (Figure ). The patient was relieved of his mid-back or thoracic radiculopathy and remained neurologically at baseline immediately post-operatively and at six months.
|
[[55.0, 'year']]
|
M
|
{'24878074': 1, '1723175': 1, '27635797': 1, '1388829': 1, '9231011': 1, '16155803': 1, '1513428': 1, '1595050': 1, '6174711': 1, '25130126': 1, '30338190': 2}
|
{}
|
3,269 |
6175265-1
| 30,338,187 |
comm/PMC006xxxxxx/PMC6175265.xml
|
Type 2M Von Willebrand Disease: A Case Report
|
We report a 24-year-old Caucasian woman who presented to the hematology clinic with a history of easy nontraumatic bruising on both thighs and legs. She had a recent history of fall, with bruises on the left hip, bilateral arms, and the lower left quadrant of the abdomen. Her family history was negative for easy bruisability, bleeding, or clotting disorder. She denied any bleeding gums, heavy menstrual blood flow, nasal bleeds, blood in stool, or blood in urine. She also had an unexplained loss of appetite and loss of weight over the last six months. Her medication history included inhaled albuterol as needed. She has not had any surgeries in the past. She smokes a pack of cigarettes per day and drinks a pint of vodka every night as well as three cans of beer per week. She is unmarried and has no children. She is sexually active with male partners. Her maternal grandmother had lung cancer.\nThe physical examination was unremarkable except for few bruises on bilateral thighs. The computed tomography (CT) scans of the chest, abdomen, and pelvis were ordered to screen for her unexplained weight loss which was unremarkable. The complete blood count, comprehensive metabolic panel, factor VIII, prothrombin time and partial thromboplastin time, D-Dimer, and antithrombin activity were normal. Her von Willebrand factor activity was much lower compared to the antigen (Table ). From the reports, it was established that her von Willebrand factor activity was 20% (reference range is 40%-163%) whereas the antigen was low normal at 45% (reference range is 45%-150%) and the ratio is less than 0.5 (normal ratio is more than 0.7). Repeat testing in a week consolidated the previous findings with the factor activity and the antigen as less than 19% and 37%, respectively. The reports of her von Willebrand factor multimer analysis were normal. The platelet count was normal.
|
[[24.0, 'year']]
|
F
|
{'9473222': 1, '22131616': 1, '17596142': 1, '25712990': 1, '28904675': 1, '29378695': 1, '23633542': 1, '25113304': 1, '30338187': 2}
|
{}
|
3,270 |
6175266-1
| 30,338,173 |
comm/PMC006xxxxxx/PMC6175266.xml
|
P/Q and N-type Voltage-gated Calcium Channel Binding Antibodies Associated with Paraneoplastic Chorea and Mixed Invasive Ductal and Lobular Carcinoma of the Breasts in an Elderly Patient
|
In December 2012, a 70-year-old woman presented with the chief complaint of “shaking” head movements. The movements began one month previously, shortly after she began taking hydroxychloroquine for seropositive rheumatoid arthritis (RA).\nIn addition to RA, the patient had a past medical history of atrial fibrillation, cardioembolic cerebrovascular accident, two transient ischemic attacks, Sjögren’s syndrome, pseudogout, calcium pyrophosphate disease, osteoarthritis, pacemaker placement, left-sided multinodular goiter, osteoporosis, chronic hypertension, heart failure with preserved ejection function, recurrent bilateral lower extremity deep vein thromboses, iron deficiency anemia, anxiety disorder, major depressive disorder, and dyslipidemia. She did not smoke tobacco, drink alcohol, or use illicit drugs. She danced once or twice a week to maintain physical fitness. Her family history was not contributory. She did not have allergies. Her medications included atorvastatin, carvedilol, cyclosporine, docusate, ergocalciferol, ferrous sulfate, folic acid, furosemide, losartan, melatonin, methotrexate, omeprazole, polyethylene glycol, prednisone, hydroxychloroquine, and warfarin.\nBlood pressure was 135/72 mmHg, temperature was 97.7 Fahrenheit (38.6 Celsius), and body mass index was 41.05 kg/m2. She was alert and oriented to person place and time, and not in acute distress. Cranial nerves 2–12, and sensation to pinprick, vibration, and joint position were intact. Reflexes were 2+ at all the tendons, and strength was 5/5 in all the extremities. Gait was ataxic and she had choreiform movements affecting her head, upper extremities, and lower extremities. There was some dysmetria with finger-to-nose testing. The heart had normal rate and rhythm with a holosystolic murmur in the aortic region. The pulmonary, abdominal, and integumentary exams were unremarkable.\nArrangements were made to contact the patient's rheumatologist to determine if the head movements were related to hydroxychloroquine and obtain medical records from outside facilities. Results from a computed tomography (CT) scan of the head performed elsewhere four months previously were unremarkable except for some abnormalities around the pituitary region.\nBy February 2013, the truncal ataxia and abnormal head movements were still present. Hydroxychloroquine was halted, and rituximab was started, in case the former medication was the cause of her abnormal movements; however, the movements continued. Complete blood count (CBC), complete metabolic panel (CMP), thyroid function tests (TFTs), parathyroid hormone, lipid panel, vitamin B12 level, human immunodeficiency virus (HIV) screen, rapid plasma reagin, iron panel with ferritin, and creatine kinase (CK), were all within the normal limits. Antinuclear antibody, anti-Ro antibodies, rheumatoid factor, and anti-cyclic citrullinated peptide were positive; anti-La antibody was negative. A paraneoplastic antibody panel demonstrated P/Q and N-type V-G calcium channel antibodies. Table shows the full results of the paraneoplastic antibody panel. By November 2013, the cerebellar ataxia had resolved; however, the patient reported occasional sensations of feeling like she was “on a ship” and had some difficulties maintaining her balance.\nIn January 2014, the cerebellar ataxia returned prompting a workup for malignancy. Based on the US Preventative Task Force's recommendations about age-appropriate cancer screening for a 70-year-old-female a colonoscopy and screening mammograms were ordered. The colonoscopy was only remarkable for diverticulosis. Bilateral screening mammograms (Figures -) and ultrasounds done in April 2014 identified a 2.1 × 2.0 × 1.7 centimeter (cm) mass and a 0.7 × 0.5 cm hypoechoic area at the upper outer quadrants of the left and right breasts, respectively. Two months later, bilateral core needle biopsies confirmed bilateral breast cancer.\nIn September 2014, she presented again with complaints of intermittent abnormal movements of the head, with choreiform and athetoid characteristics; the movements were absent at rest and present with movement. In the same month, she underwent total bilateral mastectomies. The left breast specimen was 2.2 × 1.6 × 1.4 cm with a negative sentinel lymph node, and that from the right breast was 1.1 × 1.0 × 0.6 cm, with three negative lymph nodes. Histopathology revealed mixed invasive ductal and lobular carcinoma. Immunohistochemistry was weakly estrogen receptor (ER) positive, weakly progesterone receptor (PR) positive, and human epidermal growth factor 2 (HER2) negative. Antigen Ki-67 results predicted a low risk of recurrence. Tumor protein P53 was positive in the left breast but negative in the right breast.\nIn April 2015, she continued to have intermittent episodes of abnormal movements that also were unresponsive to trails of gabapentin and clonazepam.
|
[[70.0, 'year']]
|
F
|
{'6114283': 1, '15823485': 1, '17389803': 1, '21465146': 1, '9854961': 1, '14769141': 1, '31191155': 1, '19370491': 1, '33824828': 2, '32832197': 1, '8656140': 1, '10219745': 1, '19845010': 1, '26109714': 1, '18851928': 1, '11102903': 1, '10563618': 1, '16834698': 1, '30338173': 2}
|
{'8012257-1': 1}
|
3,271 |
6175268-1
| 30,338,188 |
comm/PMC006xxxxxx/PMC6175268.xml
|
Cavernous Hemangioma of the Small Bowel: A Case Report and Literature Review
|
A 66-year-old male presented to the emergency room due to worsening leg pain. His past medical history was significant for peripheral artery disease and iron deficiency anemia. Initial laboratory tests revealed an unexpectedly low hemoglobin level of 5.4 g/dl. He received three units of packed red blood cells and subsequently the hemoglobin level increased to 6.9 g/dl. Our gastroenterology department was consulted for evaluation of occult gastrointestinal bleeding. There was no hematochezia, melena, hematemesis, fatigue, or abdominal pain. The patient had been taking oral iron supplementation for the last five years for iron deficiency anemia. Previous upper and lower endoscopies were negative. On physical examination, the patient had pale conjunctivae. The abdomen was noted to be soft and non-tender. No masses, organomegaly or vascular bruits were detectable. The vital signs were stable, and the laboratory investigations were as follows: a hemoglobin (hb) level of 6.9 g/dL, a mean corpuscular volume of 73.5, a hematocrit level of 22.7% with normal white blood cell and platelet counts. The analyses for iron-deficiency anemia showed ferritin levels of 6 ng/mL, serum iron levels of 25 μg/dL, total iron-binding capacity of 535 μg/dL, and transferrin saturation of 5%. Upper and lower endoscopy showed no active bleeding or suspicious lesions. A small bowel capsule endoscopy was performed, which revealed a suspicious lesion over the jejunum with evidence of fresh blood (Figure ).\nFor further investigation, double balloon enteroscopy was performed, which revealed a proximal jejunal soft submucosal mass (25 mm) with mild superficial ulceration/erosions of the surface mucosa. Biopsy samples were taken from the mass and the patient was referred for further management and surgical evaluation. The final pathology results revealed a cavernous hemangioma without evidence of malignancy.
|
[[66.0, 'year']]
|
M
|
{'17983812': 1, '31970182': 1, '24206746': 1, '27004239': 1, '18405648': 1, '22679168': 1, '23256111': 1, '26240811': 2, '16226971': 1, '25007019': 1, '28293061': 1, '22875598': 1, '10966205': 1, '18155208': 1, '32238724': 1, '32999791': 2, '19481664': 1, '32327915': 2, '24324488': 1, '17321267': 1, '11569713': 1, '27447475': 1, '19362610': 1, '26303132': 1, '30338188': 2}
|
{'7167414-1': 1, '4522429-1': 1, '7522049-1': 1}
|
3,272 |
6175539-1
| 29,861,043 |
comm/PMC006xxxxxx/PMC6175539.xml
|
Evaluating the causality of novel sequence variants in the prion protein gene by example
|
A 63-year-old right-handed Danish Caucasian lady, with no previous medical illnesses or family history of neurodegenerative diseases, was admitted urgently to her local stroke unit with a 5-day history of abrupt onset fluent dysphasia in October 2009. Detailed speech examination revealed preserved fluency and comprehension but markedly impaired repetition, reminiscent of conduction aphasia. Computed tomography of her brain was unremarkable, and she was subsequently discharged with secondary prevention measures for stroke, after 3 days. Nine days following hospital discharge, she returned with sudden onset right-sided paresthesia, and thereafter, her clinical complex evolved rapidly through a sequence of dysarthria, nonfluent speech, dyslexia, dysgraphia, motor and verbal perseveration, startle, myoclonus, akinetic mutism, and finally death over the period of 10 weeks.\nThe patient has 2 older sisters, both of whom are alive and well in their 70s at the present time. Her father died of cancer at the age of 80 years, while her mother lived until the age of 90 years; neither parent had neurological or cognitive symptoms in life. The patient's father had a sister who died in “old age” of an unknown cause; her mother had 2 other siblings who died of cancer at 63 and 73 years of age, respectively.\nMagnetic resonance imaging (MRI) of her brain revealed restricted diffusion in her caudate heads, anterior putamina, and predominantly left-sided cortical ribboning. Her electroencephalogram (EEG) showed left frontotemporal slowing of 1–2 Hz, with occasional sharp waves over the left hemisphere. Her cerebrospinal fluid had 3 white cells and 308 red cells but normal protein and glucose levels; protein 14.3.3 was positive, and neuron-specific enolase (NSE) was raised 101 ng/ml (<35 ng/mL); real-time quaking-induced conversion assay was not performed.
|
[[63.0, 'year']]
|
F
|
{'20880036': 1, '18624793': 1, '20694796': 1, '24224623': 1, '20583301': 1, '10079068': 1, '16597650': 1, '19218199': 1, '11476832': 1, '23315928': 1, '34182938': 2, '18576157': 1, '19321423': 1, '24487276': 1, '24059340': 1, '19773352': 1, '31340582': 1, '16391566': 1, '10440324': 1, '17991853': 1, '24252267': 1, '25741868': 1, '12764055': 1, '15539564': 1, '27535533': 1, '25623792': 1, '27830781': 1, '16415305': 1, '26135918': 1, '31447551': 1, '11283320': 1, '19204296': 1, '34696491': 1, '9811807': 1, '34578375': 1, '19561590': 1, '26791950': 1, '29861043': 2}
|
{'6175539-2': 2, '8237416-1': 1}
|
3,273 |
6175539-2
| 29,861,043 |
comm/PMC006xxxxxx/PMC6175539.xml
|
Evaluating the causality of novel sequence variants in the prion protein gene by example
|
A 76-year-old right-handed British Caucasian woman, with no family history of neurodegenerative diseases, developed abrupt onset bilateral upper limb postural and action myoclonus. In the following week, she exhibited unusual sitting postures (axial apraxia), and her gait assumed a narrow-based shuffling character (gait apraxia). She then developed a rapidly progressive nonfluent dysphasia that rendered her effectively mute within 3 weeks. In tandem with that, she became socially withdrawn, abulic, and completely indifferent to her surroundings. Subsequently, she developed visual hallucinations, exaggerated startle, severe myoclonus, incontinence, and akinetic mutism. She died 8 weeks after symptom onset; a postmortem examination was not carried out.\nThe patient was the only child. Her father died of bone cancer at the age of 73 years, while her mother died of lung cancer at the age of 57 years.\nHer MRI brain showed asymmetrical cortical ribboning with a left-sided emphasis and bilateral anterior basal ganglia diffusion restriction, while her EEG showed generalized periodic complexes. cerebrospinal fluid cell count and routine biochemistry were normal, but no sample was analyzed for protein 14.3.3, S100B, or real-time quaking-induced conversion assay.
|
[[76.0, 'year']]
|
F
|
{'20880036': 1, '18624793': 1, '20694796': 1, '24224623': 1, '20583301': 1, '10079068': 1, '16597650': 1, '19218199': 1, '11476832': 1, '23315928': 1, '34182938': 2, '18576157': 1, '19321423': 1, '24487276': 1, '24059340': 1, '19773352': 1, '31340582': 1, '16391566': 1, '10440324': 1, '17991853': 1, '24252267': 1, '25741868': 1, '12764055': 1, '15539564': 1, '27535533': 1, '25623792': 1, '27830781': 1, '16415305': 1, '26135918': 1, '31447551': 1, '11283320': 1, '19204296': 1, '34696491': 1, '9811807': 1, '34578375': 1, '19561590': 1, '26791950': 1, '29861043': 2}
|
{'6175539-1': 2, '8237416-1': 1}
|
3,274 |
6176285-1
| 30,356,339 |
comm/PMC006xxxxxx/PMC6176285.xml
|
Identification of Dietzia Species in a Patient with Endophthalmitis following Penetrating Injury with Retained Intraocular Metallic Foreign Body
|
A 47-year-old Norwegian male presented at the general causality clinic with right eye irritation. Previously, the same day he had been working using a hammer and chisel to repair his car without any eye protection, and he thought a foreign body had struck his right eye. The examination of his right eye revealed congestion and laceration of the conjunctiva, and the general practitioner started treatment with a broad-spectrum topical antibiotic (chloramphenicol). Seven days following his first presentation to the general causality clinic, he woke up with decreased vision, redness, and minimal pain in his right eye, and he presented to the nearby ophthalmology department on the same day. The best-corrected visual acuity (BCVA) decimal had decreased from 1.0 to 0.7. The orbit computed tomography scans detected a metallic intraocular foreign body (), and he was referred urgently to the Department of Ophthalmology at Oslo University Hospital for surgical removal of the foreign body. On arrival, the BCVA decimal had decreased from 0.7 to hand motion. The biomicroscopic examination revealed intense conjunctival and ciliary injection, most likely self-sealed conjunctival laceration, corneal oedema, 3+ anterior chamber cells with fibrin, and a thin layer of hypopyon in the anterior chamber and posterior synechiae. A layer of fibrin mesh covered the anterior surface of the lens. The changes in ocular media obscured the fundus view. The B-scan ultrasonography revealed an echogenic foreign body in the posterior vitreous cavity with dense vitreous opacities and attached retina and posterior vitreous. His left eye was unremarkable, and he was otherwise in good health. A clinical diagnosis of exogenous endophthalmitis secondary to penetrating eye injury with retained intraocular metallic foreign body was made.\nHe underwent an emergency 23-gauge pars plana vitrectomy with both undiluted and diluted vitreous biopsy and anterior chamber tap. The attempt to remove the intraocular foreign body was unsuccessful even after the removal of fibrin mesh layer covering the anterior surface of the lens due to poor surgical visualization of the posterior segment. At the end of the surgery, vancomycin (1 mg/0.1 ml), ceftazidime (2 mg/0.1 ml), and fungizone (0.00549 mg/0.1 ml) were administered intravitreally and gentamicin (20 mg/0.5 ml) subconjunctivally. He received treatment with topical steroids and antibiotics (Maxitrol eye drops consisting of dexamethasone, neomycin, and polymyxin B eye drops) hourly during daytime and intravenous cefuroxime (750 mg 3 times a day) postoperatively. In addition, he received oral steroids (prednisolone 60 mg daily) only for 2 days prior to repeated pars plana vitrectomy. Due to poor visualization of the posterior segment initially, he underwent surgical removal of the metallic intraocular foreign body (2 × 1.5 × 1 millimetres) 7 days after the first operation. The day after surgical removal of the foreign body, the intravenous cefuroxime was discontinued, and he was prescribed a 10-day course of ciprofloxacin (750 mg three times a day) peroral treatment. He continued with topical steroids and antibiotics (dexamethasone, neomycin, and polymyxin B eye drops) three times a day. The routine postoperative eye examination on the 9th day following removal of the foreign body revealed asymptomatic rhegmatogenous retinal detachment from 10 to 2 o'clock with fovea on and with a BCVA decimal of 0.4. He underwent his third pars plana vitrectomy with gas tamponade. Three weeks following the retinal detachment repair, he reached a BCVA decimal of 0.8, and the retina was attached. Six months following the retinal detachment repair, he reached a BCVA decimal of 1.0.\nDirect microscopy of the undiluted vitreous sample showed pleomorphic rods with coccoid or club-shaped appearance suggesting coryneform bacteria.\nA broad PCR and DNA sequencing targeting 16S rRNA-encoding gene was performed on the undiluted vitreous body sample using EZI DNA tissue kit (Qiagen, Thermo Fisher Scientific, Hilden, Germany). The 5' half of the 16S rRNA gene was amplified by PCR. The PCR product was sequenced using BigDye Terminator Cycle Sequencing Kit (Thermo Fisher Scientific, Hilden, Germany). The bacterium was identified by searching the GenBank (the NIH genetic sequence database) with the obtained DNA sequence. The obtained 740-base pair DNA sequence revealed 100% identity with GenBank sequences of the Dietzia species including D. natronolimnaea, D. dagingensis, and D. cercidiphylli. Although, additional DNA sequencing on the rest of the 16S rRNA gene (total 1462 base pairs) was performed, and this did not give an unambiguous identification.\nThe undiluted and diluted vitreous samples were cultured on sheep blood agar and chocolate agar plates (Oslo University Hospital, Oslo, Norway). The plates were incubated at 35°C in 5% carbon dioxide (CO2) for 7 days. The growth of bacteria was detected after two days under aerobic incubation at 35°C in 5% CO2. Anaerobic culture using horse blood agar (Oslo University Hospital, Oslo, Norway) did not detect any bacterial growth, and yeast culture on Sabouraud agar (Oslo University Hospital, Oslo, Norway) did not reveal any growth. No bacterial or yeast growth was detected from the anterior chamber tap aspirate.\nThe Gram stain of the bacterial colonies demonstrated Gram-positive cocci and polymorphic rods. The isolate from the culture was identified as D. natronolimnaea using MALDI-TOF MS (MALDI Biotyper, Bruker Daltonics GmbH, Bremen, Germany). MALDI-TOF was unable to distinguish D. natronolimnaea from D. dagingensis and D. cercidiphylli because the MALDI-TOF database does not contain the sequences for the latter two species.\nAntimicrobial susceptibility tests were performed on Mueller-Hinton agar (Oslo University Hospital, Oslo, Norway) using MIC test strips (Liofilchem, Teramo, Italy). There are no determined breakpoints for Dietzia species, and therefore, the results were reported with a minimum inhibitory concentration (MIC) value. The MIC values of ciprofloxacin, gentamycin, tetracycline, and vancomycin against Dietzia species were low, indicating that these antibiotics have clinical effect.
|
[[47.0, 'year']]
|
M
|
{'28101387': 2, '18175685': 1, '23438028': 1, '23945639': 1, '23536398': 1, '9783184': 1, '24635156': 1, '22984001': 1, '17670678': 1, '10739337': 1, '12900232': 1, '7857805': 1, '34917388': 1, '18033838': 1, '23035183': 1, '8659579': 1, '10524995': 1, '19159434': 1, '23993357': 1, '29094328': 1, '34905116': 1, '22151787': 1, '16514042': 1, '29477689': 1, '11427581': 1, '21478395': 1, '23245359': 1, '25600198': 1, '30356339': 2}
|
{'5215629-1': 1}
|
3,275 |
6176286-1
| 30,356,358 |
comm/PMC006xxxxxx/PMC6176286.xml
|
Two Cases of Dedifferentiated Endometrioid Carcinoma: Case Presentation and Brief Review of the Literature
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Case 1. A 68-year-old postmenopausal woman (gravida 2; body mass index [BMI], 32.4 kg/m2) presented at a local gynecology clinic 20 months ago with a chief complaint of vaginal spotting. Transvaginal ultrasonography showed no thickness of the endometrium, and endometrial cytology was negative. At the three-month follow-up visit, a repeat endometrial cytology was also negative. However, vaginal bleeding persisted, and the patient visited the clinic again a month ago. At this time, pelvic magnetic resonance imaging (MRI) was performed, which revealed irregularity and endometrial thickening, and the patient was referred to our institution—Nara Medical University, Kashihara, Nara, Japan—for further evaluation. Endometrial curettage was performed that revealed atypical cells with large nuclei and conspicuous nucleoli without gland formation, which appeared to be consistent with high-grade endometrioid carcinoma or UC. The level of tumor markers was not elevated: CA125, 17 U/ml; CA19-9, 9 U/ml; CA72-4, 2.9 U/ml; CEA, 1.1 ng/ml; and SCC, 0.9 ng/ml. Chest and abdominal contrast-enhanced computed tomography (CECT) revealed no metastatic lesions. Pelvic contrast-enhanced MRI showed multiple myomas and a 30 mm polyp-like mass projecting into the endometrial cavity without myometrial invasion. The patient underwent abdominal total hysterectomy, bilateral salpingo-oophorectomy, pelvic lymphadenectomy, para-aortic lymphadenectomy, and omentectomy. The surgical specimen of the uterus showed a 35 mm polypoid tumor developing from the uterine posterior wall. Microscopically, the polypoid tumor comprised well-differentiated endometrioid carcinoma, grades 1-2, and UC. The well-differentiated endometrioid carcinoma was confirmed on the surface of the endometrial polyp, and the coexisting UC showed a diffuse proliferation of atypical cells (). Pancytokeratin (AE1/AE3) was diffusely expressed in the differentiated carcinoma component and was focally expressed in the UC component. Estrogen receptor (ER) and progesterone receptor (PR) were well expressed only in the differentiated carcinoma component (). The UC component represented about 80% of the whole neoplasm. Endometrium invasion or lymph node (LN) metastasis was not observed. Based on these findings, the patient was diagnosed with DEC located on the endometrial polyp. The final Federation of Obstetrics and Gynecology (FIGO) stage was IA. The patient was treated with adjuvant chemotherapy (TC protocol: paclitaxel, 175 mg/m2 + carboplatin AUC 6, every three weeks, and six cycles). She has been disease-free for 15 months after the initial surgery.
|
[[68.0, 'year']]
|
F
|
{'24371688': 2, '17365829': 1, '5566365': 1, '23923084': 1, '29285365': 1, '21531695': 1, '20305618': 1, '16160474': 1, '534388': 1, '21448784': 1, '17342307': 1, '32090165': 1, '269000': 1, '16306785': 1, '28069049': 2, '26239622': 1, '26371430': 1, '22295150': 1, '30356358': 2}
|
{'6176286-2': 2, '3862303-1': 1, '5223350-1': 1, '5223350-2': 1, '5223350-3': 1, '5223350-4': 1}
|
3,276 |
6176286-2
| 30,356,358 |
comm/PMC006xxxxxx/PMC6176286.xml
|
Two Cases of Dedifferentiated Endometrioid Carcinoma: Case Presentation and Brief Review of the Literature
|
Case 2. A 58-year-old woman (BMI, 22.9 kg/m2), who had been hospitalized for several months with a diagnosis of bipolar disorder, reported that she has been experiencing atypical vaginal bleeding for >1 year, which had worsened over time. An abdominal CECT showed a large pelvic mass, and she was transferred to our institution for further evaluation. Pelvic MRI revealed a bulky mass in the whole uterine corpus, which spread to the bladder and rectum. Chest and abdominal CECT revealed multiple LN metastases, which extended from the para-aortic to pelvic LNs. Endometrial curettage revealed the foci of atypical cells arranged in sheets with numerous mitotic figures. There was no sarcoma component, and the histological pattern represented that of only a carcinoma. ER and PR tumor cell were focally expressed. As tumor markers, CA19-9, CEA, and SCC levels had risen (CA19-9, 43 U/ml; CEA, 13.9 ng/ml; SCC, 80.4 ng/ml); CA125 and CA72-4 levels were within normal range (CA125, 12 U/ml; CA72-4, 2.5 U/ml). Although the pathological diagnosis remained uncertain, based on the overall findings, the patient was diagnosed with stage IVA uterine endometrial cancer. Because of the presence of mental disorder and poor general condition (performance status 4), best supportive care was selected as the optimal treatment. However, the patient died in three months. Autopsy revealed uterine tumor invasion to the bladder, rectum, and pelvic wall with the involvement of the greater omentum and small intestine. The metastases to the pelvic and para-aortic LNs were observed. Microscopically, endometrioid carcinoma (grade 2) and UC components were present. Pancytokeratin (AE1/AE3) was diffusely expressed in the differentiated carcinoma component and focally expressed in the UC component (). ER and PR tumor cells were expressed only in the differentiated carcinoma component. There were bone marrow hyperplasia and neutrophil infiltration in the lung and myocardium. The patient died of sepsis due to urinary tract infection secondary to the tumor invasion. The final diagnosis was DEC with FIGO stage IVB.
|
[[58.0, 'year']]
|
F
|
{'24371688': 2, '17365829': 1, '5566365': 1, '23923084': 1, '29285365': 1, '21531695': 1, '20305618': 1, '16160474': 1, '534388': 1, '21448784': 1, '17342307': 1, '32090165': 1, '269000': 1, '16306785': 1, '28069049': 2, '26239622': 1, '26371430': 1, '22295150': 1, '30356358': 2}
|
{'6176286-1': 2, '3862303-1': 1, '5223350-1': 1, '5223350-2': 1, '5223350-3': 1, '5223350-4': 1}
|
3,277 |
6176294-1
| 30,356,364 |
comm/PMC006xxxxxx/PMC6176294.xml
|
Sarcoidosis and Monoclonal Gammopathy of Undetermined Significance (MGUS): A True Association or Just a Coincidence?
|
A 79-year-old male with a past medical history of hypothyroidism and benign prostatic hyperplasia presented with dry mouth for four months. Family history was significant for the presence of Crohn's disease and systemic lupus erythematosus (SLE) in his sister. He was initially referred to an oral surgeon who performed a lip biopsy two weeks prior to admission revealing nonnecrotizing epithelioid cell granulomas. The patient was prescribed a mouthwash solution containing diphenhydramine, nystatin, lidocaine, hydrocortisone, and tetracycline. He was referred to a rheumatologist. His xerostomia significantly worsened prior to his appointment with rheumatology so he decided to go to the emergency department (ED). He presented to the ED with generalized weakness and decreased oral intake secondary to mouth pain resulting in a 30-pound weight loss over four months. Physical exam was remarkable for dry oropharyngeal mucosa. Laboratory analysis revealed an elevated serum calcium of 12.71 mg/dL (reference range: 8.4–10.7 mg/dL), an increased ionized calcium of 1.9 mmoL/L (reference range: 1.10–1.30 mmoL/L), an increased creatinine level of 3.81 mg/dL (reference range: 0.7–1.3 mg/dL), a decreased parathyroid hormone level of 6.5 pg/mL (reference range: 15–65 pg/mL), and an increased erythrocyte sedimentation rate (ESR) of 55 mm/hr (reference range: 0–15 mm/hr). Despite adequate fluid hydration, his calcium level remained elevated. Further workup for hypercalcemia revealed undetectable parathyroid hormone-related peptide (PTHrp), mildly decreased 25-hydroxyvitamin D at 18.1 ng/ml (reference range: 20–100 ng/ml), and an elevated 1,25-dihydroxyvitamin D at 72 pg/ml (reference range: 18–64 pg/ml).\nFurther workup for hypercalcemia showed an elevated angiotensin-converting enzyme at 91 U/L (reference range: 18–53 U/L). Bence Jones protein revealed free lambda light chains in the urine. Serum protein electrophoresis showed an elevated gamma globulin level of 38% and an IgG monoclonal gammopathy with an M-spike of 1.47. Immunoglobulin free light chain revealed elevated kappa free light chains at 5.79 and elevated lambda free light chains at 14.1 with a kappa to lambda ratio of 0.4. A bone marrow biopsy was done and was sent for pathology.\nFurther workup for dry mouth showed positive antinuclear antibody (ANA) at a titer of 1 : 160, and the other rheumatologic workup was negative.\nThe constellation of findings prompted further workup for sarcoidosis. Chest radiograph (CXR) showed minimal hilar lymphadenopathy which was more pronounced on the right side, bibasilar infiltrates and mild bilateral pleural effusions. High-resolution computerized tomography (HRCT) of the chest showed prominent hilar densities, ground glass opacities, and bilateral pleural effusions (). He was started on prednisone 40 mg/day and noticed immediate symptomatic improvement. His calcium level normalized, and his acute kidney injury resolved. Bone marrow biopsy results revealed lambda-restricted plasma cell neoplasm with 5%–6% of bone marrow cellularity consistent with MGUS. The patient was discharged with a one-month follow-up from nephrology and oncology.
|
[[79.0, 'year']]
|
M
|
{'3756082': 1, '22534002': 1, '19561785': 1, '1344048': 1, '18032765': 1, '22422021': 1, '11734441': 1, '24424172': 1, '25340385': 1, '24761384': 2, '15888103': 1, '17560310': 1, '11860317': 1, '18307569': 1, '20472173': 1, '27651903': 2, '17917102': 1, '22461752': 1, '10641512': 1, '15855274': 1, '27542684': 1, '6454846': 1, '25078638': 1, '20088430': 1, '1583964': 1, '21071376': 1, '30356364': 2}
|
{'3994709-1': 1, '5024499-1': 1}
|
3,278 |
6176296-1
| 30,356,359 |
comm/PMC006xxxxxx/PMC6176296.xml
|
Late-Life Presentation of Unsuspected G6PD Deficiency
|
An 86-year-old retired male of African-Brazilian descent was admitted to the Clementino Fraga University Hospital for surgical correction of lumbar stenosis. He had a history of chronic arterial hypertension, stage 3 chronic kidney disease, benign prostatic hyperplasia, peripheral arterial disease, and arthrosis of the knees. He had long been treated with enalapril, hydrochlorothiazide, nifedipine, aspirin, simvastatin, finasteride, cilostazol, and tamsulosin. He had a smoking pack year equal to 30 but had quit smoking several years earlier.\nIn the immediate postoperatory period, he developed a hypertensive emergency and was treated with intravenous nitroglycerin. Soon thereafter, he developed cyanosis of the extremities, which was confirmed by pulse oximetry (SO2 = 79%), but not by arterial blood gas sampling (SO2 = 97%). He was then empirically treated with methylene blue considering the clinical suspicion of methemoglobinemia, but severe dyspnea ensued in close association with the beginning of treatment. His hemoglobin steeply decreased from 11.1 g/dL to 6.1 g/dL, but the physical exam revealed no evidence of bleeding or of liver enlargement. The patient was not aware of previous episodes of anemia. A laboratory work-up revealed an elevated reticulocyte count, macrocytosis, transient leukocytosis (leukocytes count = 14,000/mm3 with 60% neutrophils, 30% lymphocytes, 8% monocytes, and 2% eosinophils), normal platelet count (= 250,000/mm3), hemoglobinuria, and positive markers for hemolysis [LDH = 4701 U/L (normal < 250 U/L), total bilirubin = 1.6 mg/dL (normal range = 0.3-1.2 mg/dL), unconjugated bilirubin = 0.9 mg/dL (normal < 1 mg/dL), haptoglobin < 6 mg/dL (normal range = 44-215 mg/dL]. A Coombs test was negative. The peripheral blood smear was consistent with a diagnosis of hemolytic anemia (). A few days after exposure to methylene blue, the patient's methemoglobin was 4.5% (normal < 2%). Given the possibility that the hemolytic crisis had been triggered by a deficiency of G6PD, a measure of the activity of this enzyme was obtained, resulting in a value of 13.6 U/g Hb (normal > 6.7 U/g Hb). Because enzyme activity was assessed during the hemolytic crisis, a definite diagnosis of G6PD deficiency could not be confidently ruled out at the time.\nThe patient was treated with packed red blood cells and folic acid. A rapid clinical improvement, which was closely followed by normalization of the red blood cell count, was observed. Three months later, a follow-up measure of G6DP activity (5.5 U/g Hb) revealed a moderate degree of enzyme deficiency (the 10%-60% range), thus confirming the diagnosis of G6DP deficiency.
|
[[86.0, 'year']]
|
M
|
{'29305344': 1, '6015571': 1, '29592989': 1, '5641629': 1, '18177777': 1, '29217886': 2, '5771222': 1, '2633878': 1, '18156501': 1, '24715943': 1, '30356359': 2}
|
{'5704414-1': 1}
|
3,279 |
6176298-1
| 30,356,340 |
comm/PMC006xxxxxx/PMC6176298.xml
|
Combined Approach of Cryoablation and Stent-In-Stent Technique for Removal of an Embedded Esophageal Stent
|
A 72-year-old man with history of localized esophageal carcinoma with a history of neoadjuvant chemoradiation and esophagectomy presented to a local hospital with dysphagia four months after the surgery. Endoscopy revealed a benign-appearing esophageal stricture at the site of the anastomosis, and biopsies confirmed benign tissue. He was treated with a series of esophageal dilations and temporary placement of a FC-SEMS by his surgeon. This stent was removed after 3 months of placement; however, the patient developed recurrent symptoms after several weeks. Given no evidence of cancer recurrence, a 100 mm × 23 mm Wallflex PC-SEMS (Boston Scientific, Natick, MA) was placed by his surgeon as an attempt for a permanent solution to the patient's dysphagia.\nThe patient developed recurrent dysphagia after 3 months. A CT chest with oral contrast demonstrated the PC-SEMS in appropriate position at the anastomosis but demonstrated evidence of circumferential soft tissue extending approximately 2 cm in length and 7 mm in depth nearly occluding the proximal side of the stent. An upper endoscopy confirmed the above finding, and biopsies which concluded this represent benign and hypertrophic tissue.\nThis patient was then referred to our institution for further management and consideration of stent removal. At the time of referral, the PC-SEMS had been in place for almost 5 months. Repeat endoscopy demonstrated a benign-appearing stricture in midesophagus, beyond which the standard 9.8 mm endoscope could not pass. An ultraSlim 5.5 mm gastroscope was then advanced through the stricture, and the stent was identified beneath the tissue ingrowth and extending across the anastomosis. The proximal edges of the stent were not visible and fully covered by tissue ingrowth (). Cryoablation of the tissue ingrowth was performed using the CryoSpray (TruFreeze, Lexington, MA) Ablation () for 20 seconds, followed by placement of a 125 mm × 23 mm Wallflex FC-SEMS (Boston Scientific, Natick, MA) within the previously placed PC-SEMS () in order to promote tissue necrosis and permit subsequent removal of both stents. This rescue FC-SEMS was removed after 2 weeks on repeat endoscopy, with less tissue ingrowth visible on the proximal end and with no stricture evident. An attempt was made to remove the PC-SEMS but was unsuccessful. Thus, a 125 mm × 23 mm Wallflex FC-SEMS was again placed within the embedded PC-SEMS. Endoscopy was repeated after 4 months with successful removal of the rescue FC-SEMS. Less hypertrophic tissue was seen at the proximal end of the PC-SEMS and the PC-SEMS was now able to be pulled away from the embedded stent's proximal margin mucosa. Given the distal end of the stent which was still embedded, the stent was unable to be removed safely. Thus, another 125 mm × 23 mm Wallflex FC-SEMS was placed within the PC-SEMS. A repeat endoscopy was performed at 6 months with successful retrieval of both the FC-SEMS () and PC-SEMS (Figures and ) with minimal resistance with the help of rat-tooth forceps under fluoroscopic guidance. The patient was symptom-free and was started on high dose oral proton pump inhibitor with slow taper to a low daily dose.
|
[[72.0, 'year']]
|
M
|
{'20029413': 1, '24362537': 1, '20940709': 1, '27134592': 1, '28441152': 1, '14528208': 1, '26358327': 1, '10388850': 1, '20363409': 1, '12806523': 1, '21112501': 1, '23293566': 1, '22154410': 1, '28980205': 1, '17611917': 1, '27626318': 1, '26357006': 1, '30356340': 2}
|
{}
|
3,280 |
6176301-1
| 30,356,369 |
comm/PMC006xxxxxx/PMC6176301.xml
|
Pheochromocytoma in Congenital Cyanotic Heart Disease
|
We describe the case of a 23-year-old Caucasian female affected with congenital tricuspid atresia and intact ventricular septum. She had a history of palliative surgery since first days of life but her percutaneous oxygen saturation (SpO2) level remained around 80% even though a Fontan procedure was performed at 12 years of age. Persistent desaturation was related to the presence of venous collaterals between the Fontan circulation and left atrium.\nThe patient admitted to Policlinico San Donato (San Donato Milanese, Italy) for hypertensive crisis, worsening dyspnea, and hemoptysis. There was no family history of relevant morbidities. On examination, her height was 175 cm, weight was 64 kg (BMI 17.7 Kg/m2), blood pressure (BP) was 160/85 mmHg, and SpO2 was 81% (room air). Electrocardiogram (ECG) showed sinus tachycardia (heart rate 101 beats/min), first-degree atrioventricular block (PR 220 msec), and right bundle branch block (QRS 140 msec). Chest computed tomography (CT) () incidentally detected a 6-cm mass in the left adrenal lodge.\nThe presence of a heterogeneous adrenal lesion, with hyperintense spots due to hematic content, was confirmed by abdominal magnetic resonance imaging (MRI) ().\nLaboratory tests revealed increased levels of noradrenaline (NA) and its metabolites [plasma NA 5003.7 pg/ml, n.v. < 480 pg/ml; urinary NA 1059.5 µg/24 h, n.v. < 85.5 µg/24 h; urinary metanephrine 489 µg/24 h, n.v. < 320 µg/24 h; plasma adrenaline (A) 100 pg/ml, n.v.20-190 pg/ml; urinary A 15 µg/24 h, n.v.1.7-22.4 µg/24 h]. The patient reported no typical paroxysmal symptoms of catecholamine excess. Echocardiographic evaluation showed slight left atrial and ventricular enlargement, mild to moderate mitral regurgitation, and preserved systolic function (ejection fraction 65%).\nThe diagnosis of pheochromocytoma was confirmed by 123I-metaiodobenzylguanidine (123I-MIBG) scintigraphy showing abnormal accumulation of radioactive tracer in the left adrenal gland. A 18F-fluorodeoxyglucose positron emission tomography (18F-FDG-PET) performed in order to exclude any extra-adrenal uptake: no significant metabolic activity in the adrenal mass but intense uptake in supra- and subdiaphragmatic brown adipose tissue was detected, likely due to noradrenergic-stimulated glucose uptake ().\nThe patient underwent open left adrenalectomy after preconditioning with α-blockers (doxazosin) and, then, β-blockers (bisoprolol). Postoperative course was complicated by anemia due to hematoma formation in the left hypochondrium. Histopathological examination confirmed the diagnosis of pheochromocytoma with large hemorrhagic areas and scarce necrosis. No capsular or lymphovascular invasion was found. Immunohistochemistry revealed diffuse expression of chromogranin A, synaptophysin and neuron specific enolase, and S100 staining in sustentacular cells; Ki-67 was <5%. The P-PGL susceptibility genes VHL, RET, SDHA, SDHAF2, SDHB, SDHC, SDHD, MAX, and TMEM127 were analyzed for germline mutations and large deletions, via direct sequencing and multiplex ligation-dependent probe amplification methods; RET was only analyzed by direct sequencing. No aberration was found in these genes. Twelve months after surgery patient's BP and heart rate were under control and urinary NA and metanephrine levels were within the normal range. Plasma NA levels remained slightly increased (715 pg/ml n.v. 70-480), consistent with the hemodynamic changes in Fontan circulation [].
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[[23.0, 'year']]
|
F
|
{'24739310': 1, '29623675': 1, '31934081': 1, '12084585': 1, '10690869': 1, '12093776': 1, '30033572': 1, '4706179': 1, '29601261': 1, '21115164': 1, '25581599': 1, '30356369': 2}
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{}
|
3,281 |
6176302-1
| 30,356,349 |
comm/PMC006xxxxxx/PMC6176302.xml
|
Classical Hodgkin Lymphoma Presenting with Severe, Recurrent Hypothermic Episodes
|
A 39-year-old woman was admitted to the ER with a right-sided drop-foot, fever, and pancytopenia. The patient reported night sweats during the last month and a 25 kg weight loss over the last year. On physical examination, enlarged, painless right cervical and axillary lymph nodes were found; the largest of which was 1 × 2 cm. A CT-scan revealed marginally enlarged axillary and abdominal lymph nodes as well as a marginally enlarged spleen. A bone marrow biopsy was performed and bilineage dysplasia was found, possibly suggestive of a myelodysplastic syndrome. The fever and anaemia responded well to broad-spectrum antibiotics and blood transfusions, respectively. An EBV-viremia (18.500 DNA copies/mL) was detected, and the patient was treated with acyclovir followed by rituximab. The decision to initiate acyclovir and rituximab was taken due to suspected virus-associated haemophagocytic syndrome. During this treatment, three separate episodes of hypothermia occurred with an interval of approximately two weeks between each episode.\nThe first episode occurred the day after rituximab infusion and was accompanied by moderate bradycardia, hypotension, and a prolonged QT interval. The patient was subjectively unaffected. However, the patient had a syncope-like episode a few days later. Subsequent ECG monitoring at the Department of Cardiology did not reveal any arrhythmias. The second episode of hypothermia occurred 13 days later just before a planned rituximab infusion. However, the patient had already received paracetamol as premedication prior to rituximab. The patient only experienced mild symptoms related to hypothermia, that is, moderate sweating, moderate hypotension, and insecure gait. Intravenous fluids were administered with clinical effect. During the third episode, an ear temperature as low as 32.8°C was recorded. The patient experienced profuse sweating and an ECG demonstrated bradycardia along with a borderline prolonged QT interval. The blood pressure reached a low point of 85/52 mmHg and the pulse was recorded as 50 bpm. Similar to the previous episodes, the patient was relatively unaffected, and no specific treatment in order to increase the body temperature was initiated. The third episode differed from the first two since neither rituximab nor paracetamol was given prior to the onset of hypothermia ().\nA PET/CT was performed, revealing increased FDG uptake in enlarged right cervical and mediastinal lymph nodes and in focal areas of the spleen and liver. Furthermore, increased FDG uptake was found at multiple skeletal sites and in the bone marrow, but without CT correlate (). A surgical biopsy from a right cervical lymph node revealed classical HL, nodular sclerosis type. The bone marrow biopsy was without morphological and immunophenotypic evidence of lymphoma.\nIn the weeks following the last episode of hypothermia, three separate attacks with generalized seizures occurred. One of them was clinically described as a classic tonic-clonic Jackson-type attack, while the other two were less well characterized. An EEG showed focal activity compatible with epileptic state. Cerebral CT and MRI scans did not show any sign of intracranial or intraspinal tumors and did not provide any clues to clarify why the attacks occurred.\nThe patient was treated with 8 series of BEACOPP-14. The peroneal palsy which had remitted worsened again during chemotherapy, and it was therefore decided to continue without vinca alkaloids from series 3 and onwards. After 8 series the PET scan revealed a complete metabolic remission. No radiotherapy was added. Although no repeat bone marrow biopsy was done upon completion of the treatment schedule, all blood counts returned to normal making the initial diagnosis of a possible myelodysplastic syndrome unlikely. The patient received her last round of chemotherapy on December 2015. She was still in 1st complete remission and is regularly followed on an outpatient basis. No additional episodes of hypothermia have been registered so far.
|
[[39.0, 'year']]
|
F
|
{'7824016': 1, '3419084': 1, '3948197': 1, '22184521': 1, '11907792': 1, '6288883': 1, '19936661': 1, '6789938': 1, '21799410': 1, '17240740': 1, '24335335': 1, '6790005': 1, '3965953': 1, '7479230': 1, '6404384': 1, '30356349': 2}
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{}
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3,282 |
6176303-1
| 30,356,373 |
comm/PMC006xxxxxx/PMC6176303.xml
|
Urinoma: Prompt Diagnosis and Treatment Can Prevent Abscess Formation, Hydronephrosis, and a Progressive Loss of Renal Function
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A 70-year-old nonverbal female presented to the emergency department (ED) from home with her daughter who had noted that the patient has been acutely grimacing in pain from even the lightest palpation over her right flank. She had decreased urine output for the prior two days and her family had noticed an enlargement on the right side of her back one day prior to her ED visit. Of note, the patient presented with poor functional status, was totally bedridden, and was on no antibiotics. She also had a renal flow scan several months prior to her presentation, which revealed the absence of blood flow to the left kidney. A nephrectomy was ultimately rejected based on her medical history and current health status. The patient's medical history was significant for CVA with left hemiparesis, sacral stage 4 pressure ulcers, DM, HLD, failure to thrive, and asthma. Her past surgical history included a left double J-stent placement, an appendectomy, and a tracheostomy that was reversed.\nOn physical examination, the patient appeared to be in mild distress with a blood pressure of 93/50, heart rate of 116, and otherwise normal vital signs. Abdominal examination was remarkable for tenderness to palpation over the right flank with visible erythematous skin seen in the same area. Results of the initial laboratory tests were significant for a lactate of 2.9, white blood cell count of 18.4, hemoglobin of 7.1, platelet count of 933, albumin of 2.3, and potassium of 5.8, yet with a creatinine of 0.62. She underwent an IV contrast computed tomography (CT) scan of the abdomen and pelvis, which revealed a right hydronephrotic kidney that contained numerous large calcifications (Figures and ). The right previously placed ureteral stent was in satisfactory position. There was an extremely large fluid collection in the right retroperitoneum extending into the right flank consistent with leakage of urine from the obstructed right kidney ().\nWhile, in the ED, urology was consulted and requested interventional radiology to drain the urinoma and to place a Foley catheter to monitor urine output, the attending physician, at the request of interventional radiology, performed a needle aspiration of the loculated fluid collection in the right flank via ultrasound and noted a small amount of purulent and urine-like fluid from two separate areas of collection. The patient was admitted to the intensive care unit for urosepsis, urinoma with abscess, symptomatic anemia, and failure to thrive, while, in the intensive care unit, the patient was evaluated by urology, infectious disease, gastroenterology, wound care, and palliative care.\nUrology decided against emergent interventional radiology (IR) drainage as IR did not believe there was an acute need for drainage. It was postulated that the collection was more consistent with a urinoma without an apparent abscess thus not requiring emergent drainage. The patient also had been afebrile and it was reported that there were no fevers noted at home. It was discussed that emergent drainage would be performed if the patient acutely decompensated or became febrile. Additionally, the family refused surgical drainage because of her comorbid conditions. The patient was placed on empiric vancomycin and piperacillin/tazobactam.\nThe following day interventional radiology placed an 8 French pigtail drainage catheter and drained 610 ml of fluid. A subsequent IV contrast CT scan of the abdomen and pelvis showed the right retroperitoneal collection to be significantly decreased in size and nearly resolved. The contiguous component in the right flank soft tissues was slightly decreased with the drainage catheter in place. The patient was eventually discharged with the drain in place to hospice care.
|
[[70.0, 'year']]
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F
|
{'23905930': 1, '28730297': 1, '32660460': 2, '33680854': 1, '33718096': 1, '26012125': 1, '12975505': 1, '3786682': 1, '34658566': 2, '18257927': 1, '9146579': 1, '33898116': 2, '26046510': 1, '31852454': 2, '30356373': 2}
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{'8481848-1': 1, '7359582-1': 1, '8058494-1': 1, '6921490-1': 1}
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3,283 |
6176304-1
| 30,356,346 |
comm/PMC006xxxxxx/PMC6176304.xml
|
Severe Symptomatic Hypocalcemia from HIV Related Hypoparathyroidism
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A 54-year-old Caucasian female presented to our clinic with a two-year history of persistent hypocalcemia requiring multiple hospitalizations. Her symptoms included muscle cramps, tingling and perioral paresthesias. Her medical history was significant for HIV diagnosed four years ago, gastric bypass surgery done 15 years ago, hypertension, and COPD. She denied any history of prior neck surgery or radiation. She denied any history of hearing loss. She had no family history of autoimmune disease.\nHer vital signs were stable with an unremarkable physical exam. Chvostek's and Trousseau's signs were negative. Pertinent medications included calcium carbonate, vitamin D3, calcitriol, atripla (efavirenz/emtricitabine/tenofovir disoproxil), hydrochlorothiazide, and inhaled budesonide/formoterol.\nLaboratory testing showed total calcium of 5.7 mg/dL (normal range: 8.4-10.2 mg/dL), serum albumin 3.9 mg/dL, ionized calcium 2.7 mg/dL (normal range: 4.5-5.5 mg/dL), serum magnesium 1.7 mg/dL (normal range: 1.7-2.7 mg/dL), serum phosphate 6.3 mg/dL (normal range: 2.7-4.5 mg/dL), and intact PTH 7.6 pg/mL (normal range: 15-65 pg/mL). She had normal 25-hydroxy vitamin D 32 ng/mL (normal range: 30-100 ng/mL), 1,25 dihydroxy vitamin D 23 pg/mL (normal range: 18-72 pg/mL), TSH 1.2 μIU/L (normal range: 0.40-4.5 μIU/L), and creatinine 0.98 mg/dL (normal range: 0.5 -1.1 mg/dL). Absolute CD4 count was 629 cells/μL (normal range: 185-2273 cells/μL) with undetectable HIV-1 RNA viral load.\nShe was diagnosed with primary hypoparathyroidism. A serum sample was tested for anti-calcium sensing receptor (CaSR) antibodies [] and NALP5 antibodies [] to rule out autoimmune hypoparathyroidism and it was found to be negative; the CaSR antibody index was 1.09 (normal range: 0.57-1.38; upper limit of normal, 1.73) and the NALP5 antibody index was 1.12 (normal range: 0.62-1.93; upper limit of normal, 2.17). During subsequent clinic visits, doses of calcium supplements and calcitriol were titrated and she was started on magnesium oxide. She required calcium carbonate 2500 mg three times per day, calcium citrate 1900 mg twice per day, and calcitriol 0.5 mcg three times per day (). Her last corrected serum calcium level was 9.18 mg/dL. She was considered for treatment with recombinant human PTH but subsequently she was lost to follow-up.
|
[[54.0, 'year']]
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F
|
{'7698727': 1, '7989478': 1, '34504905': 1, '8014731': 1, '24587936': 1, '1827127': 1, '16044577': 1, '1406838': 1, '24423312': 1, '8957484': 1, '15068493': 1, '10095819': 1, '7915122': 1, '30356346': 2}
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{}
|
3,284 |
6176307-1
| 30,356,357 |
comm/PMC006xxxxxx/PMC6176307.xml
|
Total Knee Arthroplasty after Correction of Tibial Diaphyseal Nonunion with Clamshell Osteotomy
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A 65-year-old male with a BMI of 42 and uncontrolled type II diabetes mellitus came to our clinic with a fracture on the left tibial shaft. He was treated conservatively for 20 years. Radiographs showed a malunited fracture on the middle third left tibia in 20-degrees varus, 15-degrees apex anterior angulation with a 1 cm anterior translation of distal segment, 20-degrees internal rotation and 1.5 cm shortening. He also had severe tricompartmental osteoarthritis on the left knee (Figures and ). A CT scan confirmed the presence of malunion (). Blood sugar was controlled by an endocrine physician and a clamshell osteotomy of the tibia was planned.
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[[65.0, 'year']]
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M
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{'1914313': 1, '21519079': 1, '21196543': 1, '19181975': 1, '21248221': 1, '22691677': 1, '23138705': 1, '25270959': 1, '15386160': 1, '26542874': 1, '10984710': 1, '21210313': 1, '30356357': 2}
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{}
|
3,285 |
6176309-1
| 30,356,361 |
comm/PMC006xxxxxx/PMC6176309.xml
|
Endobronchial One-Way Valve Therapy Facilitates Weaning from Extracorporeal Membrane Oxygenation in a Patient with ARDS and Persistent Air Leak
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A 60-year-old healthy male patient (no comorbidities, never-smoker) with ARDS due to influenza A pneumonia was admitted to our specialised lung clinic for further treatment. Endotracheal intubation due to severe hypoxemic respiratory failure was already performed prior to admission (day 0). Transference of the patient to the hospital occurred on day 6. The first chest X-ray after admission revealed an apical left-sided pneumothorax of approximately 2 cm, accompanied by a large subcutaneous emphysema. Two chest tubes were inserted, one on each side. After that, the left lung was again fully expanded, the subcutaneous emphysema resolved, and no air leak could be observed. On day 14, the patient developed once again spontaneously a massive and progressive subcutaneous emphysema, accompanied by a large air leak of about 5000 ml per minute on the left side. A second and a third chest tube were inserted on the left, one in Monaldi's position (3rd intercostal space mid-clavicular) and the other in Bülau's position (5th intercostal space slightly anterior the mid-axillary line). However, the chest X-ray and chest CT-scan on day 16 showed a complete, left-sided pneumothorax (). Central venous catheter placement on the left (internal jugular vein) was performed six days before the onset of the air leak. We interpreted the occurrence of the air leak, the pneumothorax, and the subcutaneous emphysema as a result of barotrauma due to invasive mechanical ventilation. Because of progressive hypercapnia and severe respiratory acidosis, a tracheostomy was performed and a vvECMO (PLS Set and ROTAFLOW Console) was established (day 16), using an Avalon Elite™ Bi-Caval Dual Lumen Catheter (Maquet Cardiopulmonary GmbH, Germany). Blood gas analysis immediately before the start of the extracorporeal lung assistance revealed a PaCO2 of 88 mmHg with a pH of 7.30, and PaO2 was 90 mmHg. At this point, the patient was ventilated in the assist-controlled mode (BIPAP-ASB, Evita 4, Dräger®). FiO2 was 0.85, and Pinsp was set at 28 mBar with a PEEP of 7 mBar. This resulted in a tidal volume of approximately 400 ml and a minute ventilation of 8.4 l/min. After the cannulation of the patient and the commencement of vvECMO support, a lung protective ventilation strategy with low tidal volumes (Pinsp 20 mBar, PEEP 10 mBar, FiO2 0.6, VT 250 ml) was established. This resulted in acceptable blood gas values (PaCO2 49 mmHg, PaO2 74 mmHg, pH 7.52) on vvECMO (blood flow 2.5 l/min, FiO2-vvECMO 1.0, sweep gas flow 4.0 l/min); however, the air leak persisted (day 17), and in the chest X-rays the left lung remained collapsed. In the further course of treatment, the blood gas analyses revealed persistent hypercapnia with a PaCO2 of approximately 60–65 mmHg, and even though the sweep gas flow was increased, a state of normocapnia could not be achieved. Therefore, an interventional closure of the fistula with endobronchial valves was planned.\nOn the day of the procedure (day 21), FiO2 on the ventilator was 0.6, and Pinsp was set at 17 mBar and PEEP at 5 mBar, resulting in tidal volumes of about 450 ml and minute ventilation of approximately 9.2 l/min. vvECMO blood flow was 2.6 l/min with a sweep gas flow of 5.5 l/min. Valve placement was done bedside on the intensive care unit. The patient was under deep sedation/analgesia with midazolam and sufentanil, respectively. Cis-Atracurium (10 mg) for muscle relaxation was administered immediately before the procedure. Bronchoscopy was performed through the tracheal cannula. The exact bronchoscopic localisation of the fistula was assessed by occlusion of the upper and lower lobe bronchus on the left, using a bronchus blocker while measuring the fistula flow with the Thopaz Digital Chest Drainage System (Medela AG, Switzerland). First of all, as we blocked the left upper lobe bronchus (corresponding to the segment bronchi LB1–5), the air leak was stopped entirely. Then we occluded each segment of the left upper lobe separately, but we did not achieve any significant result. The occlusion of the lingula bronchus (LB4/5) had no significant effect on the air leak as well. Thus, decision was made to close LB1/2 and LB3 with two Zephyr® endobronchial valves (2 × 4.0-LP, Pulmonx®, Redwood City, USA). This initially led to an immediate decrease of the air leak to about 400–700 ml/min, and the left lung was then again fully expanded (). After valve placement, PaCO2 decreased slowly during the following six days, while there were no major adjustments of the ventilator settings or the vvECMO parameters. Normocapnia was detected for the first time on day 27, so that blood flow and sweep gas flow on vvECMO could be slowly reduced. During the following two weeks, the air leak stopped completely and the patient could be weaned from vvECMO on day 48. The patient was transferred from the intensive care unit to the weaning unit on day 61. Removal of the endobronchial valves occurred on day 62, after which the chest X-rays showed a persistently expanded left lung (). As there was no evidence of an air leak once again, the chest tubes were removed one after another, liberation from the ventilator on day 72 and discharge to neurological rehabilitation on day 89.
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[[60.0, 'year']]
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M
|
{'12730823': 1, '24193288': 1, '23207358': 1, '28367339': 2, '29110704': 1, '34527361': 1, '20172150': 1, '9631785': 1, '31723383': 1, '32133366': 2, '16354867': 1, '33138976': 1, '26282263': 1, '19349382': 1, '30356361': 2}
|
{'5359445-1': 1, '5359445-2': 1, '5359445-3': 1, '7040219-1': 1}
|
3,286 |
6176312-1
| 30,356,382 |
comm/PMC006xxxxxx/PMC6176312.xml
|
Intrathecal Pump Implantation in the Cisterna Magna for Treating Intractable Cancer Pain
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The patient was a 54-year-old male with multiple metastasis of axillary lymph nodes, lung, and intracranial and cervical vertebrae after liver cancer surgery. He had been experiencing severe, persistent needle-like pain in the right shoulder, back and right arm since 3 months. Other doctors treated the pain with fentanyl transdermal patch 29.4mg q72h and 100mg tramadol sustained release tablet q.d. oral prior to admission. However, neither analgesic therapy was effective in treating his pain. In addition, the patient had breakthrough pain (BTP) more than ten times in 24 hours, and NRS (Numerical Rating Scale) score was 7. Due to the poor analgesic effect of the tramadol sustained release tablets, they were discontinued, and the patient's condition was reassessed after admission. The patient felt pricking, numbness, and electrical shocks, suggesting an ID Pain scale [] (Neuropathic pain screening scale) score of 3. Since the ID Pain score accurately indicates the presence of a neuropathic component of pain, his pain was considered to be a combination of pathological neuralgia, and thus 600mg Gabapentin capsules were given t.i.d. orally starting on the day of admission.\nNRS score was 4 at rest on day 2 of admission, BTP was 4 times at night, and NRS score was 7. One hour after administering 10mg morphine tablets, NRS score decreased to 3. Due to the weak effect of 29.4mg fentanyl, the concentration was increased to 42mg in the transdermal patch. At the same time, 5mg dexamethasone injection IV q.d., oral 25mg amitriptyline tablets 25mg q.n., and oral 2mg Clonidazepam tablets q.n. were given.\nOn day 7 of admission, the patient still complained of obvious pain in the back, shoulder, and right arm, NRS score was 5 at rest, BTP was 3 times at night and NRS score was 8. In our patient, imaging showed multiple soft tissue masses in the neck space, corresponding to metastases. Since the spinal canal becomes narrow and results in cerebrospinal fluid reflux in such a condition, the tip of the catheter was inserted in the cerebellomedullary cistern. Intrathecal pump was implanted in the cisterna magna under DSA without any complications in the First Affiliated Hospital, Zhejiang University School of Medicine (). Morphine is one of the FDA recommended drugs for full implantable infusion pumps, and a conservative starting dose is recommended for intrathecal administration. The patient was given 50mg morphine dissolved in 200ml saline via the intrathecal pump. Since the patient was treated with 42mg fentanyl transdermal patch before surgery, the initial parameters of drug infusion were continuous background dose (Con) of 0ml and single enhancement dose (bolus) of 0.8ml for 0.2mg morphine. Some studies recommend that the maximum dose of morphine in cerebellomedullary cistern should not exceed 0.5mg [], with locking time 20min and electrocardiogram (ECG) and O2 saturation monitoring. The intrathecal pump parameters could be adjusted according to the degree of pain and drug reaction experienced by the patient. In the period between operation and 8:00am on day 8 after operation, the patient pressed bolus 15 times and the effective number was 8 times. Since the pain was not relieved even after pressing, the parameters were adjusted to Con of 0.3ml/h and bolus of 1ml with 0.25mg morphine. Meanwhile, fentanyl dose in the transdermal patch was reduced to 33.6mg. After adjusting the pump's parameters, the NRS score was 1 at rest, the time of BTP was 4, and the NRS score was 4. According to the equivalent dose of opioid drugs and related efficacy conversion, the intrathecal dose of morphine is about 300 times more than its intravenous form. When the pain stabilized, fentanyl dose in the transdermal patch was further reduced to 25.2mg after expiration, and the amount of morphine infused via the intrathecal pump was reduced daily. The degree of pain was significantly reduced compared with that before surgery. Taken together, administration of analgesic via intrathecal pump implantation in the cisterna magna reduced pain levels and reduced the number of BTPs. The patient experienced considerable pain relief (see ). However, the patient had terminal cancer and died of multiple organ failure on day 13 after admission.
|
[[54.0, 'year']]
|
M
|
{'8677660': 1, '17355955': 1, '16870080': 1, '28042904': 1, '7501106': 1, '3478979': 1, '22150811': 1, '1702248': 1, '34422413': 1, '6886783': 1, '30356382': 2}
|
{}
|
3,287 |
6176314-1
| 30,356,399 |
comm/PMC006xxxxxx/PMC6176314.xml
|
Sertoli-Leydig Cell Tumour and DICER1 Mutation: A Case Report and Review of the Literature
|
A 15-year-old girl presented with a background of erratic menstrual periods following menarche at age of 12 years. By first contact she had experienced amenorrhoea for 6 months followed by continuous daily vaginal bleeding for 3 months. She had noticed hair loss, receding hairline, and coarse dark hair on her abdomen, thighs, and bottom. Clinical examination revealed a normally developed female without virilisation of the external genitalia or a change in voice. She was pain free.\nHormone profile revealed raised testosterone (10.1nmol/l Ref: 0.5-3.0 nmol/l), suppressed FSH (<0.1 IU/L Ref: 1-11 iu/L), and borderline SHBG (21 nmol/l Ref: 18 – 114 nmol/L). AFP was raised (137 kU/L Ref: 0-5.8 kU/L) but all other tumour markers, including Beta-HCG and Inhibin, were normal. Urine steroid profile was normal.\nUltrasound examination of the abdomen and pelvis, , revealed a complex 7 cm left ovarian lesion with internal vascularity but otherwise normal pelvic organs and adrenal glands. MRI, , confirmed an abnormal but well-defined 7 cm left adnexal lesion of predominant intermediate T2 signal interspersed with high signal cystic areas separated by low signal septa. The clinical picture was of a primary ovarian tumour with ectopic production of androgens, and not the more common germ cell tumour.\nThe case was discussed at the paediatric and gynaecologic oncology MDT. A laparoscopic left oophorectomy with preservation of the ipsilateral fallopian tube was performed with a secondary Pfannenstiel incision used to extract intact the specimen. The tumour which was more solid than cystic was 11 cm in size with no discernible normal ovarian tissue visible. A small nodule on the right ovary was excised. There were no other sites of disease. All other organs and peritoneal surfaces were normal. The postoperative course was uneventful.\nHistological analysis, Figures and , indicated a predominantly poorly differentiated Sertoli-Leydig cell tumour, retiform pattern, with heterologous mucinous elements. The right ovarian nodule was benign.\nFollowing multidisciplinary team discussion and parental consent, adjuvant chemotherapy was commenced, in a monthly regime of Bleomycin 28500 IU on Day 1, Etoposide 190 mg daily on Days 1-5, and Cisplatin 38 mg daily on Days 1-5 for 3 cycles. Starting prior to chemotherapy commencement, a GNRH analogue, Leuprorelin 3.75mg per month, was administered for 4 months for ovarian protection. The patient became neutropenic following cycle 1 and received Filgrastim 300mcg for 6 days on Days 6-10 of Cycle 2. There were no further episodes of neutropenia. Following cessation of Leuprorelin, menstruation resumed on a regular monthly cycle. She completed her treatment 2 years ago and been reviewed every 3 months. She has had normal tumour markers, including testosterone and AFP, and normal abdominopelvic ultrasound scans throughout this period. Following genetic analysis a germline DICER1 mutation was discovered, inherited from her father and shared by her 19-year-old sister.
|
[[15.0, 'year']]
|
F
|
{'26408257': 1, '23132766': 1, '33028642': 1, '32280807': 1, '28323992': 1, '25794098': 1, '26925222': 1, '28960912': 1, '28654427': 1, '22850410': 1, '25176334': 1, '24136150': 1, '28474256': 1, '28748527': 1, '28620008': 1, '29037807': 1, '30356399': 2}
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{}
|
3,288 |
6176323-1
| 30,356,387 |
comm/PMC006xxxxxx/PMC6176323.xml
|
The Fire Service for the Removal of a Metallic Penile Constricting Device: A Ready Help When All Else Fail
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We present the case of a 30-year-old Nigerian male who was brought to the Surgical Emergency Department of the Lagos State University Teaching Hospital Ikeja 22 hours after he had inserted a constricting ring over his penis. He had developed a painful penile shaft swelling distal to the ring with suprapubic pain and swelling secondary to acute urinary retention. There was associated urethral bleeding.\nThere had been failed attempts at removing the ring by self and the resulting severe pain drew the attention of his relatives who brought him to the emergency room.\nHe had a history of a psychiatric illness and the patient claimed he was under a spell and had heard a voice that instructed him to insert a ring over his penis. He denied using the ring to sustain erection and claimed it was his first time of inserting a ring over his penis.\nThe patient had a history of deterioration in personal and general performance with underachievement dating back to 7 years prior to presentation when he voluntarily dropped out of the university and had done nothing tangible thereafter.\nTwo weeks prior to presentation, the patient's relatives had noticed some unusual behavior in him characterized by talking to self and rubbing salt over his body and the patient claimed he was being chased by unseen people.\nHe had a history of alcohol, cigarette, and cannabis abuse for about 15 years.\nOn examination, he was in acute urinary retention with a tender suprapubic distention up to the level of the umbilicus.\nThere was a thick constricting ring at the root of his penis. There was a markedly swollen oedematous penis distal to the ring with marked reduction in sensation over the penis and glans ().\nWe made a diagnosis of Constrictive Penile Injury (Bhat Grade III) with acute urinary retention [].\nHe had a suprapubic cystostomy done to relieve the acute urinary retention as a urethral catheterization was impossible.\nAttempts were made to remove the constricting ring by the use of aspiration, application of cold compress, and lubrication initially and later by the use of the string method.\nFollowing failed attempts at removing the device with these different manipulations and unsuccessful attempt at cutting with the manual saws available in the hospital coupled with the fact that the patient appeared to have imminent penile gangrene, a decision was made to call the fire service for a power driven saw.\nThe ring was successfully removed by cutting it at two different points () with a power driven arc saw () under conscious sedation at the emergency room.\nThermal injury was prevented by intermittent cooling with ice packs and injury to underlying tissue was prevented by insinuating a pair of artery forceps between the penis and the ring ().\nDressing of the resulting penile skin ulceration was done and the plastic surgery team was invited for possible additional wound care.\nThe patient was also reviewed by the psychiatric team who made a diagnosis of schizophrenia and commenced the patient on haloperidol. He was to be followed up on an outpatient basis in the psychiatry clinic.\nThe patient reported normal nocturnal erections while on admission. Further evaluation of the suspected urethral injury with urethrogram and a urethroscopy was planned but this was declined by the patient who opted to retain his suprapubic catheter.\nThe patient also declined any additional wound care by the plastic surgery team and the wound was healing satisfactorily by secondary intention as at 2 weeks after the initial presentation ().\nHe subsequently defaulted from care.
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[[30.0, 'year']]
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M
|
{'6740843': 1, '26670412': 1, '19416581': 1, '24579040': 1, '21091882': 1, '17888068': 1, '15183986': 1, '10368261': 1, '1773293': 1, '9014727': 1, '20646187': 1, '18631393': 2, '11212451': 1, '18507720': 1, '30356387': 2}
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{'2491652-1': 1}
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3,289 |
6176343-1
| 30,356,381 |
comm/PMC006xxxxxx/PMC6176343.xml
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Fatal Septic Shock in a Patient with Hemophagocytic Lymphohistiocytosis Associated with an Infectious Mononucleosis
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A 24-year-old woman was admitted to the Department of Infectious Disease with fever (T = 38,3°C) which was attributed to a relapse of a IM-HLH occurring about two months prior to the current hospitalization. At that time, the diagnosis of IM was confirmed by the presence of EBV DNA in the bloodstream and the diagnosis of HLH was suspected on the basis of the clinical findings such as persisting fever, the enlargement of the liver and the spleen as well as of blood abnormalities including pancytopenia, abnormally elevated values of ferritin (> 15.000 mcg/ml), triglycerides (789 mg/dl), and liver enzymes (AST 175 U/L, AST 120 U/L); a bone marrow biopsy confirmed the presence of hemophagocytosis and viral RNA in many cells by means of in situ hybridization (EBER) []; a genetic screening excluded the presence of gene mutations associated with HLH. During that hospitalization, she received steroids, etoposide, rituximab, cyclosporine, granulocyte-stimulating factor, and intravenous immunoglobulins (IvIg) and was ultimately discharged 38 days after the initial admission without viral DNA detectable in the bloodstream. During her stay at home, which lasted 3 weeks, the patient received prednisone, cyclosporine, trimethoprim-sulphametoxazole and acyclovir through a peripherally inserted central venous catheter (PICC). Thirty-six hours after the current admission during which rituximab was added to the ongoing treatment she was transferred to the ICU due to the deterioration of the consciousness, arterial hypotension, and fever. At the ICU admission, the patient presented high fever (40,5°C), disseminated intravascular coagulation, arterial hypotension, and acute kidney injury requiring renal replacement therapy (RRT): a methicillin-resistant Staph. aureus (MRSA) was isolated from the blood cultures and a septic shock-related MODS possibly in association with a cytokine storm caused by the HLH were hypothesized; the patient was intubated and mechanically ventilated and treated with IV vasopressors at incremental doses, IV vancomycin, meropenem, and caspofungin; the PICC was removed and replaced with a central venous catheter; as the patient remained unresponsive to the treatment, a Coupled Plasma Filtration and Adsorption treatment (CPFA, LYNDA®, Bellco, Mirandola, Italy) that aimed at removing the inflammatory mediators was added to the RTT along with the IV administration of IgM and IgA-enriched IvIg (Pentaglobin®, Biotest; Dreieich, Germany). Despite this increasingly aggressive approach, the MODS further worsened and the patient died 18 hours after the ICU admission.\nAt the autopsy, the liver and the spleen appeared enlarged, weighting 3110 g and 1230 g, respectively. Microscopically, the spleen showed lymphocyte depletion and the scattered necrosis of Malpighi's follicles () combined with subversion of the general architecture due to a proliferation of T-lymphocytes (CD3+) with predominant expression of CD8 (). The lymphocyte population B (CD20+, PAX-5+) was virtually absent, while there was a significant increase in monocyte-macrophage component sometimes associated with hemophagocytosis. The EBER highlighted several lymphocytes with integrated EBV RNA in the nucleus (). The liver showed several perivascular infiltrates of polymorphic lymphocytes likewise those found in the spleen and many monocyte-macrophage cells (CD14+, CD64+). In the bone marrow there were multiple lymphocyte with polymorphic or abnormal nucleuses () that appeared to be almost exclusively CD8+ T-lymphocytes (). Most of these cells were EBER positive (); B-lymphocytes (CD20+, PAX-5+) were almost absent while there was an expansion of the monocyte-macrophage series (CD14 +, CD64 +). The three hematopoietic lines appeared contracted but with preserved maturation. Mediastinal lymph nodes showed a diffuse proliferation of medium/large sized lymphoid elements, sometimes with single or multiple polymorphic nuclei (). The lymphocyte population was composed by CD3+ CD8+ T-lymphocytes with a limited presence of lymphocytes CD3+ CD4+ and absence of B cells (CD20 +, PAX-5 +).
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[[24.0, 'year']]
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F
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{'29907163': 1, '24792320': 1, '11009000': 1, '25959150': 1, '31583137': 2, '24438142': 1, '23968282': 1, '20505178': 1, '25998991': 1, '28101605': 1, '26492511': 1, '20532477': 1, '25003566': 1, '23206255': 1, '17707260': 1, '25758828': 1, '30356381': 2}
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{'6754887-1': 1}
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3,290 |
6176504-1
| 30,301,456 |
comm/PMC006xxxxxx/PMC6176504.xml
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Castleman disease of the hyaline vascular variant transforming to POEMS syndrome as endpoint: a case report
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A 66-year-old male presented with the left cervical and submaxillary lymph node enlargement with size of 30 mm × 30 mm. The following lymph node biopsy was completed and the pathological evaluation showed reactive lymphoid hyperplasia characterized by vascular, atrophic germinal lesions with surrounding concentric “onion skin” layers of lymphocytes (Fig. ), defined as the hyaline vascular variant of CD. He denied weight loss, lymphadenopathy, tuberculosis, diabetes mellitus and hypertension. He gave no history of bone pain and drug abuse. The bone marrow (BM) cytology indicated no clonal plasma cell infiltration. Thereafter the patient was treated with irradiation dose of 30 Gy in 10 fractions with clinical response. The clinical evaluation remained stable in annual follow-up visits. In the 4th visit, the patient was diagnosed in an outside hospital with 2-diabetic mellitus on basis of increased blood glucose, C peptide release test and oral glucose tolerance test (OGTT). The blood glucose was well-controlled by the hypoglycemic and diet therapy for three years when he presented to the previous hospital with progressive hand-foot numbness spreading from the proximal extremes to distal ends. The electromyography test confirmed the hampered nerve conduction velocity of bilateral ulnar, median and peroneal nerves. The cerebrospinal fluid (CSF) biochemistry from lumbar puncture indicated the slightly elevated protein (1.1 g/L, normal, 0.1~ 0.4 g/L) with normal cell count. The blood monoclonal protein level and bone marrow cytology was normal. Based on the resultant diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP), the patient was treated with daily intravenous pulse methylprednisolone therapy of 1.0 g for three consecutive days. Due to the minor clinical response, the diabetic peripheral neuropathy was suspected with following insulin injection and oral mecobalamin therapy. However, the manifestation of hand-foot numbness remained constant. One and half years after the first sign of numbness, the muscular dystrophy of palms was noticed with finger fine hypoactivity. In the next 2 years, the patient was admitted to the previous hospital with the progressive muscular atrophy, numbness of hands and myasthenia of limbs along with interphalangeal deformity. The CSF test showed slightly elevated protein concentration (1.6 g/L) with normal pressure, cell count and the level of glucose and chloride. Other laboratory results were normal. The electromyography test was performed with severe neuro-electrophysiological damage in bilateral median, ulnar, peroneal and tibial nerves. Despite the intensive glucose control and oral mecobalamin therapy for the next seven years, the symptom of limb numbness and trembling was significantly worsened. In parallel, the skin pigmentation with increasing body hair and skin elasticity loss was also noted. He gave the history of insomnia for seven years but denied smoking and alcohol abuse history. Insulin and oral anti-diabetic drugs was thereafter withdrawn at the normal level of HbAlc and blood glucose.\nThe physical examination revealed that skin was thickened with hyperpigmentation over the toes (Fig. ). Other abnormal neurological examinations include the limb hypoesthesia, static tremor of hands, tendon hyporeflexia and positive Romberg sign. The thorax and abdominal CT scanning showed interstitial pneumonia and nodules located in right lobe, a small amount of pericardial effusion, hemorrhagic cyst on the pole of right kidney and splenomegaly (Fig. ). The pituitary gland MRI showed the shrunk size of pituitary gland concurrent with partial empty-sella and nasosinusitis. The ultrasonography excluded lesions of adrenal glands but discovered bilateral thoracic effusion post CT scanning. The electromyography test was repeated with severe to complete neuro-electrophysiological damage in bilateral median, ulnar, peroneal and tibial nerves and movement loss of tibialis anterior muscle and abductor muscle of right little finger. Laboratory investigations revealed a platelet count of 454 × 1012/L (normal, 125~ 350 × 109/L), triglycerides level of 1.8 mmol/L (normal, 0.5~ 1.7 g/L), albumin of 20 g/L (normal, 35~ 50 g/L), adrenocorticotropic hormone (ACTH) level of 322.0 pg/ml which fell to 227.0 pg/ml (normal, 0~ 46 pg/ml) after one week. Her CRP level was 17.7 mg/L but rose to 21.3 mg/L (normal, 0~ 3.0 mg/L) within 2 weeks. The blood cortisol level in the morning was 220.3 nmol/l (normal, 138~ 690 nmol/L) within one week. The coagulation function showed PT-SEC of 15.6 s (normal, 10.0~ 14.0 s), PT% of 49.4% (normal, 70.0%~ 130.0%) and APTT-SEC of 44.2 s (normal, 20.0~ 40.0 s). The serum immunoglobin test indicated moderately increased IgG level of 11.9 g/L (normal, 7.6~ 11.6 g/L) and decreased complement C3 level of 0.5 g/L (normal, 0.8~ 1.4 g/L). Viral serology (EBV and HSV not included), urine free cortisol, tuberculosis antibody, sex hormone test, thyroid hormone and tumor biomarkers were undertaken and came back with normal value. BM cytology revealed significant hypercellularity and thrombocythemia. Genetic tests from BM biopsy showed negative expression of JAK-2 gene and BCR/ABL gene fusion, therefore the primary thrombocytosis was diagnosed instead of multiple myeloma. Abnormal hyperimmunoglobulinia appeared as minimal IgG-lambda monoclonal protein variant (Fig. ). The clinical presentation and investigations consisted with features of POEMS syndrome. The patient was managed with daily oral prednisone of 20 mg and azathioprine of 150 mg for 2 weeks. The numbness was apparently relieved with improved performance status. Thus, thalidomide with oral dose of 50 mg daily was taken as maintenance therapy. Clinical monitor of response and toxicity was evaluated periodically within the next 2 years and the patient rejected medical treatment and died of hypoalbuminemia, electrolyte disturbance and pneumonia.
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[[66.0, 'year']]
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M
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{'9771661': 1, '21881050': 1, '12456500': 1, '21221584': 1, '26331353': 1, '23398538': 1, '6539431': 1, '15975949': 1, '28405536': 2, '30301456': 2}
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{'5384847-1': 1}
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3,291 |
6176516-1
| 30,296,944 |
comm/PMC006xxxxxx/PMC6176516.xml
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Description of a novel RyR2 mutation in a juvenile patient with symptomatic catecholaminergic polymorphic ventricular tachycardia in sleep and during exercise: a case report
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A 17-year-old Caucasian boy was admitted to our intensive care unit (ICU) after successful resuscitation by emergency services. While performing running exercise in a fitness center, he suddenly collapsed. Because neither pulse nor breathing could be detected by the bystanders, immediate resuscitation was performed. In the first heart rhythm analysis conducted by the paramedics, ventricular fibrillation (VF) was seen and immediately defibrillated into sinus rhythm. The patient recovered quickly and was transferred to our ICU by the ambulance service. At admission, the patient was in hemodynamically stable condition with normal vital signs (heart rate 95/min, blood pressure 125/79 mmHg, auricular temperature 36.5 °C, respiration 15 breaths/min, oxygen saturation of 100% on 4-L nasal cannula). The physical examination revealed no abnormal findings. Auscultation of the heart showed a regular rate and rhythm with normal S1 and S2 and no murmurs or rubs. The breath sounds of the lungs were equal and clear bilaterally with no wheezes, rhonchi, or rales. The patient was awake (Glasgow Coma Scale score of 15) and orientated in all aspects. No focal sensory or motor deficits, aphasia, or inadequate balances were noted in the neurological examination. Deep tendon reflexes and cranial nerves II through XII were intact. Because there were no cerebral or other sequelae at the time of hospital admission, we decided not to obtain a cranial computed tomographic scan, owing to the patient’s young age. When asked about the event, he told us that he had no symptoms prior to the collapse. However, in the years before, he had syncopated several times while climbing stairs, playing soccer, and once when he got frightened. A general practitioner previously performed an exercise ECG, which showed multiple premature beats under submaximal stress (Fig. ). As a result, beta-blockers were prescribed (metoprolol succinate 47.5 mg once per day). Apart from this, the patient had no medical history or prior medication. The patient was a nonsmoker with no regular alcohol consumption and an unremarkable family, social, and environmental history.\nAt ICU admission, initial medical treatment included the first surface ECG after cardiac arrest, which showed negative T-waves in V1 and biphasic T-waves in V2 (Fig. ). The results of blood tests showed normal findings without signs of cardiac ischemia or metabolic disorders (Table ). Respiratory disorders (bronchospasm, aspiration) or neurovascular events seemed to be unlikely because the physical examination, blood gas analysis, and a pulmonary x-ray showed normal findings. An echocardiogram revealed normal left ventricular function without wall motion abnormalities, right heart strain, or valve disease. Additionally, a cardiac magnetic resonance imaging scan was performed and showed normal findings. Therefore, we ruled out hypertrophic and dilative cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and acute myocarditis as potential differential diagnoses. Further diagnostic workup included coronary angiography and electrophysiological testing, but none of those resulted in any relevant finding.\nBecause no extracardiac cause or structural heart disease was found, diagnostic workup focused on channelopathies and genetic heart diseases. Owing to the patient’s medical history of stress-dependent syncope, we strongly suspected a CPVT as the underlying mechanism for VF. Genetic screening was performed and confirmed the diagnosis of CPVT, revealing a new heterozygous point mutation in the gene for ryanodine receptor type 2, which, to the best of our knowledge, has not been described to date in the literature. The heterozygous mutation c.12520T>A (p.F4174 l, exon 90, RyR2 gene) results in an exchange of phenylalanine to isoleucine at position 4174 of the RyR2 protein. Forty-five percent of the relevant mutations of RyR are located in this region []. This novel identified missense mutation is located in the C-terminal channel region as a residue of the hydrophobic side chain of the S6/U motif interface of RyR2 [].\nPrediction algorithms for forecasting functional effects of a mutation clearly identify this mutation to potentially cause CPVT []. Genetic screening of both parents showed that neither of them were carriers of the mutation. Results of further screening of the patient and family members for other pathogenic mutations (long or short QT syndrome, Brugada syndrome) were also negative.\nOn the basis of of our findings, the patient received an ICD device to protect him from recurrent episodes of VF. Additionally, oral medication with a beta-blocker was continued with the maximum tolerable dose. Because of the relatively small number of documented arrhythmic episodes, we did not add flecainide at that point. Left ventricular sympathetic denervation was discussed with the patient and the family, but in the end it was deferred.\nAt hospital discharge, the patient was included in our home monitoring program for ICD surveillance. Shortly after implantation, the ICD terminated a sustaining VT by antitachycardic pacing (Fig. ). This episode occurred early in the morning while the patient was asleep, which is an uncommon situation for arrhythmic events in patients with CPVT. However, the patient had no memory of a possible emotional stress due to dreams. In the following 6 months, a single episode of VF occurred during a physical activity (cycling), this time terminating spontaneously.
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[[17.0, 'year']]
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M
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{'21832802': 1, '28158428': 1, '21659649': 1, '28596175': 1, '34725342': 1, '11208676': 1, '12837242': 1, '17556193': 1, '27789712': 1, '26837728': 1, '25463374': 1, '15197150': 1, '30296944': 2}
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{}
|
3,292 |
6176649-1
| 30,338,071 |
comm/PMC006xxxxxx/PMC6176649.xml
|
Shisha smoking as a possible cause of bilateral granulomatous lung lesions
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A 19-year-old male presented to the emergency department with a two-week history of pleuritic chest pain, dyspnoea, and non-productive cough. He denied fevers, night sweats, or weight loss. He had no articular, cutaneous, or ocular symptoms. He had mild childhood asthma in the past. He was not on any regular medications. There was no significant family history. He had moved to New Zealand from Fiji eight years earlier. He had regularly smoked tobacco through a “shisha” pipe for the preceding 3 months.\nOn examination, he was afebrile, with a heart rate of 90 beats per minute, blood pressure of 110/80 mmHg, and oxygen saturations of 98% on air. His cardiac and respiratory examination was normal. His abdomen was non-tender without evidence of masses. He had no peripheral lymphadenopathy. His testicular examination was normal.\nA full blood count showed normal haemoglobin of 147 g/L (normal range 130–175), white blood cell count of 8.8 × 109 (normal range 4–11), and eosinophil count of 0.2 × 109 (normal range 0–0.5). C-reactive protein was 25 mg/L (normal range 0–5).\nHis chest radiograph showed multiple ill-defined opacities in both lower lung fields. A subsequent computed tomography (CT) scan of the chest and abdomen (Fig. ) showed multiple poorly marginated and irregularly contoured enhancing nodules through both upper and lower lobes bilaterally, more numerous at the bases. There were no pleural effusions or lymphadenopathy, and appearances of the abdomen were normal.\nFurther blood tests showed a negative antinuclear antibody (ANA), extractable nuclear antigen (ENA) panel, anti-neutrophil cytoplasmic antibodies (ANCA), serum angiotensin-converting enzyme (ACE), alpha-feto protein, Beta human chorionic gonadotropin (hCG), and Quantiferon-Gold.\nHe proceeded to a CT-guided fine needle aspirate and core biopsy of the most peripheral lesion in the left lower lobe. Histology (Fig. ) demonstrated preserved lung alveoli but prominent expansion of the lung interstitium with frequent necrotizing granulomas. There was a mixed inflammatory infiltrate of lymphocytes and occasional plasma cells and eosinophils. Fungal and mycobacterial stains were negative, as was culture for bacteria, mycobacteria, and fungi. Mycobacterium tuberculosis polymerase chain reaction (TB PCR) on biopsy specimen was negative. There was no evidence of malignancy, vasculitis, or foreign bodies, nor any features of Langerhans cell histiocytosis (LCH). Cell marker studies showed no evidence of monoclonality. Overall, the pathology impression was of necrotizing granulomatous inflammation.\nThe patient was given no specific treatment other than simple analgesia. While awaiting the histology results, he was discharged home with advice to avoid further shisha tobacco. Serial chest radiographs were performed at intervals of two weeks, six weeks, 12 weeks, and nine months. These demonstrated progressive resolution of the pulmonary opacities, with a clear chest radiograph at 12 weeks (Fig. ). A spirometry performed at nine months was normal.\nThe impression was of bilateral pulmonary granulomatous nodules most likely related to shisha smoking, with complete resolution following cessation.
|
[[19.0, 'year']]
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M
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{'24577678': 1, '34720796': 1, '11911432': 1, '27938776': 1, '14575812': 1, '26843673': 1, '25233010': 1, '22045884': 1, '20207606': 1, '12971670': 1, '12577995': 1, '32015968': 2, '28932746': 1, '21545223': 1, '30338071': 2}
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{'6993912-1': 1}
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3,293 |
6176746-1
| 30,310,678 |
comm/PMC006xxxxxx/PMC6176746.xml
|
Fibro-osseous pseudotumor of the digit: Case report and surgical experience with extensive digital lesion abutting on neurovascular bundles
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Our patient is a 27-year old female that denied any past medical and surgical history. Her family and drug history were also unremarkable. The patient presented with a 7-month history of progressively enlarging mass on her left ring finger. The patient mentioned that the mass appeared suddenly with no history of trauma and that she was concerned about the potential malignant nature of the mass. The patient also mentioned that she underwent incision and drainage of that mass 2 months after its appearance with no improvement and provided no detailed surgical or pathological reports, which was the reason for her delayed presentation. Upon her assessment, the mass was located over the ulnar side of the proximal phalanx of left ring finger with extensive involvement of the 4th web space. The overlying skin coverage was ulcerative with no active signs of infection. Range of motion of the involved digit was limited, however neurovascular examination was normal. ().\nRadiological evaluation of the involved hand showed a soft tissue swelling with no evidence of bone involvement (). Further magnetic resonant (MRI) evaluation showed a mass on the volar aspect of the ring finger encasing about 50% of the flexor tendons of that digit with low signal intensity on T1 and high signal intensity on T2 evaluation with strong enhancement in post contrast evaluation. Assessment of neurovascular structures showed partial abutment of the radial sided bundle together with complete encirclement of the ulnar sided neurovascular bundle. The surrounding bone was free of any masses and associated mass effect.\nThe patient was taken to the OR for exploration and mass excision by the senior author. Possible risks associated with such intervention were explained. Intra-operatively, bruner type incision was designed together with island of skin involved in the mass. Exploration revealed extensive subcutaneous mass with fibro-fatty consistency with extensive fascia like extension to the surrounding soft tissue. The mass was encircling the ulnar neurovascular bundle with mass abutment over the radial bundle as seen in pre-op assessment. The mass was dissected freely from its attachment to those bundles preserving both radial and ulnar structures. The mass was then excised en-bloc having a dimension of 3.5 × 4x2.5 cm (). Histological assessment showed a lesion with fasciitis like features, myofibroblastic proliferation and scattered foci of osteoid formation that was positive for Alpha-Smooth Muscle Actin (ASMA 1A4) immune staining and no evidence of malignancy (). The resected margins were however, positive for residual lesion with difficulty in obtaining negative margins due to the extensive nature of the mass. Post-operatively, the patient had an un-eventual course. She was informed about the need for close follow-ups for both clinical and/or radiological signs of lesion recurrence, pending early surgical intervention (see ).
|
[[27.0, 'year']]
|
F
|
{'3463398': 1, '8864927': 1, '19678826': 1, '11392292': 1, '8356273': 1, '27613565': 1, '24405807': 2, '6837834': 1, '23210090': 2, '32362989': 2, '34409128': 2, '18164411': 1, '8367203': 1, '6945056': 1, '22623814': 1, '21199633': 1, '30310678': 2}
|
{'7180200-1': 1, '8366670-1': 1, '3507031-1': 1, '3898666-1': 1}
|
3,294 |
6176846-1
| 30,308,425 |
comm/PMC006xxxxxx/PMC6176846.xml
|
A case of obstructive jaundice due to early carcinoma of the cystic duct protruding into the common bile duct
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A 76-year-old man visited a local clinic with icteric conjunctivae. He had sick sinus syndrome and used a pacemaker. Blood biochemistry revealed significantly high levels of total bilirubin and transaminase, and US imaging demonstrated intrahepatic bile duct dilatation. Therefore, he was referred to our department for examination of suspected obstructive jaundice.\nOn admission, the patient’s body temperature was 35.9 °C, and yellowing of the conjunctivae and skin was evident. The patient had medium build, and no abnormal findings were evident in the neck or thoraco-abdominal region. Blood tests on admission showed no abnormality, but blood biochemistry revealed significant increases in the levels of transaminases and biliary enzymes (glutamate oxaloacetate transaminase (GOT): 260 U/L, glutamate pyruvate transaminase (GPT): 420 U/L, γ-glutamyl transpeptidase (γ-GTP): 1166 mU/mL, and alkaline phosphatase (ALP): 1163 U/L). The total bilirubin level was 6.0 mg/dL. Examination of tumour markers revealed a carcinoembryonic antigen (CEA) level of 3.0 ng/mL and a high level of cancer antigen 19-9 (CA19-9) (194.1 U/mL) ().\nEndoscopic retrograde cholangiopancreatography (ERCP) revealed disruption of contrast medium flow from the confluence of the cystic and common hepatic ducts through the distal bile duct, as well as significant dilatation of the common and intrahepatic bile ducts. Therefore, an endoscopic retrograde biliary drainage (ERBD) stent was inserted for biliary drainage (a). Brush cytology at the site of distal bile duct stricture demonstrated class V (adenocarcinoma).\nAbdominal computed tomography (CT) scan revealed a contrast-enhanced lesion that filled the lumen of the bile duct from inside the distal bile duct. This lesion did not extend beyond the walls of the bile duct, and neither infiltration into other organs nor no clear lymphadenopathy was observed (b). Positron emission tomography (PET)-CT scan revealed accumulation of fluorodeoxyglucose (FDG) that coincided with the lesion in the bile duct, and there were no clear findings of distant metastasis (c). Based on these results, we made a preoperative diagnosis of distal bile duct carcinoma (T1N0M0) according to the Union for International Cancer Control (UICC) classification and performed pancreatoduodenectomy with regional lymphadenectomy.
|
[[76.0, 'year']]
|
M
|
{'18193129': 1, '26155272': 1, '31783817': 2, '27613565': 1, '5765677': 1, '14886607': 1, '19096752': 1, '6468218': 1, '13914434': 1, '6318950': 1, '18224484': 1, '708242': 1, '30308425': 2}
|
{'6883593-1': 1}
|
3,295 |
6176965-1
| 31,020,164 |
comm/PMC006xxxxxx/PMC6176965.xml
|
Immunoglobulin G4-related disease of the thickened aortic valve extending to the left ventricular outflow tract causing severe aortic regurgitation and complete atrioventricular block: a case report
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A 62-year-old man with diabetes presented with general malaise, shortness of breath, and bradycardia. His medical history included retroperitoneal fibrosis, enlargement of the pancreas, and symmetrical swelling of the lacrimal glands with elevated serum IgG4 levels (175 mg/dL). He had received steroid therapy for 1 year for suspected IgG4-RD.\nA physical examination revealed a blood pressure of 90/42 mmHg, a pulse rate of 42 b.p.m., and body temperature of 36.6°C. An early diastolic murmur was noted on auscultation. The laboratory test results revealed elevated levels of white blood cells (WBC, 17 800/mm3), C-reactive protein (CRP, 4.07 mg/dL), and erythrocyte sedimentation rate (ESR, >120 mm) in the first hour. The serum IgG4 level was within the normal range (101 mg/dL) under oral prednisolone treatment (10 mg/day). An electrocardiogram revealed a complete atrioventricular block. A chest radiograph showed a normal cardiac silhouette and clear lung fields. Although echocardiography revealed a normal aortic valve 1 year ago, a transthoracic and transoesophageal echocardiography now revealed a thickened tricuspid aortic valve and the LVOT wall with severe aortic regurgitation, but no evidence of aortic stenosis and LVOT obstruction (Figure ). The left ventricular (LV) systolic function was preserved, without wall motion abnormalities, and the LV end-diastolic diameter was slightly increased (Table ). A contrast-enhanced computed tomography (CT) of the chest showed a thickened aortic valve extending to the LVOT wall and normal thickness of the ascending aortic wall (Figure ). A cardiovascular magnetic resonance (CMR) revealed a high-intensity signal around the aortic valve in the late gadolinium enhancement, whereas there was no significant change in the myocardium, the ascending aortic wall, and the surrounding structures.\nWe increased the oral prednisolone to 30 mg/day after three days (1 g/day) of high-dose methylprednisolone for clinically suspected IgG4-RD of the aortic valve. The complete atrioventricular block improved to a first-degree atrioventricular block within a few days. Thus, he avoided permanent pacemaker implantation. He received an angiotensin receptor blocker (olmesartan 10 mg/day) and a long-acting loop diuretic (azosemide 60 mg/day) as a medical therapy for aortic regurgitation-related heart failure. The inflammatory markers CRP and ESR gradually returned to within the normal range, and his serum IgG4 level decreased further (56.3 mg/dL). A follow-up echocardiography demonstrated a slight regression of the thickened aortic valve and the LVOT wall. We thus decreased the oral prednisolone to 25 mg/day after 1 month of administration and initiated azathioprine (50 mg/day). A follow-up contrast-enhanced CT showed regression of the thickened aortic valve and the LVOT wall (Figure ).\nNevertheless, he presented with worsening shortness of breath and malaise three months after increasing the corticosteroid dose. Plasma brain natriuretic peptide increased from 69 pg/mL to 414 pg/mL, whereas the serum IgG4 level decreased to 27.6 mg/dL. The chest radiograph showed pulmonary congestion and cardiomegaly. The transthoracic echocardiography revealed the progression of aortic regurgitation and an enlarged LV dimension, whereas the aortic valve and LVOT wall thickening regressed. The LV systolic function was preserved, with no evidence of significant aortic stenosis and no LV wall motion abnormalities (Table ).\nHe underwent aortic valve replacement for severe symptomatic aortic regurgitation and heart failure deterioration. The patient received a bioprosthetic aortic valve (25-mm Carpentier-Edwards PERIMOUNT; Edwards Lifesciences, Irvine, CA, USA), as we were concerned about the risk of anticoagulation-related bleeding and the possibility that there could be problems further down the line with complications from multiple organs and ongoing anticoagulation. During the operation, we observed the thickening and shortening of the tricuspid aortic valve (Figure ). The entire LVOT wall was also thickened. In contrast, the ascending aorta was normal. The pathological examination of the excised valve leaflets showed a dense lymphoplasmacytic infiltrate mixed with fibrotic tissue. The immunohistochemical staining revealed a ratio of IgG4-positive plasma cells to IgG-positive plasma cells greater than 0.5 (Figure ). Thus, he was diagnosed with IgG4-RD of the aortic valve.\nThe dose of prednisolone was tapered by 2.5 mg every 2 months in combination with azathioprine 50 mg after surgery. The transthoracic echocardiography 1 year after the surgery showed regression of the LV dilatation and normal function of the prosthetic valve.
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[[62.0, 'year']]
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M
|
{'28219556': 1, '25283128': 1, '22316447': 1, '23706467': 1, '32447609': 1, '11236777': 1, '20403026': 1, '24898599': 1, '20213336': 1, '28027743': 1, '31020164': 2}
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{}
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3,296 |
6177024-1
| 31,020,154 |
comm/PMC006xxxxxx/PMC6177024.xml
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Vasopressin antagonist-like effect of acetazolamide in a heart failure patient: a case report
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An 83-year-old male patient was emergently admitted to the hospital with the chief complaint of progressive dyspnoea over several days due to acutely decompensated HF (NYHA-IV) with hypotension (60/42 mmHg), bradycardia, and an irregular pulse (30 b.p.m.). The patient was uneventful for recent several years, and was not on any regular medication, including cardiovascular drugs, before the present admission. Table shows the clinical course of his HF-related tests, peripheral blood and urinary tests, and medications given to treat the decongestion and electrolyte disturbance. Physical examination on admission revealed jugular venous distension, systemic oedema, bilateral basal pulmonary rales, distant heart sound, and peripheral coldness. A 12-lead electrocardiogram revealed sinus arrest with a junctional escape rhythm and an irregular heart rate of 30 b.p.m. A chest X-ray revealed mild cardiomegaly (cardiothoracic ratio 55%) and prominent vasculature in the upper lung fields. Transthoracic cardiac ultrasound revealed a moderate degree of aortic regurgitation (III/IV), but the left ventricular ejection fraction (60%) was preserved, and its diastolic volume was almost within the normal range (143 cc). Thoracic and abdominal ultrasound showed massive bilateral pleural effusion and an expanded inferior vena cava with minimal respiratory change.\nUrgent initiation of a noradrenaline drip infusion (2–3 μg/kg/h) and beta stimulant adhesive skin patch (Tulobuterol 2 mg/day) promptly restored the sinus rhythm (70 b.p.m.) and the normality of conduction and the QRS complex on electrocardiography, resulting in the recovery from hypotension with a systemic blood pressure of 117/56 mmHg. Blood tests on admission revealed moderately elevated b-type natriuretic peptide (BNP 576 pg/mL; normal range <18.4 pg/mL), hyponatraemia (128 mEq/L; normal range 135–147 mEq/L), hypochloraemia (95 mEq/L; normal range 98–108 mEq/L), hyperkalaemia (5.7 mEq/L, normal range 3.6–5.0 mEq/L), and preserved renal function (creatinine 1.0 mg/dL; normal range 0.61–1.04 mg/dL) under no particular cardiovascular medications. Immediately after resolving the bradycardia and hypotension, low-dose oral acetazolamide (500 mg/day) and 20% polystyrene sulfate-Ca jelly (Argamate 25 g/day for 3 days) were prescribed to correct the decompensated HF status and electrolyte disturbance. Three days later, both the serum sodium and chloride concentrations had recovered to normal levels (136 mEq/L and 104 mEq/L, respectively), and the serum potassium concentration had decreased to 4.5 mEq/L.\nTwo weeks later, the patient’s body fluid retention was ameliorated and the serum BNP concentration was near normal (55 pg/mL). Serum chloride and potassium concentrations remained in the normal range, but the serum sodium concentration was slightly reduced (133 mEq/L) compared to that at Day 4 of the hospital admission, which could be managed by changing the diuretic prescription and/or dietary salt adjustment in accordance with the ‘chloride theory’ for HF pathophysiology. Three weeks later, the patient was discharged in an acceptable HF status. Two months later after discharge under the same medication, the patient’s HF status remained stable (serum BNP level of 65 pg/mL) and both the serum sodium and chloride concentrations were normal (139 mEq/L and 108 mEq/L, respectively).
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[[83.0, 'year']]
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M
|
{'28673579': 1, '27278221': 1, '3183367': 1, '13209842': 1, '6303178': 1, '32378135': 1, '13165901': 1, '29154432': 1, '28062134': 1, '28965280': 1, '19007589': 1, '30546691': 1, '31114959': 1, '30279861': 1, '3532823': 1, '18454727': 1, '34398440': 1, '18645067': 1, '31020154': 2}
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{}
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3,297 |
6177026-1
| 31,020,128 |
comm/PMC006xxxxxx/PMC6177026.xml
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Successful transcatheter aortic valve implantation for severe aortic stenosis of a bicuspid valve with situs inversus totalis guided by advanced image processing: a case report
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A 71-year-old man was admitted to our hospital with dyspnoea due to severe aortic stenosis complicating a calcified type 0 bicuspid aortic valve. His medical history included diabetes mellitus, atrial fibrillation, chronic respiratory failure, and coronary artery bypass grafting surgery for left main artery stenosis, which uncovered a situs inversus totalis (Figure ). On physical examination the patient had a systolic murmur predominantly located in the second left intercostal space on cardiac auscultation and bilateral crackles regarding the inferior parts of the lungs on pulmonary auscultation. Because of his medical history and a high Society of Thoracic Surgeons (STS) score of 11.9%, the Heart Team recommended TAVI rather than open surgery. The pre-operative multi-slice computed tomography (MSCT) evaluation of the aorta, and its branches confirmed patency of femoral arteries that allowed transfemoral approach (Figure ) and absence of significant thoracic aortic aneurysm.\nPre-operative sizing was performed with the new ValveAssist 2 (Discovery IGS 730, GE Healthcare, Chalfont St Giles, UK) image processing software. Comparatively to the standard fluoroscopy, the new software allows the projection of the MSCT-extracted, manually drawn virtual aortic annulus on the live fluoroscopy screen, and the enhancement of the aortic valve calcifications and aorta calcifications that are used as anatomical landmarks for operator guiding for the positioning of the THV during the procedure (Figures ). A Sapien 3 (Edwards lifesciences, Irvine, CA, USA) 26 mm was directly implanted in a high position (regarding the leaflet extremities rather than the annulus, to reduce the risk of paravalvular regurgitation and need for permanent pacemaker), without post-dilatation, prosthesis constriction and no angiographic leak. The patient did not require permanent pacemaker implantation. A transthoracic echocardiography one week later confirmed an excellent result with no intra or paravalvular regurgitation, and the patient reported improved symptoms. In follow-up consultation 3 months after the procedure the patient reported improved symptoms and had no periprosthetic leak on transthoracic echocardiography.
|
[[71.0, 'year']]
|
M
|
{'27609682': 1, '27101906': 1, '28893961': 1, '22645293': 1, '23375925': 1, '32617485': 2, '27609683': 1, '34812240': 1, '25465419': 1, '31020128': 2}
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{'7319830-1': 1}
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3,298 |
6177029-1
| 31,020,131 |
comm/PMC006xxxxxx/PMC6177029.xml
|
A case of left ventricular pseudoaneurysm presenting with a visible apex beat
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A 72-year-old man with a history of anteroseptal acute myocardial infarction was admitted to our hospital with acute heart failure. He underwent left ventricular (LV) reconstruction due to LV aneurysm, coronary artery bypass grafting from the left internal thoracic artery to the left anterior descending artery, mitral valvuloplasty with artificial ring for moderate to severe mitral regurgitation, and tricuspid valvuloplasty with artificial ring 18 months earlier. On admission, his blood pressure was 86/55 mmHg, heart rate was 60 b.p.m., and a visible apex beat was present at the 6th left intercostal space just medial to the left mid-clavicular line (, Video S1). Computed tomography revealed a pseudoaneurysm with mild calcification, protruding outside the thorax around the apex of the heart (Figure ). Echocardiogram showed akinesis of the anteroseptal wall and a 40 × 27-mm pseudoaneurysm around the apex of the heart, moving in synchrony with the heartbeat, and a 17% LV ejection fraction (Figure , , Video S2). The connection was confirmed between the pseudoaneurysm and the left ventricle with a spontaneous echo contrast. An underlying infection could have contributed to the formation of the pseudoaneurysm. We theorize that as the pseudoaneurysm progressed, the tissue along its path of progression was mechanically damaged. This gradual damage could have resulted in impaired structural integrity of the surrounding tissue which ultimately allowed certain segments of the heart to protrude into regions beyond the normal anatomical confines of the heart. Left ventricular ejection fraction slightly improved from 17% to 25%, before and after the operation, respectively. The patient was discharged after a protracted hospital course. After discharge, the patient is now coming for follow-ups at regular intervals. Most LV pseudoaneurysm patients present with various clinical observations and abnormal findings on physical examination, such as heart failure, dyspnoea, and chest pain; however, 10% of patients are asymptomatic. In the present case, the pseudoaneurysm protruded into the left thoracic cavity with the pericardium and perforated subcutaneously from the intercostal space. Post-myocardial infarction LV pseudoaneurysm has been reported,; however, a pseudoaneurysm presenting with a visible apex beat is exceptionally rare.
|
[[72.0, 'year']]
|
M
|
{'9741493': 1, '27751338': 1, '28986350': 2, '31020131': 2}
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{'5633050-1': 1}
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3,299 |
6177097-1
| 31,020,159 |
comm/PMC006xxxxxx/PMC6177097.xml
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A rare case of accessory mitral valve tissue causing left ventricular outflow tract obstruction associated with parachute mitral valve, ventricular septal defect, bicuspid aortic valve, unruptured aneurysm of aortic sinus: a case report
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A 22-year-old female patient was referred to the Department of Cardiology with exertional shortness of breath and a history of congenital heart disease with mitral stenosis (MS), VSD and pulmonary hypertension as an outpatient. Five days previously, her condition had deteriorated rapidly, the patient became progressively dyspnoeic and developed orthopnoea, and she was unable to perform daily activities due to severe shortness of breath associated with exertional atypical chest pain. An electrocardiogram showed an ectopic rhythm (78 b.p.m./m), rapid atrial arrhythmias, and a left QRS axis. Upon physical examination, her blood pressure was found to be normal (100/60 mmHg) and the cardiac auscultation showed a 3/6 systolic murmur along the left sternal border. On auscultation of the chest, there were normal vesicular breath sounds. Scoliosis was observed in chest findings. There were no peripheral oedema and jugular venous distention. Blood and biochemical laboratory tests revealed leucocytosis, white blood cell count 10.18 × 109 cells/L (normal value: 3.5–9.5 × 109 cells/L), elevated C-reactive protein levels 25.36 mg/L (normal value: 1–10 mg/L) and NT-proBNP 628 ng/L (normal value: 133–450 ng/L). Chest radiography showed a cardiothoracic ratio of 60%, pulmonary congestion, bilateral pleural thickening and scoliosis.\nNext, we performed a transthoracic echocardiography (TTE) that revealed an abnormal membranous structure (1.3 cm × 1.2 cm) attached to the ventricular side of anterior mitral valve (MV) leaflet, with a subaortic chordal attachment. The abnormal tissue was similar to a MV leaflet. The parasternal short-axis view showed the relationship between the normal MV and the accessory valve (Figure ). Therefore, we diagnosed it as AMVT. The peak blood flow velocity across LVOT had accelerated to 5.0 m/s (Figure ). The MV had a parachute-like appearance. There were two normally positioned papillary muscles in the left ventricle, but they did not have chordae tendineae inserted into it. The chordae tendineae were located in the left ventricular wall between the two papillary muscles (). Therefore, we described it as a parachute-like MV. Doppler assessment yielded a peak MV gradient of 27 mmHg and a mean MV gradient of 16 mmHg. Pressure half-time method yielded a valve area of 0.8 cm2. There was also a mild degree of mitral regurgitation. In addition, echocardiography revealed a peri-membranous VSD ( and ) and BAV. The diameter of the VSD was 1.0 cm, and the shunt flow through VSD was left-to-right with a peak velocity of 4.5 m/s. From these findings, we hypothesized that LVOT obstruction was due to the accessory MV, MS was due to PMV and the left-to-right shunt was due to VSD. The pulmonary and tricuspid valves were normal. The pulmonary artery systolic pressure was slightly high (44 mmHg). There was also a mild dilatation of the left atrium (4.2 cm) and left ventricle (left ventricle end-diastolic diameter = 5.2 cm). Systolic function of the left ventricle was estimated to be within normal limits (ejection fraction = 60%). right ventricle function as well as the dimensions and morphology of the aortic arch and the ascending and descending aorta were normal.\nIn addition, we performed transoesophageal echocardiography (TOE) that confirmed the TTE findings, showing a fixed, membrane-like structure arising from the anterior mitral leaflet causing the LVOT obstruction (). This also confirmed the presence of PMV and VSD ( and ). Transoesophageal echocardiography showed a BAV with only two sinuses: left coronary and right coronary. The right coronary sinus appeared aneurysmal, but not ruptured (). The valve area of BAV was 2.5 cm2 by planimetry, BAV was functioning normally with no aortic valve stenosis or regurgitation.\nAfter a comprehensive clinical evaluation, elective surgical treatment was performed because of the presence of VSD, severity of the MV stenosis and LVOT obstruction. The BAV was functioning normally and was not replaced. The operative findings correlated with the imaging diagnosis. During the operation, excision of the AMV and MV replacement were performed. In addition, the peri-membranous VSD and aneurysm of the aortic sinus were repaired. Grossly, the membranous structure specimens confirmed that it was AMVT (Figure ). Histological examination showed valvular tissue associated with mucous degeneration and inflammatory cell infiltration.\nA post-operative echocardiography showed complete resection of AMV, no residual shunt, no left ventricular outflow gradient or mitral regurgitation. The mosaic flow signals in the left ventricular outflow were diminished using colour Doppler, and the peak blood flow velocity decreased to 1.4 m/s. The peak pressure of rapid filling phase and atrial systolic phase across the prosthetic MV were 16 mmHg and 4 mmHg, respectively. The post-operative course was uneventful, and the patient was most recently reviewed 1 week, 1 month, 3 months after the surgical procedure by ultrasound, electrocardiogram, and chest radiography. The function of BAV was evaluated by ultrasound regularly. In the most recent follow-up, the patient’s shortness of breath disappeared, with no further episodes of chest pain.\nIn this study, we report an extremely rare case of AMVT causing LVOT obstruction associated with PMV, VSD, BAV, and an unruptured aneurysm of the aortic sinus. This combination of symptoms has not been previously reported in literature.
|
[[22.0, 'year']]
|
F
|
{'32377426': 1, '15891764': 1, '22044509': 1, '24165118': 1, '23236337': 1, '34622793': 1, '10892953': 1, '12824963': 1, '23288193': 1, '34317218': 1, '31020159': 2}
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{}
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