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2,000 |
6099022-1
| 30,147,886 |
comm/PMC006xxxxxx/PMC6099022.xml
|
Renal infarction in vascular Ehlers–Danlos syndrome masquerading as pyelonephritis
|
A 29-year-old female presented to the emergency department with a 1-day history of acute right flank pain, fever, and vomiting. She had a known history of a mutation in COL3A1 gene associated with vascular Ehlers–Danlos syndrome (vEDS) and a strong family history of arterial aneurysms and rupture. On examination, her abdomen was soft and not distended, and with costovertebral angle tenderness. White blood cell count was elevated at 15 000 cells per cubic millimeter (normal range, 4000-11 000). Urinalysis showed 5-20 white blood cells per field with small leukocyte esterase. An abdominal computed tomography (CT) without contrast showed multiple hypo-densities at the right kidney, initially interpreted as “severe pyelonephritis” but ultimately thought to be related to multiple renal infarcts. Because of the clinical suspicion of kidney infarction, CT angiogram was pursued and showed asymmetric contrast enhancement of the right kidney with nearly no perfusion of the renal parenchyma in the posterior aspect of the upper and lower pole (Figure , Panels A and B). A 3-dimensional reconstruction of the CT demonstrated similar findings (Figure , Panel C). Renal duplex had findings consistent with renal artery dissection. The patient was admitted to the hospital, where she received supportive care and heparin therapy and beta-adrenoceptor blocker. Antibiotics were withheld, and both blood and urine cultures were without growth. Over the next 3 days, her abdominal symptoms resolved.
|
[[29.0, 'year']]
|
F
|
{'10575421': 1, '8160237': 1, '21549076': 1, '24653803': 2, '15127738': 1, '28306229': 1, '18328988': 1, '17640391': 1, '26698927': 1, '20825986': 1, '26175915': 2, '17276805': 1, '30147886': 2}
|
{'3958580-1': 1, '4484843-1': 1}
|
2,001 |
6099024-1
| 30,147,912 |
comm/PMC006xxxxxx/PMC6099024.xml
|
Metabolic acidosis after sodium thiosulfate infusion and the role of hydrogen sulfide
|
A 68-year-old Caucasian woman with end-stage renal disease on dialysis was admitted to our facility for a stroke and a non-ST segment elevation myocardial infarction. The stroke caused a right facial droop and right upper extremity flaccid paralysis, without any other sensory or cognitive disturbances. Her chronic medical conditions included type 2 diabetes mellitus (20-year history, hemoglobin A1C 6.6% on admission), atherosclerotic coronary vascular disease, ischemic cardiomyopathy with an ejection fraction of 35%, congestive heart failure, paroxysmal atrial fibrillation on warfarin anticoagulation, hypertension, and hyperlipidemia. She had been receiving dialysis for 2 months and was anuric. Concurrently, she was found to have tender, nonhealing, necrotic, violaceous, ulcerating plaques of her right shin and left posterior calf, which were evaluated by dermatology and thought to be consistent with CUA. Biopsies were not obtained due to supratherapeutic INR and concern for inability to heal from biopsy. Antibiotics (clindamycin, later changed to vancomycin) were initiated. Blood pressure and rate control therapies with beta-blockers were initiated to mitigate myocardial demand ischemia. She was beyond the time range for thrombolytic therapy, but her neurologic symptoms did not progress under observation.\nThe patient continued her scheduled intermittent hemodialysis (dialysate of 4 mEq/L potassium, 2.5 mEq/L calcium, and 35 mEq/L bicarb, duration of therapy 4 hours, ultrafiltration 3 kg) on the day of her admission after medical stabilization. During the last hour of the dialysis session that evening, 25 g of STS was also administered intravenously to treat her CUA ulcers. The morning following, the patient was found to have delirium, hypotension, and a metabolic acidosis with an elevated anion gap (Table ). ABG revealed a primary metabolic acidosis with an increased anion gap, mixed with metabolic alkalosis with full respiratory compensation. Lactate and β-hydroxybutyrate were not elevated. Sepsis was suspected; however, three sets of blood cultures were obtained and revealed no growth, and helical computed tomography scan of chest, abdomen, and pelvis revealed no nidus of infection. Her metabolic acidosis with anion gap did not resolve despite daily dialysis with dialysate of 35 mEq/L bicarb and stabilized with a supplemental bicarbonate drip; her anion gap trended downward over the next 4 days and eventually returned to her baseline.\nAfter investigations for potential sepsis, ketosis, lactic acidosis, and uremia, STS was considered to be the probable instigating drug in her metabolic derangement. Due to the life-threatening nature of this profound anion gap academia, the clinical team discontinued STS. She was treated conservatively with the help of our wound care team.\nWithout STS therapy, her ulcers continued to worsen. She was judged to not be a candidate for surgical debridement due to her multiple comorbidities. Her hospital stay was complicated by poor nutrition, health care-associated pneumonia, and a Clostridium difficile infection. Thirty days into her hospital stay, she elected to switch to hospice care and died shortly thereafter.
|
[[68.0, 'year']]
|
F
|
{'9426423': 1, '23581969': 1, '26877209': 1, '15168392': 1, '24824185': 1, '32336746': 1, '23991830': 1, '21834598': 1, '25461301': 1, '26563786': 1, '21566113': 1, '6600205': 1, '25029979': 1, '22036943': 1, '32967516': 1, '26992479': 1, '25960299': 1, '25506005': 2, '33935760': 1, '30147912': 2}
|
{'4254074-1': 1, '4254074-2': 1}
|
2,002 |
6099025-1
| 30,147,882 |
comm/PMC006xxxxxx/PMC6099025.xml
|
Excimer laser in contrast for the treatment of acute MI caused by thrombosis of underexpanded stent
|
A 79-year-old male with a history of hypertension, hyperlipidemia, and polycythemia vera underwent PCI of the left anterior descending artery (LAD) 1 week prior to admission at an outside institution with overlapping 3.0 × 15 mm Integrity bare-metal stents (Medtronic) to the mid-LAD (Fig. A). He developed chest pain approximately 40 min prior to arrival in the ER where he was found to have anterior ST elevations with hemodynamics consistent with shock. He was taken emergently to the laboratory where angiography with a 6 Fr system was performed via the right radial approach demonstrated a 100% occlusion of the LAD with in-stent thrombosis (Fig. B). There was also angiographic underexpansion of the stents at the site of occlusion (Fig. C). In the interim from arrival, we were able to obtain his catheterization report from the other hospital, and it was reported that an attempt was made to postdilate the stents with a 3.0 and 3.25 noncompliant (NC) balloon without resolution of the “waste” in the midportion of the stent. Bivalirudin was administered, and a Runthrough wire (Terumo) was passed distally restoring antegrade TIMI 1 flow. We then advanced a 0.9 laser to the lesion (Fig. D). The catheter would not advance through the lesion. Given the recent issues encountered by the previous operator, we performed laser with contrast injections at a setting of 80/80 (fluency/rate) for approximately 1 min. We then did aggressive dilation with a 2.5 and then a 3.0 NC balloon with expansion of the stent (Fig. E). He stabilized hemodynamically at this point. We then performed intravascular ultrasound (IVUS) demonstrating severe concentric calcification and lumen diameter of about 3.75–4.0 mm. Postdilation was performed with a 4.0 × 12 Quantum balloon (Boston Scientific) with an excellent angiographic result (Fig. F). Final IVUS demonstrated good stent expansion; however, on pullback, there was evidence of significant distal left main and ostial LAD disease with heavy calcification; this was also appreciated in the LAO cranial views. After the patient was stabilized and recovered from his event (echo demonstrated a decline in the ejection fraction (EF) to approximately 25% with anterior wall motion abnormality compared with a previously reported normal EF), a heart team approach was used to determine the best revascularization option for the patient. Given the extent of calcification and anatomic concerns, he eventually underwent bypass and was discharged home on postoperative day five.
|
[[79.0, 'year']]
|
M
|
{'15894747': 1, '10785758': 1, '7728846': 1, '12112890': 1, '33747064': 1, '1999636': 1, '8023778': 1, '8462152': 1, '8496518': 1, '19171852': 1, '8313578': 1, '18324694': 1, '25754354': 1, '29086727': 1, '15028347': 1, '24290659': 1, '27862848': 1, '10762799': 1, '1999637': 1, '8294681': 1, '10151024': 1, '26643071': 1, '18377975': 1, '23703809': 1, '33849433': 2, '11170330': 1, '7594041': 1, '24561145': 1, '22865316': 1, '30147882': 2}
|
{'6099025-2': 2, '8042855-1': 1}
|
2,003 |
6099025-2
| 30,147,882 |
comm/PMC006xxxxxx/PMC6099025.xml
|
Excimer laser in contrast for the treatment of acute MI caused by thrombosis of underexpanded stent
|
A 73-year-old male with history of hypertension, hyperlipidemia, and esophageal reflux presented to an outside hospital with a non-ST elevation myocardial infarction and underwent PCI of the LAD with overlapping 3.0 × 38 and 3.5 × 18 Resolute DES (Medtronic). There was a suboptimal stent expansion in the LAD, and he was discharged on dual antiplatelet (DAPT) therapy. He presented to the same institution 6 days later with acute ST elevation and stent thrombosis. They were able to pass a wire and did sequential balloon inflations sizing up to a 4.0 balloon. Antegrade flow was restored, but despite aggressive dilation, the lesion did not expand. He was transferred to our institution for bypass. The surgical team evaluated him, and it was felt PCI would be a better option if feasible rather than surgery in the acute situation. In the interim, the patient developed cardiogenic shock and chest pain and was taken emergently to the laboratory where an Impella CP (Abiomed) was placed to stabilize the patient. A decision was made to perform laser atherectomy of the stent to try and expand the stent. Right radial access was obtained with a 6/7 slender sheath (Terumo). Angiography revealed a patent LAD with TIMI 1 flow (Fig. A) and underexpansion of the stents at the overlap (Fig. B). A 0.9 ELCA catheter was easily advanced through the lesion (Fig. C). Laser atherectomy was performed with contrast at 80/80 (fluency and rate) for 2 min and then an attempt to dilate with a series of 2.5 and 3.0 NC balloons was performed. Despite high-pressure inflation at 26 atm, the lesion did not yield (Fig. D). Perhaps rupturing the balloon would have resulted in some plaque modification as well; however, this did not occur. It was felt that the 0.9 ELCA did not have enough contact with the underlying plaque given the preexisting channel (although underexpanded). Therefore, a 1.4 ELCA catheter was advanced to the lesion; however, it would not advance through the lesion. Atherectomy was performed at 60/40 for 1 min with contrast puffs during atherectomy (Fig. E) followed by attempted dilation with a 3.0 NC balloon without resolution of the lesion (Fig. F). It was decided to use an atherotomy balloon at this time to increase the radial force. A 3.0 × 10 Flextome was advanced with an initial inflation at 14 atm (Fig. G) without resolution. The lesion yielded at 24 atm (Fig. H). Postdilation was then performed with a 3.75 NC balloon with restoration of TIMI 3 flow (Fig. I and J). The patient was weaned off the Impella and had no acute issues postprocedure.
|
[[73.0, 'year']]
|
M
|
{'15894747': 1, '10785758': 1, '7728846': 1, '12112890': 1, '33747064': 1, '1999636': 1, '8023778': 1, '8462152': 1, '8496518': 1, '19171852': 1, '8313578': 1, '18324694': 1, '25754354': 1, '29086727': 1, '15028347': 1, '24290659': 1, '27862848': 1, '10762799': 1, '1999637': 1, '8294681': 1, '10151024': 1, '26643071': 1, '18377975': 1, '23703809': 1, '33849433': 2, '11170330': 1, '7594041': 1, '24561145': 1, '22865316': 1, '30147882': 2}
|
{'6099025-1': 2, '8042855-1': 1}
|
2,004 |
6099027-1
| 30,147,893 |
comm/PMC006xxxxxx/PMC6099027.xml
|
A case of Extrapulmonary intrathoracic hydatidosis with pseudochylothorax
|
A 79-year-old Iranian man was admitted to Imam-Khomeini hospital with 6-month history of dyspnea, nonproductive cough, fatigue and weight loss. Previous clinical history and family history was unremarkable. He had no history of smoking or being passive smoker. He did not use alcohol or opium in the past, and his job is animal husbandry. Six month before recent admission, he had been admitted into another hospital, due to dyspnea. His spiral thoracic computed tomography scan revealed left massive pleural effusion with multiple cysts inside pleural effusion. The patient refused more investigation and discharged with his satisfaction. From first to second hospitalization, a little relief of his symptoms was seen. On February 2017, the patient was admitted again and his complaint was dyspnea and dry cough.\nGeneral physical examination revealed an oral temperature of 37°C, a heart rate of 90 beats per minute, a respiratory rate of 14 breaths per minute, and a blood pressure of 110/70 mm Hg and the oxygen saturation of 92% with room air. Aside from this, the clinical examination was unremarkable. Blood samples revealed an elevated CRP of 97 mg/L, leukocytosis (15400/microL) with a strong component of granulocytosis, but no eosinophilia. Physical chest examination showed decreased breath sound in left hemithorax. The remainder of the examination was normal.\nThe chest radiography showed left pleural effusion. Spiral thoracic computed tomography scan revealed left loculated pleural effusion (Figures and ). Echocardiography was normal and abdominal sonography revealed one cyst with 59 mm diameter and many wrinkle membranes in pleural space (Figure ). Thoracentesis obtained a milky fluid (Figure ) with the following biochemical values: 4800 leukocytes/mm3 with polymorphonuclear predominancy leukocytes/mm3; total protein 10.8 g/dL; lactate dehydrogenase (LDH) 5744 U/L; glucose 81 mg/dL; pH 7.34; Cholesterol 189 mg/dL triglycerides 68 mg/dL. A great number of cholesterol crystals were observed on microscopic examination. H & E stain of pleural fluid showed many scolices of hydatid cyst. Immunoglobin-G enzyme-linked immunosorbent assay for Echinococcus was positive, and then pseudochylothorax pleural effusion and spontaneously ruptured hydatid cyst was diagnosed.\nThe patient declined any surgical treatment; therefore he was prescribed antihelminthic treatment with albendazole 400 mg, two times daily. He was discharged with satisfaction. After 9 months follow up dyspnea was improved and the pleural effusion resolved gradually. After this time albendazole was discounted.
|
[[79.0, 'year']]
|
M
|
{'19568393': 1, '14982612': 1, '21695106': 1, '18291609': 1, '19369124': 1, '21333077': 1, '23604185': 1, '19931502': 1, '16157340': 1, '20216420': 1, '19350321': 1, '27621864': 1, '30147893': 2}
|
{}
|
2,005 |
6099029-1
| 30,147,906 |
comm/PMC006xxxxxx/PMC6099029.xml
|
Successful treatment of dens invaginatus type 3 with infected invagination, vital pulp, and cystic lession: A case report
|
A 14-year-old male patient was referred to the Clinic of Dental and Oral Pathology at Lithuanian University of Health Science, Kaunas, Lithuania, by his general dentist for evaluation and treatment of the maxillary lateral right incisor (tooth #12). The patient complained about constant mild pain, tenderness to bitting and touching mucosa near the tooth #12. He reported swelling history in the infraorbital region about a month ago.\nOn the appointment day, the extra-oral examination revealed no abnormalities. The intraoral examination showed infra-occlusion of tooth #12. Sinus tract was observed in the alveolar mucosa, proximally to the apical area of tooth #12. The tooth reacted normally to percussion, however, was somewhat sensitive to palpation. Response to cold test was positive, indicating the unaffected vitality of the pulp. There was no evidence of caries in the hard tissues as well as no increased tooth mobility and probing depths (Figure ).\nThe tooth presented with an open and unsealed endodontic cavity. Drainage of pus through the cavity was observed. The radiographic examination revealed a huge radiolucent lesion in the periapical region of tooth #12 and signs of a Oehlers' type 3 invagination (Figure ). The invagination extended from the crown to the root apex (“pseudocanal”), and apparently did not communicate with the regular canal.\nWith the consent of the patient's mother, a cone beam computer tomography (CBCT) scan (Picasso-Trio, Vatech Global) with exposure parameters of 80 kVp, 5 mA, and 12-24 seconds was taken of the area of interest. The CBCT scan revealed the presence of a large periapical radiolucency related to the tooth #12. Radiolucency had a quite well-circumscribed sclerotic border and no connection with maxillary sinus or the nasal cavity. Coronal and axial CBCT images showed that the invagination was separated from a circular vital root canal and had a different portal of exit (Figure ).\nThe final diagnosis was defined as chronical apical periodontitis with a cyst-like lesion of tooth #12 with an infected Oehlers' type 3 invagination and the surrounding vital pulp. The treatment plan was to perform endodontic treatment of the invagination and then to enucleate the cystic lesion surgically, while maintaining the pulp vitality.\nOn the first visit, the endodontic cavity of tooth #12 was carefully reshaped without penetrating the pulp using local anesthesia (1.7 mL Ubistesin forte, articaine, 1:100 000 epinephrine) and rubber dam isolation. Under the dental operating microscope (OPMI pico, Carl Zeiss, Jena, Germany), a wide infected invagination in the middle of the cavity was observed. It was not possible to visualize the end of invagination because of the curvature. The pulp horns were hidden behind a thin layer of dentin and located in the mesial and distal corners of the cavity.\nThe space of invagination was instrumented with K-files (Dentsply Maillefer, Ballaigues, Switzerland) and generously irrigated with 2.5% NaOCl and 17% EDTA, using an ultrasound activation. Calcium hydroxide paste was inserted for 2 weeks, and the cavity was sealed with temporary material (IRM, Dentsply Maillefer).\nOn the second appointment, the patient had no complaints, and the sinus tract was closed. The tooth was anesthetized as previously described and isolated with a rubber dam. Then, the apical entrance of the invagination was sealed with mineral trioxide aggregate (MTA, Angellus, Lordina, Brazil) and condensed with hand pluggers and paper points.\nAfter allowing 20 min for setting of MTA, the remaining space of invagination was filled with thermoplastic gutta-percha (Callamus Dual, Dentsply Mailefer) and AHplus sealer (Dentsply, De Trey, GmbH, Konstanz, Germany). Furthermore, the dentin walls near the vital pulp were covered with “Biodentine” (Septodont, Saint Maur des Fosses, France), and the final composite restoration was placed (3M, Filtek Supreme).\nIn 3 months, the surgical enucleation of the cyst was performed. Under the dental operating microscope, using intrasulcular incision and vertical release, a full-thickness flap was reflected and thin cortical bone was removed to create the bony window. The cystic lining/granulation tissue was carefully enucleated, without damaging the periapical region of teeth #11, #12, #13. The integrity of maxillary sinus and nasal cavity was not damaged. The histological evaluation of the biopsy confirmed the diagnosis of a radicular cyst.\nThe follow-up visits of the patient were made after 1, 2, 3, 6, 12, and 24 months. Tooth #12 maintained a normal response to cold test for the entire period. The clinical examination revealed normal function of tooth #12 (Figure ). The patient had no complaints or signs of infection. After 12 months, the radiographic examination showed a fully repaired bone structure (Figures , , ).
|
[[14.0, 'year']]
|
M
|
{'10332241': 1, '26874642': 1, '24815882': 1, '25146043': 1, '13477660': 1, '25728098': 1, '24767572': 1, '25127930': 1, '21978185': 1, '25595467': 1, '25799535': 1, '24238434': 1, '20491983': 1, '27497511': 1, '19133104': 1, '20500234': 1, '18699792': 1, '21564517': 1, '19133103': 1, '23137215': 1, '22794224': 1, '22244638': 1, '26514867': 1, '23265156': 1, '20728729': 1, '23522541': 1, '28231977': 1, '30147906': 2}
|
{}
|
2,006 |
6099033-1
| 30,147,904 |
comm/PMC006xxxxxx/PMC6099033.xml
|
Discordance for placental mesenchymal dysplasia in a monochorionic diamniotic twin pregnancy: A case report
|
A 34-year-old gravida 3 para 2 was referred at 20 weeks because of growth restriction in one twin of a spontaneous monochorionic diamniotic pregnancy. Twin 1 had normal amniotic fluid and appeared structurally normal (estimated fetal weight [EFW] 335 g). Umbilical artery and ductus venosus Doppler studies were unremarkable, whereas the middle cerebral artery showed decreased peak systolic velocities (19 cm/s-0.74 multiples of the median [MoM]) suggestive of polycythemia. Twin 2 had severe growth restriction (65% growth discordance compared to twin 1, EFW 118 g) and had a pericardial effusion. Additionally, there was an anhydramnios and its bladder was empty. Doppler studies of the umbilical artery showed an absent end diastolic flow, accompanied by a reversed a-wave of the ductus venosus and increased peak systolic velocities of the middle cerebral artery (52 cm/s, 2 MoM) suggestive of anemia. Its placental part was thickened (7 cm) and contained multiple cysts (Figure A). The working diagnosis was that of severe early-onset discordant growth probably related to a chromosomal discordancy with diandric triploidy or partial mole in one of the twins with associated twin anemia polycythemia sequence. The parents were offered genetic testing by amniocentesis of twin 1 and by chorionic villous sampling of twin 2. We discussed the likely poor outcome with expectant management, the option of selective reduction of twin 2, if twin 1 was confirmed to be normal as well as a termination of the entire pregnancy. However, the parents wished to continue the twin pregnancy and therefore declined invasive testing.\nSubsequent scans at 26 and 30 weeks showed an improvement of the condition of twin 2 with positive flow in the umbilical artery, a positive a-wave in the ductus venosus, increased amniotic fluid, and a normalization of the middle cerebral artery peak systolic velocity. From 30 weeks onwards, the patient was seen twice weekly for fetal monitoring and a course of lung maturation was given.\nAt 34 weeks, an elective cesarean section was performed with the birth of 2 boys. Twin 1 had a birthweight of 2130 g and Apgar scores of 8, 9, 9 after 1, 5, and 10 minutes, respectively. Twin 2 weighed 970 g with Apgar scores of 7, 8, 9, after 1, 5, and 10 minutes, respectively. Both had normal hemoglobin levels. Twin 1 was hospitalized for 22 days without any major neonatal problems. Twin 2 stayed in the neonatal intensive care unit for 58 days and required nasal CPAP for 4 days and 2 units of packed cells for anemia on day 30 and day 50 after birth. Additional postnatal examinations in twin 2, such as serial brain scans, abdominal ultrasound scan, echocardiography, and metabolic tests, were normal. Conventional karyotype and single-nucleotide polymorphism array analysis of both twins showed 46, XY and absence of pathologic copy number variants, respectively. DNA fingerprinting confirmed a monozygotic twin pregnancy. Developmental assessment by Bayley scores at the age of 5 months showed a mild developmental delay in both children.\nPlacental injection studies did not show any vascular anastomoses between the vascular territories (Figure B). Macroscopic examination showed a normal part of twin 1 and a cystic enlarged part of twin 2 (Figure C). Pathological examination confirmed a monochorionic diamniotic twin placenta with normal findings in the part of twin 1. In the part of twin 2, the chorionic vessels were strongly dilated. In the stem villi, the stroma was severely hydropic with the formation of central cisterns. Starting from the stem villi and extending into the intermediary and terminal villi, there was also a diffuse capillary proliferation (chorangiomatosis). No trophoblastic hyperplasia was seen. In the stem villi, the trophoblastic cells were p57 positive, whereas the stromal fibroblasts were p57 negative. Pathology therefore confirmed discordancy for placental mesenchymal dysplasia in a monochorionic placenta.
|
[[34.0, 'year']]
|
F
|
{'23239538': 1, '19442969': 1, '16411235': 1, '21934458': 1, '16522413': 1, '17460014': 1, '16231321': 1, '30147904': 2}
|
{}
|
2,007 |
6099035-1
| 30,147,910 |
comm/PMC006xxxxxx/PMC6099035.xml
|
A novel technique for lead sparing tricuspid valve replacement in the case of a transvenous ICD lead
|
A 35-year-old female patient was presented to our center for TV replacement due to stenosis. At the age of 11 years, the patient suffered from endocarditis supported by a small ventricular septal defect. At that time, the ventricular septal defect was closed and a mechanical tricuspid valve (SJM, 28 mm) implantation and epicardial single chamber pacemaker implantation due to concomitant third degree AV block without escape rhythm were performed. At the age of 17 years, the abdominal pacemaker was replaced, due to battery depletion (Biotronik). Six months later, a second surgery followed with replacement of the dysfunctional mechanical valve for a 27 mm Porcin-Baxter biological TV. Another PM replacement (Medtronic) was performed at the age of 27 years, again, due to battery depletion. At the age of 30 years, the abdominal pacemaker was explanted and a two chamber transvenous ICD (Medtronic Egida DR) was introduced, as the patient suffered a syncope during documented sustained ventricular tachycardia. The ICD lead was implanted passing the tricuspid valve into the right ventricle. Six years later, severe TV stenosis developed, caused by an ICD lead, that stuck to the posterior leaflet of the biological valve and ventricular myocardium, and the TV had to be replaced a third time. To avoid future TV dysfunction due to lead related complications, we discussed several options with the patient. These included first TV replacement in combination with epicardial pacemaker leads and a subcutaneous ICD (S- ICD, EMBLEM™ Boston Scientific) or alternatively placing a pacing lead in the coronary sinus in combination with an S- ICD. As the patient disagreed on both options, despite a higher risk of TV dysfunction by placing another transvenous ICD lead through the TV, we discussed another option and opted for a lead sparing replacement of the TV. The TV ring was cut open on both sides beneath the original ICD lead, and the TV prosthesis was excised. A new bioprosthetic valve was implanted, leaving the ICD lead outside the ring of the new TV prosthesis. As the lead was stuck to the former TV annulus and posterior ventricular wall, no further fixation of the lead was needed. The new valve (SJM biological 28 mm) was implanted using 14 Coreknots (Figures , , ).\nThe postoperative course was unremarkable, and the patient was dismissed on the 11th postoperative day/postoperative day 11. Follow-up after 4 months showed a well functioning TV prosthesis without stenosis or regurgitation and no deterioration in pacing or sensing parameters. No artifacts or other hints to a lead dysfunction were recorded (Table ).
|
[[35.0, 'year']]
|
F
|
{'24803079': 1, '25527426': 1, '28339945': 1, '27075814': 1, '28473139': 1, '24886320': 1, '28109394': 1, '30147910': 2}
|
{}
|
2,008 |
6099042-1
| 30,147,897 |
comm/PMC006xxxxxx/PMC6099042.xml
|
Perinatal findings in a patient with a novel large chromosome 19p deletion
|
Twin B of a spontaneous dichorionic and diamniotic twin pregnancy of a 30-year-old multigravida was found to have symmetrical intrauterine growth restriction (IUGR) at 25-week gestation (estimated fetal weight (EFW) <3rd percentile, intertwin weight discordance 28%), with abnormal Dopplers indicating increased placental resistance and cranial sparing with cephalization of blood flow. Also noted were mild right lateral cerebral ventriculomegaly, small stomach, and enlarged gallbladder. Aneuploidy screening results were low-risk, with cell-free DNA negative for trisomy 21, 18, and 13. Amniocentesis was declined. Maternal viral serology for cytomegalovirus, toxoplasmosis, and parvovirus was negative for recent infection. From 27 weeks onward, persistently absent end-diastolic flow of the umbilical artery was noted. Ventriculomegaly worsened to moderate range at 28 and 33 weeks, with bitemporal skull narrowing and strawberry-shaped skull appearance noted at 31 weeks (Figure ). Anhydramnios for Twin B was noted at 36-week gestation. As diagnosis of aneuploidy would affect postnatal management, bladder aspiration of Twin B was performed, but cell culture was without growth. At 38 weeks, the EFW for Twin B was 1559 g, with twin discordance of 48%.\nThe patient was born at 38 weeks and 3 days gestation, via scheduled repeat cesarean delivery. Apgar scores were 5, 7, and 8 at 1, 5, and 10 minutes of life, respectively. He was small for gestational age (SGA) with birthweight 1133 g (Z-score: −5.49), birth length 39.4 cm (Z-score: −4.43), and head circumference 29.5 cm (Z-score: −3.23). Physical examination was significant for small facies with underdeveloped chin, relative macrocephaly, overlapping cranial sutures, mild crumpling of the ears, wide-spaced nipples, second and fifth fingers of the right hand overlapping the third and fourth fingers, and a small sacral hemangioma (Figure ). The patient developed hypoglycemia and hypophosphatemia, likely secondary to his IUGR/SGA status, which responded to modifications in intravenous fluids. He tolerated full enteral feeds by the second week of life, but due to poor oromotor skills, he was fully nasogastric tube-dependent. Patient developed self-resolving leukopenia. Thrombocytopenia, reaching a nadir on day of life (DOL) 2, responded to 1 platelet transfusion. Mild self-resolving anemia was noted with a high reticulocyte count. Second anemia nadir at fourth week of life was treated with epoetin alfa, with normalization of erythrocyte indices. From DOL 5 onward, patient had a prolonged need for respiratory support, attributed to chronic microaspirations, with a waxing-and-waning degree of respiratory distress, which was subsequently attributed to a hiatal hernia. Gastrointestinal contrast study showed approximately half the stomach within the thoracic cavity, along with an incidental finding of inguinal hernia.\nDuring the patient's hospital course, extensive workup was completed as part of evaluation for the chromosome 19p deletion (see Section ). Initial head ultrasound showed a small hyperechogenic focus inferior to the third ventricle. Noncontrast brain MRI performed on DOL 23 showed normal findings. Follow-up head ultrasound performed on DOL 50 showed resolution of the previously described echogenic focus, with a new finding of mild dilation of frontal horns of lateral ventricles. Spinal ultrasound was significant for a low lying conus and a tethered spinal cord. Whole spine MRI confirmed this finding, additionally showing 6 lumbar vertebrae. Abdominal and focused renal ultrasounds were normal. Echocardiogram was significant for suspected interrupted inferior vena cava with hemiazygos continuation to the left superior vena cava draining to the coronary sinus; no right superior vena cava was noted. Suspected cervical aortic arch was present with mild tortuosity of transverse arch without evidence of coarctation. Normal pulmonary venous drainage and a patent foramen ovale with left-to-right shunt were also seen. Ophthalmologic examination performed on DOL 13 showed a thin iris with rugged pupils. Mild stippling of the left retina with irregularly shaped optic disk was also noted.\nOn DOL 53, laparoscopy was performed to repair the hiatal hernia. Intraoperative diagnoses were: type I paraesophageal hernia with almost the entire stomach located within the chest, and a significant pyloric stenosis. The infant underwent paraesophageal hernia repair, Nissen fundoplication, G-tube placement, and pyloromyotomy. On postoperative day four, the patient developed a firm abdomen and respiratory compromise. Abdominal X-ray revealed intestinal pneumatosis and presence of portal vein gas. Emergent laparotomy found a 3 mm gastric perforation and necrotic small bowel. Unfortunately, the patient passed away intraoperatively. Cause of death was shock secondary to gastric perforation, peritonitis, and bowel necrosis.
|
[[30.0, 'year']]
|
F
|
{'18775991': 1, '26260137': 1, '17112790': 1, '19855400': 1, '24571724': 1, '6609675': 1, '19353584': 1, '19842200': 1, '15937949': 1, '19215039': 1, '12642666': 1, '17928360': 1, '26966713': 1, '19874387': 1, '29379197': 1, '16239148': 1, '20673863': 1, '16740480': 1, '24963350': 1, '20648052': 1, '17353270': 1, '30147897': 2}
|
{}
|
2,009 |
6099043-1
| 30,147,924 |
comm/PMC006xxxxxx/PMC6099043.xml
|
Florid dermatopathic lymphadenopathy—A morphological mimic of Langerhans cell histiocytosis
|
A 21-year-old male presented with fever, generalized pruritus and nonblanching petechial and papular skin rash. The rash had a centripetal distribution, initially appearing on the extremities and spreading to the trunk. Laboratory tests revealed normal white blood cell count with mild lymphopenia of 0.8 × 109/L, elevated C-reactive protein, positive antinuclear antibody and elevated liver function tests (serum alanine transaminase: 277 U/L, serum aspartate transaminase: 81 U/L, alkaline phosphatase: 170 U/L). He was suspected to have Rocky Mountain spotted fever (RMSF) and initiated therapy with doxycycline. However, viral and tick serologies (RMSF, Lyme, Ehrlichia) were negative. He continued to have persistent fever with a significant malaise, and developed bilateral uveitis and a palpable mass in the right chest wall. Imaging studies showed ground glass opacities of right middle and lower lobes of the lungs and moderately fluorodeoxyglucose (FDG)-avid mediastinal, hilar, and axillary lymph nodes. Eventually, an excisional biopsy of a right chest wall lymph node was performed and he was diagnosed with Langerhans cell histiocytosis (LCH). Flow cytometry showed phenotypically normal T-cell and B-cell populations. He was initiated on vinblastine and prednisone for treatment of LCH, and after 3 cycles, he had symptomatic improvement and a decrease in FDG-avid lesions on imaging studies. Next-generation sequencing on tissue biopsy did not reveal any mutations, including mitogen-activated kinases (MAPK) pathway alterations. The patient came to our institution for a second opinion. Histopathological review of his lymph node biopsy showed that the paracortex was expanded by a mixed population of Langerhans cells, pigment-laden histiocytes, and small lymphocytes (Figure , Panel A). Although the presence of numerous Langerhans cells was confirmed with immunohistochemistry for CD1a and Langerin, the morphology and pattern of distribution of these cells pointed away from LCH, since the latter is characterized by a sinus-based infiltrate of Langerhans cells (Figure , Panel B). Based on this, we arrived at a diagnosis of florid dermatopathic lymphadenopathy, a reactive pattern seen in lymph nodes of patients with rashes or other inflammatory skin conditions. The patient continued to improve clinically after discontinuing chemotherapy. This case emphasizes the importance of histopathological re-evaluation when the clinicopathological correlation is under ambiguity.
|
[[21.0, 'year']]
|
M
|
{'31004029': 1, '30147924': 2}
|
{}
|
2,010 |
6099054-1
| 30,147,884 |
comm/PMC006xxxxxx/PMC6099054.xml
|
Prenatal diagnosis of Pallister-Killian syndrome in one twin
|
A 34-year-old Chinese woman, gravida 1, para 0, was referred to our hospital for thickened nuchal translucency (3.4 mm) in one fetus of dichorionic diamniotic twins at 13 weeks of pregnancy. She underwent in vitro fertilization and embryo transfer (IVF-ET) because her husband was oligoasthenospermia. Two embryos were transferred to the uterus. Transvaginal ultrasound revealed an unremarkable dichorionic twin pregnancy in the first trimester. Noninvasive prenatal testing (NIPT) was performed at 15 weeks of gestation, showing a low-risk for fetal 21, 13 and 18 trisomy. After informed consent was obtained, she underwent amniocentesis for further molecular analysis at 17 weeks of gestation. The results of CMA showed a gain of the entire short arm of chromosome 12 in approximately 80% of cells in the fetus with thickened nuchal translucency, while normal in the other fetus (Figure E). SNP array analysis confirmed that the twins were dizygotic. Then, a second amniocentesis was offered to confirm the tetrasomy using FISH and G-banding karyotyping at 20 weeks of gestation. The karyotyping showed that the abnormal fetus was 47,XX,i(12p)[40]/46,XX[10] (Figure A). FISH analysis confirmed tetrasomy 12p in 80% (20/25) of cells (Figure B). Both the karyotype and FISH results of the other fetus showed a normal female (Figure C,D).\nThe decision to terminate the abnormal fetus was difficult for the parents due to the wide spectrum of PKS manifestations. At 20 weeks of gestation, more abnormalities, including severely shortened humerus and femur (<−6 SD) and mild lateral ventriculomegaly, were revealed by three-dimensional ultrasound. Meanwhile, head circumference, abdominal circumference, and biparietal diameter were in the normal ranges. In consideration of the ultrasonic and cytogenetic findings, the parents opted for selective termination. Transabdominal intrathoracic injection of potassium chloride (KCl) into the heart of the fetus with 12p tetrasomy was performed successfully at 23 weeks of gestation. Before the injection of KCl, heart blood was obtained and the karyotype analysis of heart blood in the abnormal fetus showed 47,XX,i(12p)[12]/46,XX[23]. Subsequently, ultrasounds were performed regularly, and the remaining fetus showed normal biometric parameters. A healthy female baby was born by normal vaginal delivery at term.
|
[[34.0, 'year']]
|
F
|
{'19353629': 1, '23169682': 1, '15861199': 1, '17880035': 1, '2002482': 1, '28233318': 1, '23169763': 1, '23169773': 1, '25425112': 1, '3180504': 1, '10951480': 1, '24826207': 1, '12116305': 1, '22315202': 1, '25329894': 1, '30147884': 2}
|
{}
|
2,011 |
6099055-1
| 30,147,915 |
comm/PMC006xxxxxx/PMC6099055.xml
|
A case of lateral medullary infarction with severe dysphagia and worsening of respiratory failure in the chronic phase of recovery
|
A 62-year-old man lost consciousness and was admitted to an emergency hospital. He was comatose (Hunt and Kosnik grade) and diagnosed with subarachnoid hemorrhage (SAH) due to rupture of a right vertebral artery dissecting aneurysm. Artery occlusion was performed, followed by ventricular drainage due to hydrocephalus. Nutrition was administered via a nasogastric tube. He gradually recovered consciousness but required ventilation for 1 month. After he was weaned from the ventilator, a speech cannula was installed at the tracheotomy site. The patient developed pneumonia and was treated with antibiotics. Two-and-a-half months after SAH onset, he was transferred to our hospital for rehabilitation.\nHe had a history of hypertension and hyperlipidemia; however, he did not have a history of respiratory diseases or sleep disturbance. He did not smoke. The Epworth sleepiness scale (ESS) score was 7 before SAH.\nOn physical examination, the patient was 180 centimeters tall and weighed 82.6 kg with blood pressure 126/81 mm Hg, pulse 76/min, and respiratory rate 19 breaths/min with an O2 saturation (Spo2) of 88% on room air and 97% on 1 L of oxygen per minute. Cardiovascular examination was normal, the lungs were clear on auscultation, and abdominal examination was unremarkable. On neurological examination, he was alert with a MMSE score of 28. Eye movements were normal. There was mild narrowing of right palpebral fissure and a constricted pupil with preserved light reflex of the right eye. There was mild arm and hand paresis and moderate leg paresis on the right side. Deep tendon reflexes were brisk on the right side. The Babinski reflex on the right side was extensor. The right arm was ataxic, but the presence of ataxia was unequivocal in the right leg due to moderate paresis. Superficial sensation on the left side, including the face, was decreased, and deep sensation was preserved. The patient could not sit up or maintain a sitting posture and had bladder and bowel dysfunction.\nInitial investigations revealed slight anemia (hemoglobin: 12.5 g/dL, mean cell volume: 94 μm3), hypoalbuminemia (3.5 g/dL), and low-density to high-density lipoprotein (HDL) cholesterol (26 mg/dL). Blood gas analysis revealed hypoxemia and hypercapnia (PaO2: 49.5 mm Hg, PaCO2: 73.4 mm Hg on room air and PaO2: 111.0 mm Hg, PaCO2: 77.7 mm Hg on 1 L of oxygen per minute). Other blood tests, including inflammatory markers (C reactive protein: 0.3 mg/dL), were normal. Respiratory function test results were vital capacity (VC) 3,022 mL, %VC 73%, forced expiratory volume in 1-second (FEV1.0) 2,540 mL, and FEV1.0% 78%.\nHead magnetic resonance imaging (T2-weighted MRI) revealed a focal high-intensity area in the dorsolateral medulla oblongata and the upper cervical cord on the right side (Figure ).\nThoracic computed tomography (CT) was normal.\nNeurological examination and MRI showed lateral medullary syndrome with ipsilateral palsy.\nThrough physical and occupational therapy, he gradually developed his physical strength. The right leg paresis recovered from a moderate to slight degree of impairment, and the presence of ataxia became apparent.\nWe evaluated his swallowing ability by videofluorography and videoendoscopy. Videofluorography showed that relaxation of the upper esophageal sphincter (UES), especially on the right (ipsilateral) side, was insufficient. Barium jellies hardly passed the UES with passage of small amounts along the left (contralateral) side, and after several swallowing actions, aspiration into the trachea occurred. Videoendoscopy showed insufficient movement of the right vocal cord. We conducted dysphagia rehabilitation. However, improvement was limited, and gastrostomy tube was installed. He received combined cricopharyngeal myotomy and laryngeal elevation 1 year and 7 months after SAH onset. After surgery, swallowing ability improved. Finally, he could take almost all nutrition orally in an upright sitting position.\nWe removed the speech cannula soon after admission. We observed his respiratory condition, and it was expected to improve. However, blood gas analysis did not ameliorate and PaCO2 began to worsen. Nine months after SAH onset, PaCO2 became 90.3 mm Hg without the presence of respiratory infection. Portable polysomnography (PSG) showed that consecutive apnea-hypopnea indices (AHIs) were 48.6 and 63.0/h. He was diagnosed with sleep apnea syndrome (SAS). Continuous positive airway pressure (CPAP) or bilevel positive airway pressure (bilevel PAP) was tried under various conditions, and an appropriate condition was eventually found. He received nasal bilevel PAP under the condition of spontaneous timed (ST) mode (IPAP of 8 cm H2O, EPAP of 4 cm H2O, and backup breathing frequency of 12/min) during the night. His nocturnal SpO2 dramatically improved under this condition. Blood gas analysis during the daytime also improved (PaO2: 92.9 mm Hg and PaCO2: 54.7 mm Hg on 1 L of oxygen per minute) (Figure ).\nHe was eventually discharged home 2 years and 2 months after SAH onset. Then, he needed no oxygen supply (PaO2: 75.4 mm Hg and PaCO2: 50.6 mm Hg on room air). His weight decreased to 74.9 kg at the time of discharge. However, it recovered to 80.3 kg 9 months after discharge. His neurologic manifestation remained unchanged.
|
[[62.0, 'year']]
|
M
|
{'8143712': 1, '9595998': 1, '1992369': 1, '24807272': 1, '23296134': 1, '1798888': 1, '11760386': 1, '16087770': 1, '17562836': 1, '12933911': 1, '24218531': 1, '12805095': 1, '21688613': 1, '30147915': 2}
|
{}
|
2,012 |
6099056-1
| 30,147,874 |
comm/PMC006xxxxxx/PMC6099056.xml
|
Prolonged third complete remission after busulfan, thiotepa, and autologous stem cell transplant in a primary central nervous system lymphoma patient
|
A 38-year-old male patient, with no relevant medical history, was admitted to the hematology department of the Henri Becquerel Center in Rouen in May 1999 for diplopia with clinical signs of intracranial hypertension. A cerebral CT scan shows left frontal, left parietal, right occipital, and right lateral lesions strongly enhanced after injection of contrast medium with perilesional edema and mass effect on the lateral ventricles. An encephalic MRI is performed which confirms the visible lesions on the initial CT scan. A stereotaxic biopsy is performed and histological samples indicate a large B-cell lymphoma with a centroblastic phenotype. The initial assessment therefore concludes with the diagnosis of multiple-site PNCSL of the brain.\nThe patient presented with a Karnofksy Performance status (KPS) of 70% (ECOG PS = 2), LDH were not elevated, cell blood count and standard chemical test revealed no abnormalities, CSF protein was mildly increased (0.47 g/L) with negative cytology and there were no deep brain lesions. CSF flow cytometry was not performed. The patient’s IELSG prognostic index was considered “intermediate” and the patient was treated with debulking chemotherapy (cyclophosphamide, vincristine, prednisone) followed by 2 cycles of COPADEM induction (Vincristine 1.4 mg/m² day (D) 1, methotrexate 3000 mg/m² D1, doxorubicin 60 mg/m² D2, cyclophosphamide 250 mg/m²/12 h D2 to D4, methylprednisolone 60 mg/m² D1 to D6 with intrathecal cytarabine injection on D3) followed by 2 cycles of CYM consolidation (methotrexate 3000 mg/m² D1, cytarabine 100 mg/m² D2 to D6, methylprednisolone 60 mg/m² D1 to D6, with intrathecal injection of cytarabine on D3) and whole-brain radiotherapy with 40 Grays in 16 fractions enabling a first complete remission (CR) lasting 2 years.\nFirst relapse occurred in February 2001 with appearance of gait disorder and micrographia; KPS was still at 70%; the cerebral CT was in favor of a recurrence, with multiple localizations, notably in the basal ganglia (data not shown). These lesions were too deep to biopsy; salvage chemotherapy was decided and the patient was treated with 3 cycles of DIAM, 21 days apart (cytarabine 1500 mg/m² × 2/d on D1-D2, ifosfamide 1500 mg/m² D1 to D5, dexamethasone 40 mg D1 to D4, methotrexate 3000 mg/m² on D3, with intrathecal injection of methotrexate 15 mg), then therapeutic intensification was conditioned by BEAM-ARAC high dose (VP 16: 200 mg/m² from D-7 to D-4, Cytarabine: 2000 mg/m² infused over 1 hour, ie 3900 mg from D-7 to D-4, melphalan: 140 mg/m² or 270 mg at D-3, dexametasone: 20 mg/day from D-7 to D-4) and autologous stem cell transplant (ASCT). Peripheral blood progenitor cells were obtained after 2 cycles of DIAM with 14 × 106/kg CD34(+) cells in the graft with one apheresis collection. No complications occurred during the ASCT and a second CR was obtained.\nSecond relapse was diagnosed in October 2007 with the appearance of a decrease in left visual acuity with uveitis and left-sided hemiparesis, with KPS at 80%. A brain MRI was performed showing a gadolinium-enhanced tissue lesion, measured at 23 × 19 × 15 mm, of the right front-parietal supracentricular white matter with significant perilesional edema, and discreet mass effect on the roof of the right lateral ventricle (Figure ). The patient initially benefited from a left vitrectomy, which identified a very high concentration of interleukin-10 (500 IU/L vs normal <10 IU/L). A cerebral stereotactic biopsy of a right prerolandic lesion was performed, confirming the presence of PCNSL. There was no extra-cerebral involvement. The patient benefited from 4 courses of R-DIAM (rituximab 375 mg/m² IV at D1 combined with the DIAM chemotherapy previously described), was mobilized by the use of Granulocyte colony-stimulating factor (GCSF, lenograstim) 34 MUI/d, starting at D12 after the 2nd cycle of R-DIAM, with apheresis performed at D17 (quantification of hematopoietic progenitors in blood at D17: CD34(+) = 145/μL,) with 9.5 × 106/kg CD34(+) cells in the graft with one apheresis collection. The patient received then a second therapeutic intensification conditioned by thiotepa, busulfan, and cyclophosphamide (thiotepa 250 mg/² on D-9, D-8, and D-7, intravenous busulfan 0.8 mg/kg × 4/on day D-6, D-5, and D-4, cyclophosphamide 60 mg/kg on D-3 and D-2) and ASCT. The second ASCT was marked by Grade IV mucositis and Enterobacter asburiae and Pseudomonas aeruginosa septicemia, which improved over the course of antibiotic therapy. Absolute neutrophil count (ANC) recovery above 0.5 × 109/L and white blood cell (WBC) recovery above 4 × 109/L for 3 consecutive days was achieved at D14 with filgrastim administration from D5 to D14. Platelet count exceeding 20 G/L without transfusion support was obtained at D50.\nA third CR was achieved (Figure ), and is clinically persisting 9 years after the end of treatment. After this third line treatment, no cognitive disorder was observed, and the patient’s medical follow-up was marked by:\nEar, nose, and throat infectious complications with mastoiditis, right rock lysis, and chronic otitis. Immunological deficiency with compensated hypogammaglobulinemia. Renal failure related to chronic tubulointerstitial nephropathy post-antibiotherapy, relatively stable since 2010.
|
[[38.0, 'year']]
|
M
|
{'1476655': 1, '22581000': 1, '12697892': 1, '8055462': 1, '25204639': 1, '26951382': 1, '28559537': 1, '27132696': 1, '11157026': 1, '30147874': 2}
|
{}
|
2,013 |
6099059-1
| 30,147,920 |
comm/PMC006xxxxxx/PMC6099059.xml
|
Foreign body-associated endobronchial inflammatory polyps
|
A 59-year-old woman was referred to our hospital because an abnormal shadow was found in the right middle lung field in a chest X-ray taken during a routine medical checkup. Her medical history was unremarkable, including no history of cerebrovascular disease or neuromuscular disease. Chest CT showed atelectasis of the middle lobe of the right lung (Figure A). Bronchoscopy revealed that the right middle lobe bronchus was occluded by a foreign body (Figure A). The foreign body was removed bronchoscopically, but the bronchial mucosa could not be examined adequately during the initial procedure due to substantial bleeding (Figure B). The foreign body turned out to be of plant origin and was considered to be a piece of vegetable although the patient did not remember having experienced an episode of aspiration. Seven days later, chest CT showed that the atelectasis had resolved (Figure B). On the same day, bronchoscopy revealed several polypoid lesions in the middle lobe bronchus (Figure C,D). The histopathological examination of the biopsy specimens revealed hyperplasia of the bronchial glands and nonspecific granulomatous inflammation, findings which were compatible with the diagnosis of inflammatory polyps (Figure A,B). Eight weeks later, the polypoid lesions were observed to have regressed spontaneously (Figure E,F).\nEndobronchial polypoid lesions can be observed after removal of a foreign body and usually regress without treatment. Some previous reports suggested that corticosteroid therapy may facilitate regression of endobronchial inflammatory polyps., ,
|
[[59.0, 'year']]
|
F
|
{'8347043': 1, '6845268': 1, '6468011': 1, '436503': 1, '30147920': 2}
|
{}
|
2,014 |
6099467-1
| 29,214,746 |
comm/PMC006xxxxxx/PMC6099467.xml
|
Case of idiopathic and complete appendiceal intussusception
|
The patient was a 20-year-old woman. She visited the hospital with a primary complaint of lower abdominal pain with repeated remission and exacerbation that had lasted for 3 months.\nThere was no abnormality in vital signs at the time of her initial visit. There was tenderness in the lower abdomen, and a neoplastic mass with mobility was palpable. Blood biochemistry confirmed that white blood count was 8700/μL and C-reactive protein was 0.3 mg/dL, indicating mild inflammation. Abdominal CT confirmed invagination of the intestinal tract inside of the transverse colon, which led to a diagnosis of intestinal intussusception (Figure ).\nThe patient was hospitalized for emergency treatment, and a colonoscopic disinvagination was attempted without preparation. Invagination of a neoplastic lesion into the cecum was confirmed (Figure ). A histopathological examination confirmed only inflammatory cells, but there was no clear finding of a neoplasm. However, the possibility of a malignant tumor could not be ignored as a cause of invagination. The patient was diagnosed with appendiceal neoplasm, and surgery was performed.\nWith the patient under general anesthesia, a 25-mm midline incision was made in umbilical region. With a Lap-Protector® (Hakko Medical, Tokyo, Japan) and EZ Access® (Hakko Medical), three 5-mm ports were inserted in the same area to perform SILS. Intraperitoneal observation showed that the appendix had invaginated into the cecum, leading to a diagnosis of appendiceal intussusception (Figure ). The tumor was probably resectable in the peritoneal cavity, but there was a risk of damaging the tumor. Therefore, the ileocecal region was extracted through the umbilical wound. With a small incision in the cecum, the intussuscepted appendix was retracted (Figure ), and the cecum was partially resected with an automatic suturing device to keep the safe margin.\nThere were no malignant findings in the frozen section. Additional resection was deemed unnecessary, and the surgery was completed. In histopathological findings, the appendix was completely invaginated into the cecum. Because only inflammatory changes were confirmed in the appendiceal mucous membrane, there was no clear neoplastic component. The findings led to a diagnosis of idiopathic type V appendiceal intussusception.\nThe postoperative course was good, and the patient was discharged on the fifth day postoperatively.
|
[[20.0, 'year']]
|
F
|
{'14098730': 1, '19249733': 1, '33285741': 2, '20871809': 2, '18435897': 1, '17090846': 1, '29214746': 2}
|
{'7717731-1': 1, '2943109-1': 1}
|
2,015 |
6100429-1
| 30,151,468 |
comm/PMC006xxxxxx/PMC6100429.xml
|
Paget’s Disease Mimicking Bone Metastasis in a Patient with Neuroendocrine Tumor on 68Ga-DOTANOC PET/CT
|
A 65-year old male patient who was diagnosed with gastrointestinal stromal tumor at bulbus of duodenum by gastric endoscopy was referred for a 68Ga-DOTANOC PET/CT for investigation of metastasis. PET/CT demonstrated increased tracer uptake in the right ischium, right iliac, and pubic bones (Figure ). He was asymptomatic without any complaint. Subsequent conventional radiography and CT images confirmed the presence of Paget disease in the right hemi-pelvis (Figure ).
|
[[65.0, 'year']]
|
M
|
{'17225119': 1, '20896492': 1, '34002161': 1, '33489200': 2, '23877528': 1, '23543506': 1, '12707737': 1, '9293817': 1, '17229011': 1, '21524738': 1, '10551483': 1, '15277976': 1, '11762353': 1, '30151468': 2}
|
{'7813063-1': 1}
|
2,016 |
6100433-1
| 30,151,498 |
comm/PMC006xxxxxx/PMC6100433.xml
|
Unusual CT Appearance of Bony Metastases from Malignant Peripheral Nerve Sheath Tumor
|
An 83-year-old man underwent surgical excision of a malignant peripheral nerve sheath tumor (MPNST) at the right knee at another hospital and was then referred to our hospital for further chemotherapy. Three months after the start of chemotherapy, the patient complained of severe pelvic and low back pain. A PET CT was performed which showed multiple bony lesions with a variable (moderate to high) degree of metabolic activity raising suspicion that these were metastases. The lesions, however, had a very unusual appearance and evolution as seen on CT.\nInitially, the lesions presented as small rounded lytic lesions with a well-defined sclerotic margin (Figure ). They exhibited a rapid growth but the initial appearance of central lysis and surrounding sclerotic margin was preserved. Follow up PET CT scan was performed after seven weeks to evaluate the response to chemotherapy. It revealed a second concentric band (halo) around some of the lesions. This band (halo) had a ground-glass appearance and was surrounded by a second sclerotic rim. This rim was thinner and less sharply demarcated than the more central rim (Figure ). The multiple lesions were in different phases of evolution and as such had a different appearance at any given time.\nPresence of multiple lesions, a known primary tumor and moderate to high uptake of FDG tracer on PET scan (Figure ) suggested metastatic disease, despite the unusual appearance of the lesions.\nOther bony metastases were also evident on CT. Some were entirely sclerotic and a few had an ill-defined lytic appearance. Collapse of a vertebral body and fracture of the upper endplate of another vertebra due to metastases were also present.\nBone biopsy of a lesion with the above described doughnut appearance located in the left pubic bone was performed. A biopsy was obtained in the central lytic area and another biopsy in the peripheral halo (Figure ). Histological evaluation of both the samples showed infiltration of bone marrow by malignant spindle-shaped cells arranged neatly in bundles. Histological and immunohistochemical studies were compatible with metastases from a spindle cell tumor (in this case MPNST).
|
[[83.0, 'year']]
|
M
|
{'18635627': 1, '9362421': 1, '6697319': 1, '22773934': 1, '30151498': 2}
|
{}
|
2,017 |
6100443-1
| 30,151,441 |
comm/PMC006xxxxxx/PMC6100443.xml
|
Ultrasound Findings in a Case of Myeloid Sarcoma of the Breast
|
A 21-year-old female patient was admitted with bilateral painless palpable breast masses for four months, which had increased in size over that period. The patient had given birth approximately one year before, but her medical and family histories were otherwise unremarkable.\nOn physical examination, there were multiple palpable mass lesions in the lower quadrant in both breasts, with the largest being 4.5 cm in diameter in the right breast. There were no palpable axillary mass and no breast discharge or retraction of the areola. The ultrasonographic examination (Hitachi-Preius, 13–8 MHz) revealed multiple lobulated, hypoechoic, solid masses with circumscribed contours (Figure ). The largest mass measured 4.5 × 2.7 cm (Figure ). Power Doppler examination demonstrated increased vascularity in the masses (Figure and ).\nSince the patient was 21-years-old and without family risk, no further diagnostic modalities, such as mammography or MRI, was recommended.\nThese findings were evaluated as BI-RADS 4, and biopsy was recommended. Core biopsy was non-diagnostic. After excisional biopsy, microscopic examination revealed infiltrating uniform, monotonous tumor cells with scanty cytoplasm between the breast lobules, showing lactational changes. These morphologic features suggested a hematolymphoid neoplasm. A broad immunohistochemical study was performed for confirmation and subtyping, and the results were as follows: The tumor cells showed strong positivity for CD34, CD43, CD99, Tdt, and bcl-2 protein (Figure and ). CD79a and CD117 were weak-to-moderate positive in most cells, whereas some cells were strongly positive. There was focal positivity with myeloperoxidase. With CD68, there was strong positivity in some cells and faint positivity in others.\nPeripheral smear and bone marrow examination were performed after the diagnosis of myeloid sarcoma, but revealed normal findings.\nIn the laboratory examination, the only pathological finding was a mild elevation in CA19-9 levels. In the whole body radiological examination, there were no other organ pathologies. The patient was diagnosed with myeloid sarcoma and chemotherapy was started. High dose cytarabine and idarubicine regime was used. This resulted in nearly total disappearance of the masses in both breasts. During two years follow-up the patient was disease free.
|
[[21.0, 'year']]
|
F
|
{'7023656': 1, '25890617': 1, '15628906': 1, '14717760': 1, '11920536': 1, '25213180': 1, '11099329': 1, '11135470': 1, '17958995': 1, '23593091': 2, '21941971': 1, '31030205': 1, '34263159': 1, '30151441': 2}
|
{'3625757-1': 1, '3625757-2': 1}
|
2,018 |
6100465-1
| 30,151,444 |
comm/PMC006xxxxxx/PMC6100465.xml
|
Quadriscupid Aortic Valve with Concurrent Aortic Stenosis and Insufficiency
|
A 22-year-old asymptomatic man presents at the cardiology department for follow-up of a congenital mixed aortic valve disease that presented first in childhood. Cardiac auscultation reveals a systolic decrescendo high-frequent ejection 2/6 murmur and diastolic 2/6 murmur. Transthoracic echocardiography shows a normotrophic mildly dilated left ventricle (end-diastolic diameter 63 mm) and a grade three aortic regurgitation combined with moderate aortic stenosis. The ascending aorta is also moderately dilated (48 mm). The left ventricular and ascending aorta dilatation appears to have advanced compared to previous sonographic measurements, indicating progressive regurgitation. Surgical intervention is advised and a preoperative cardiac MRI is planned.\nOn cine MRI images in the aortic valve plane, a four-leaf-clover aortic valve with one large cusp, two medium-sized cusps, and one smaller cusp is seen (Figure ). Flow velocity encoded images and cine MRI show a marked holodiastolic regurgitating jet and early diastolic regurgitation in the ascending aorta. A regurgitation fraction of 49%, a regurgitating volume of 81 ml and a regurgitant orifice area of 0.5 cm2 are measured, indicating a severe aortic regurgitation (Figure ). The high peak systolic velocity across the aortic valve, measured by flow velocity encoded imaging (328 cm/s) and a narrowed aortic valve orifice during systole, demonstrated by cine MRI confirm the aortic stenosis (Figure ). The patient underwent a Bentall procedure. The aortic valve, aortic root and ascending aorta were replaced by a composite graft with re-implantation of the coronaries. Follow-up consultations up to one year after surgery show normal valve function and cardiac testing.
|
[[22.0, 'year']]
|
M
|
{'15311857': 1, '6702660': 1, '12492123': 1, '22592485': 1, '30151444': 2}
|
{}
|
2,019 |
6100481-1
| 30,151,458 |
comm/PMC006xxxxxx/PMC6100481.xml
|
Vascular Leiomyoma Presenting as Anterior Knee Pain (Case Report)
|
A 38-year-old woman presented with painful, mobile swelling in the right knee. There was no trauma history, and the onset of pain was sporadic and had reduced her mobility. On physical examination, there was a mobile painful swelling on the lateral aspect of her right knee. The laboratory findings were normal. Plain orthogonal radiographs including lateral and skyline views of the knee demostrated no bone abnormalities (Figure ). But there was a soft tissue swelling on the lateral aspect of the patella (Figure ). MRI examination with and without contrast was performed. An MRI of the right knee revealed a subcutenous, ovoid, well-circumscribed, homogenous, capsulated soft tissue mass adjacent to the lateral patellar retinaculum (Figure ). The tumor was hyperintense on proton density (PD) images and hypointense on T1-weighted images according to muscles. On post-contrast T1-weighted (Figure ) and PD-weighted (C) images there was a sharp thin hypointense rim surrounding the lesion. The tumor showed marked homogeneous gadolinium enhancement after contrast administration (Figure ). There was no joint effusion or soft tissue edema. The muscles and bones were normal.\nThe patient underwent surgery and complete excision of the tumor was performed. Gross examination revealed a 10×10 mm firm, well-circumscribed, bean-shaped mass with a white-beige cut surface. Histological sections demonstrated a solid tumor composed of intersecting fascicles of mature smooth muscle cells surrounding vascular structures (Figure ). The smooth muscle cells showed no cellular atypia, and mitotic figures were rare. Immunohistochemical analysis showed diffuse positivity for smooth muscle actin (SMA) (Figure ). After the operation, her symptoms disappeared.
|
[[38.0, 'year']]
|
F
|
{'10901934': 1, '9762979': 1, '6722737': 1, '13818517': 1, '23396993': 1, '30151458': 2}
|
{}
|
2,020 |
6100495-1
| 30,151,480 |
comm/PMC006xxxxxx/PMC6100495.xml
|
Primary Angiosarcoma of the Central Nervous System: Case Report and Review of the Imaging Features
|
A 61-year-old Caucasian male with no significant medical history was admitted to the emergency department in 2006 with subacute, aggravating headaches. He had been vomiting for two days. Further clinical investigation and anamnesis revealed a mild fever of 38.0°C as well as alternating but progressive confusion and anomic aphasia for several months.\nAn unenhanced CT yielded a 5.8 cm large and well-defined spontaneously hyperattenuating lesion in the left frontotemporal lobes, abutting the tentorium cerebelli, with a small component of the tumor expanding into the left cerebellopontine angle of the posterior fossa (Figure ). Within this lesion, cystic components were apparent. The posterior part of the tumor was more heterogeneous with both hypoattenuating and hyperattenuating areas. There was mild to moderate vasogenic edema surrounding the lesion with significant mass effect, contralateral displacement of the midline, obliteration of the sulci, and compression of the left lateral ventricle with secondary dilatation of the temporal horn.\nMRI showed that the lesion was mainly isointense with grey matter on both T1- and T2-weighted images. Multiple small T2-hyperintense and T1-hypointense cystic components could be seen within the lesion (Figure ). No hyperintense spots could be depicted on the unenhanced T1-weighted images. Enhancement was diffuse and mildly heterogeneous, with accentuated rim enhancement both at the periphery of the lesion and surrounding the cystic areas. The posterior part of the lesion appeared strongly hypointense on the T2-weighted images and slightly hypointense on the T1-weighted images, without enhancement after intravenous administration of gadolinium. These findings most probably reflected the presence of acute bleeding. Thickening and abnormal enhancement of the tentorium cerebelli could be seen on the left side.\nThe treatment for this patient consisted of surgical excision with postoperative radiotherapy. The patient was still free of macroscopic recurrence on follow-up MRI 105 months after the initial diagnosis.
|
[[61.0, 'year']]
|
M
|
{'1501943': 1, '24171128': 2, '22909122': 2, '16972889': 1, '2014445': 1, '10765122': 1, '1715839': 1, '25388456': 1, '19574803': 1, '568026': 1, '10701536': 1, '8837814': 1, '2045922': 1, '23717792': 1, '11071573': 1, '17495298': 1, '18039756': 1, '7566378': 1, '1039997': 1, '16023347': 1, '18314334': 1, '2421549': 1, '3357039': 1, '30151480': 2}
|
{'3792530-1': 1, '3459733-1': 1, '3459733-2': 1}
|
2,021 |
6100498-1
| 30,151,435 |
comm/PMC006xxxxxx/PMC6100498.xml
|
Large-Sized Bilateral Atherosclerotic Axillary Artery Aneurysms: A Case Report
|
The 72 year old male patient was referred to our clinic with the complaint of bilateral axillary masses and numbness in the right hand. In his medical history, he had hypertension for 4 years but no history of trauma. A physical examination showed the presence of palpable pulsatile masses in his both axillae (12 cm in size in the right axilla and 8 cm in size in the left axilla) (Fig. ). His neurological and systemic examinations were within normal limits. An upper-extremity ultrasound examination revealed an aneurysm in a 12-cm segment of the right axillary artery, reaching 67 × 45 mm in dimension. There was a 27-mm thick thrombus at the edge of the aneurysm lumen. Adjacent to the aneurysm, there was a 48 × 40 mm hyperechogenic mass not related to the aneurysm. There was also an aneurysm reaching 40 × 43 mm in dimension in a 9-cm segment of the left axillary artery, with a 17-mm thick thrombus. A Doppler ultrasonic examination revealed a thrombus surrounding the lumen and a turbulent, pulsatile flow in the center. The aneurysmal segment was continuous with the brachial artery. There was no blood flow in the region adjacent to the right axillary artery (Figs. and ). On CT angiography, giant fusiform aneurysms were detected, measuring 140 × 77 mm in the right axillary artery and 93 × 45 mm in the left axillary artery. There were thrombi in both aneurysms, allowing the flow in the lumen. There was also an extension to the brachial artery and contour irregularities at the distal end of the right-side aneurysm. These latter findings were proposed to be due to a spontaneously healed rupture. A physical examination of the eyes, bones, skin and joints revealed no signs of collagen tissue disease, nor was it detected through laboratory examinations. Because the patient was symptomatic and had a high risk of aneurysm rupture, endovascular closure was initially planned. However, appropriate size stents could not be found for aneurysms so large and tortuous. Besides, the long-term success of the stenting procedure could not be guaranteed due to the large sizes and high mobility of the aneurysms, so the patient was referred for surgery.
|
[[72.0, 'year']]
|
M
|
{'23714201': 2, '9753997': 1, '22328621': 1, '9786267': 1, '24732088': 1, '20719737': 1, '21050698': 1, '17218655': 1, '1533393': 1, '25246010': 1, '15707819': 1, '30151435': 2}
|
{'3673813-1': 1}
|
2,022 |
6100555-1
| 30,151,437 |
comm/PMC006xxxxxx/PMC6100555.xml
|
Temporal Lobe Parenchyma Herniation into the Transverse Sinus: MRI Findings in a Case
|
A-50-year-old female presented with history of headache for a long time. Her neurological examination was normal. The laboratory results were within normal limits. Brain MRI demostrated a small herniation of a temporal lobe with surrounding CSF rim into the left transverse sinus (Figures , arrows). The herniation material was isointense to brain parenchyma on all sequences in the contiguous brain tissue images. T2-weighted axial image showed loss of signal void in the left transverse sinus (Figure ). After contrast media administration, no pathological parenchymal or meningeal opacification was seen, the herniation tissue was seen to bulge into left transverse sinus and it was caused the narrowing of the sinus (Figure ). On MR venography imaging, there was left transverse sinus stenosis but no venous thrombosis (Figure ).
|
[[50.0, 'year']]
|
F
|
{'23810237': 1, '24311424': 1, '20920939': 1, '9672025': 1, '24571834': 1, '19035698': 1, '8433155': 1, '12427634': 1, '30151437': 2}
|
{}
|
2,023 |
6100576-1
| 30,151,476 |
comm/PMC006xxxxxx/PMC6100576.xml
|
Forgotten Ureteral Double-J Stent Complicated by Severe Encrustation in the Bladder
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A 58-year-old man was referred to our medical imaging department with complaints of urinary frequency and dysuria associated with suprapubic and hypogastric pain. There was a clinical suspicion of colonic diverticulitis. An unenhanced abdominal CT was performed because the patient’s renal function was unknown. Numerous centimetric stones were found in the bladder, and various volume-rendering reconstructions (Figures and ) confirmed that these stones had developed like beads on a necklace along the distal intravesical pigtail loop of a double-J ureteral stent. Fortunately, the rest of the stent appeared free from encrustation. Anamnesis of the patient revealed a previous history of a ureteral stone treated with a double-J stent three years earlier in another institution. The diagnosis of encrustation of a forgotten stent was confirmed when the patient underwent a successful cystolithotripsy (Figure ).
|
[[58.0, 'year']]
|
M
|
{'33244059': 1, '12235330': 1, '30151476': 2}
|
{}
|
2,024 |
6100592-1
| 30,151,453 |
comm/PMC006xxxxxx/PMC6100592.xml
|
Atypical Feeding and Drainage of Dural AV Fistula
|
A 39-year-old man presented a one-year history of pulsatile tinnitus in the right ear without a previous history of trauma, surgery, or any other disease. His ear, nose, and throat (ENT) examination and laboratory tests were normal. The patient was referred to our department for carotid Doppler sonography to exclude vascular causes of pulsatile tinnitus. B-mode CDS revealed normal carotid intima-media thickness and no plaque formation. Doppler mode demonstrated increased peak systolic and end diastolic velocities and a decreased resistive index (RI) of the right common carotid artery (75 cm/sec, 33 cm/sec, and 0.49, respectively) compared to the left common carotid artery (63 cm/sec, 20 cm/sec, and 0.65, respectively). The blood flow volume (1370 ml/min) of the right common carotid artery (CCA) was substantially higher than that of the left CCA (500 ml/min). Likewise, the blood flow volume (760 ml/min) of the right external carotid artery (ECA) was higher than that of the left ECA (390 ml/min), and the resistive index of the right ECA (0.53) was lower than that of the left ECA (0.70) (Figure ).\nIn addition to these findings, a subcutaneous vascular structure that showed high flow rate (128 cm/sec) and low resistance (RI = 0.48) was demonstrated in the right suboccipital-mastoid region (Figure ). Considering all these vascular abnormalities, a CT angiography (CTA) was planned. CTA revealed a Cognard type I DAVF in the right mastoid region; its feeding artery was the occipital branch of the right ECA, and its venous drainage was to the ipsilateral transverse-sigmoid sinus. Interestingly, we noted an additional extracranial venous drainage path to the right brachiocephalic vein passing between the trapezius and levator scapulae muscles (Figure ). Digital subtraction angiography (DSA) confirmed the diagnosis and the findings (Figure ). The fistula was successfully treated by coil and cyano-acrylat embolization via a combined transarterial-transvenous approach.
|
[[39.0, 'year']]
|
M
|
{'22976238': 1, '15802633': 1, '16444095': 1, '7815143': 1, '7862961': 1, '888091': 1, '15244302': 1, '30151453': 2}
|
{}
|
2,025 |
6100612-1
| 30,151,479 |
comm/PMC006xxxxxx/PMC6100612.xml
|
Imaging in Myotonic Dystrophy Type 1 – Case Reports
|
Patient A, a 43-year-old woman, presented to the neurologist with increased difficulty swallowing and speaking, stiffness in the jaw muscles, and weight loss. Previous history reveals partial thyroidectomy (unknown cause), hypothyroidism, and an episode of atrial fibrillation due to overcompensated hypothyroidism. On clinical examination, there was a myotonic handshake, myopathic facial expression, and a positive Gower’s sign (weakness of the proximal muscles). Electromyography showed frequent myotonic discharges. Electrocardiography was normal. A barium study of the hypopharynx showed decreased motility of the hypopharynx and a deficient closing of the upper gastrointestinal sphincter.\nAn MRI of the brain showed multifocal T2 and FLAIR hyperintensities, with beginning confluence (Fazekas grade 1–2) located in the periventricular white matter and in the subcortical white matter of the frontal, parietal, and temporal lobes (anteromedial). There were also hyperintense lesions in the white matter posterior and superior to the trigone (Figures and ). Enlarged Virchow-Robin spaces were found in the centrum semiovale and less pronounced in the basal ganglia (Figure ). Brainstem, cerebellar hemispheres, and gray matter were unremarkable. Diffusion-weighted and contrast-enhanced imaging were normal.
|
[[43.0, 'year']]
|
F
|
{'11598331': 1, '22815033': 1, '12031621': 1, '12242535': 1, '23803495': 2, '22131273': 1, '30151479': 2}
|
{'3701470-1': 1}
|
2,026 |
6100616-1
| 30,151,447 |
comm/PMC006xxxxxx/PMC6100616.xml
|
Friday: Fish Day
|
A 78-year-old man presented with diffuse abdominal pain and nausea without vomiting for two days. Patient had his last bowel movement three days before. Physical examination confirmed diffuse abdominal pain and showed rebound tenderness in the periumbilical region suggestive of localized peritonitis. Laboratory analysis showed an elevated C-reactive protein (CRP) level of 261 mg/L (normal value < 5 mg/L) and elevated leucocyte count of 15,400/µL (normal values 3,400–9,800/µL). Plain film of the abdomen (not shown) demonstrated dilatation of a few small bowel loops in the lower abdomen with air fluid levels and absence of pneumoperitoneum. Computed tomography (CT) of the abdomen, after intravenous administration of iodinated contrast material, showed an inflammatory mass in the mesentery of the small bowel with a central air fluid level. A linear high-density structure was noted within the inflammatory mass and was in continuity with the adjacent small bowel lumen (Figure and , arrow). Sagittal (Figure , arrow) reformatted images confirmed a foreign body, suggestive of a fish bone, perforating the small bowel wall and with abscess formation. Patient admitted to ingestion of a fish bone eight days earlier. Subsequently, laparoscopy was performed. Patient was successfully treated with abscess drainage, fish bone removal, segmental resection of the inflamed bowel segment with an ileo-ileal anastomosis.
|
[[78.0, 'year']]
|
M
|
{'16928935': 1, '30151447': 2}
|
{}
|
2,027 |
6100622-1
| 30,151,446 |
comm/PMC006xxxxxx/PMC6100622.xml
|
Intragastric Rupture of a Splenic Artery Aneurysm Associated with a Pancreatic Cancer
|
A 61-year-old male was admitted to our hospital for unconsciousness followed by melena. On admission, he remained hemodynamically stable with a hemoglobin level at 12 g/dl (normal values: 14–18 g/dl). The patient underwent an upper endoscopy which revealed a stomach full of fresh blood. Neither esophageal varices nor ulcer were found. The patient rapidly progressed to hemodynamic instability, requiring intubation and polytransfusion. He was then taken to the angiography suite. The global aortic angiogram demonstrated the existence of a saccular aneurysm of 2.5 cm in diameter on the distal third of a splenic artery which also showed irregular contours (Figure ). This irregularity was not associated with the usual findings of spasticity (Figure ). However, it prevented the distal selective catheterization of the artery, using a 3F microcatheter. Given the impossibility of a “sandwich” coiling, we opted for a postostial embolization with microcoils, enabling hemodynamic stabilization (Figure ).\nIn the wake, a CT scan was performed. A distal pancreatic tumor abutting the posterior gastric wall was demonstrated. We speculate it could be responsible for the splenic artery erosion, with the development and secondary rupture of a false aneurysm in the gastric cavity (Figure ). The intravenous injection of contrast material did not reveal persisting blood extravasation. A new gastroscopy was performed the next day. As the stomach was no longer filled with blood, a posterior subcardial perforation was discovered, and biopsies were performed on its margins. Histological examination revealed invasive pancreatic ductal adenocarcinoma.\nSix days later, the patient presented a slow decrease of his blood hemoglobin (7.4 g/dl). A new contrast-enhanced CT scan revealed a new retrogastric blood extravasation originating from the distal third of the splenic artery (Figure ). A superselective catheterization of the gastroepiploic arteries by a 3F microcatheter allowed coil embolization of the distal splenic artery (“sandwich” method in two stages, see infra), hence stopping the bleeding (Figure ). After three months of chemotherapy, there was a reduction of the size of the pancreatic adenocarcinoma but also occurrence of liver and bone metastases. The patient died eight months later.
|
[[61.0, 'year']]
|
M
|
{'12731169': 1, '22293886': 1, '23024869': 2, '21628100': 1, '20166498': 1, '22840901': 1, '32587452': 2, '24353598': 2, '30151446': 2}
|
{'7304111-1': 1, '3457606-1': 1, '3809230-1': 1}
|
2,028 |
6100634-1
| 30,151,456 |
comm/PMC006xxxxxx/PMC6100634.xml
|
Congenital Agenesis of Right Internal Carotid Artery: A Report of Two Cases
|
A 19-year-old female patient with a few days history of severe headache, dizziness, nausea, vomiting and syncope was admitted for cranial CT examination. Her physical and neurological examinations were normal and her medical history was unremarkable. The color Doppler sonography revealed absence of the right ICA and a changing flow pattern of common carotid artery, from a low peripheral resistance pattern proximally into a high peripheral resistance pattern similar to that seen in the external carotid artery distally (Figure ). The brain CT showed absent right ICA and bony carotid canal without any intraparanchymal pathology (Figure ). MRI and MR angiography findings showed right ICA agenesis and as well as anomalous origin of the ophthalmic artery derived from right middle cerebral artery (MCA). The aortic arch and major aortic branches were normal (Figure ).
|
[[19.0, 'year']]
|
F
|
{'30559562': 1, '12063218': 1, '9929551': 1, '13234998': 1, '16440235': 1, '32952758': 1, '19190881': 1, '16286414': 1, '15671382': 1, '30151456': 2}
|
{'6100634-2': 2}
|
2,029 |
6100634-2
| 30,151,456 |
comm/PMC006xxxxxx/PMC6100634.xml
|
Congenital Agenesis of Right Internal Carotid Artery: A Report of Two Cases
|
A 27-year-old male patient with an unremarkable medical history presented with acute onset of severe headache, dizziness and disequilibrium, and left sided weakness. Unenhanced CT revealed a hypodense lesion in the right thalamic and subthalamic region about 1 cm in diameter and an absent right ICA and bony carotid canal (Figure ). On MRI, a well defined T2-hyperintense, T1-hypointense, contrast-enhancing lesion was seen in the right thalamus and subthalamic region consistent with sub-acute infarction (Figure ). Cranial and cervical MR angiography showed right ICA agenesis and anomalous origin of the ophthalmic artery derived from right MCA. The aortic arch and major aortic branches were normal.
|
[[27.0, 'year']]
|
M
|
{'30559562': 1, '12063218': 1, '9929551': 1, '13234998': 1, '16440235': 1, '32952758': 1, '19190881': 1, '16286414': 1, '15671382': 1, '30151456': 2}
|
{'6100634-1': 2}
|
2,030 |
6100642-1
| 30,151,454 |
comm/PMC006xxxxxx/PMC6100642.xml
|
Caesarean Scar Choriocarcinoma: Ultrasound and Magnetic Resonance Imaging Findings
|
A 33-year-old female, gravida 2 para 1, was referred to our university hospital from a local medical clinic with a history of a positive serum beta-Human chorionic gonadotropin (β-hCG) level but no visible intrauterine gestational sac. Her laboratory findings were all normal except for the serum β-hCG, which was 146.762 mIU/mL. A gynecological examination revealed a closed cervical os and mild adnexal tenderness. The patient had regular 28-day menstrual cycles. Her first pregnancy had ended with a full-term delivery by caesarean section approximately nine years earlier. There was no history of cancer in her family.\nA grayscale transabdominal ultrasound showed an empty uterine cavity, but a round hyperechoic lesion was identified in the anterior inferior wall of the uterus, measuring 23x32 mm in diameter (Figure ). There was no visible embryo or yolk sac within the lesion. The patient underwent careful dilatation and curettage (D&C) procedure, and the histopathological results were consistent with an ectopic molar pregnancy. The post-D&C period was uneventful, without excessive bleeding. The patient scheduled for methotrexate therapy, and the patient’s serum β-hCG level showed significant decrease.\nThe β-hCG level that became available to us on the twenty-third day of the treatment was still as high as 15.947 mIU/mL, and it then rose again. Therefore, the patient underwent an magnetic resonance imaging (MRI) examination, which demonstrated a peripherally hyperintense and centrally hypointense lesion on coronal and sagittal T2-weighted images of the uterine CSS. After gadolinium administration, the lesion demonstrated peripheral contrast enhancement on T1-weighted fat-suppressed axial images (Figure ). The differential diagnosis included a malignant GTD, and surgery was planned. Selective uterine artery embolization was performed immediately before the surgery to reduce the risk of intraoperative bleeding, and a total abdominal hysterectomy was then performed. The patient’s postsurgical recovery was uneventful and her serum β-hCG level decreased. The histopathological examination confirmed a friable hemorrhagic mass in the anterior inferior wall of the uterus, adherent to the previous CSS. It was composed of atypical cytotrophoblastic cells with high mitotic activity and myometrial invasion, and intensive necrosis and hemorrhage were present centrally. Immunocytochemical staining for β-hCG was positive and the Ki-67 index was as high as 80%. The final pathologic diagnosis was choriocarcinoma.\nA metastatic workup revealed multiple lung metastases. There was no evidence of metastasis to the brain. Adjuvant chemotherapy was planned and the patient received four cycles of the EMA/CO regimen (etoposide, methotrexate, actinomycin D, cyclophosphamide, and vincristine). She tolerated the therapy well, and weekly serum β-hCG measurements showed a significant drop, from 12.459 mIU/ml after the surgery to 0.7 mIU/ml following chemotherapy. A follow-up CT scan showed a significant reduction in the size of the lung metastases.
|
[[33.0, 'year']]
|
F
|
{'24887563': 2, '9292652': 1, '1848902': 1, '8946542': 1, '1033657': 1, '15027012': 1, '33768867': 2, '30046213': 2, '11437936': 1, '8640741': 1, '24393333': 1, '30151454': 2}
|
{'4026121-1': 1, '7981746-1': 1, '6055209-1': 1}
|
2,031 |
6100651-1
| 30,151,440 |
comm/PMC006xxxxxx/PMC6100651.xml
|
A Rare Cause of Calcified Subdural Empyema and Ventriculitis in a Pediatric Patient: Achromobacter Denitrificans
|
A 2-year-old male patient presented with acute onset of seizures and loss of consciousness to our emergency department. His past history revealed that he was being followed for hypogammaglobulinemia over the past year without any change of consciousness nor seizures. He had no history of head injury, trauma, or infectious diseases. Neurological examination disclosed a Glasgow Coma Score (GCS) of 3, his pupillary were anisocoric, direct light reflex and indirect light reflex were found to be negative. The laboratory examinations showed: ESR 120, CRP 6.27 mg/dL, white blood cell count 18,400 μL (neutrophils 70%) and platelets 512,000/μL. Unenhanced computerized tomography scan of the brain revealed a right frontoparietal peripherally calcified extraaxial collection, brain edema and a left sided shift (Fig. ). A contrast enhanced magnetic resonance imaging showed the presence of a subdural empyema associated with the ipsilateral lesion in the brain parenchyma and extension of the infection to the ventricular system was demonstrated (Fig. ). Neurological situation showed brain herniation symptoms, so the patient underwent emergency operation. A right sided wide decompressive craniectomy with extensive trauma incision was performed. Dura mater was tense and fibrotic, when it was passed a 15 × 7 cm fibrotic and thickened abscess with full of pus was encountered. An aspiration about 50 cc of purulent material was discharged and abscess walls were excised (Fig. ). A decompression procedure was performed for the parenchymal mass and 15 cc collection was aspirated. Postoperative imaging studies disclosed the successful decompression procedure. Aspirate samples showed numerous polymorphonuclear leukocytes without bacteria at gram staining, cultures were positive for Achromobacter denitrificans, negative for anaerobic bacteria or fungi. The isolate was susceptible to ampicillin-sulbactam, trimethoprim-sulfamethoxazol, tigecycline, ceftazidime, levofloxacin and ciprofloxacin. But in spite of subsequent antibiotic therapy patient’s neurological situation got worse in the postoperative period. The patient’s GCS remained 3 and he succumbed on the postoperative day 9.
|
[[2.0, 'year']]
|
M
|
{'15822825': 1, '21629191': 1, '22707140': 1, '15205140': 1, '8879782': 1, '23970185': 1, '25917804': 1, '25031900': 2, '22404460': 1, '12490479': 1, '24525606': 1, '30151440': 2}
|
{'4083727-1': 1}
|
2,032 |
6100657-1
| 30,151,436 |
comm/PMC006xxxxxx/PMC6100657.xml
|
Atypical Distribution of Late Gadolinium Enhancement of the Left Ventricle on Cardiac Magnetic Resonance in Classical Anderson-Fabry Disease
|
A 48-year-old man who had been aware of exertional breathlessness for two years was referred to our hospital because an echocardiogram (ECG) of his medical checkup was abnormal. His medical history included juvenile onset asthma and deafness. Regarding his familial medical history, his paternal grandfather had asthma, his mother had deafness and died from a stroke, and his older sister had asthma. He presented with hypertension and apical systolic murmur. Laboratory data showed moderate renal failure (eGFR: 41 ml/min/1.73 m2), high serum level of brain natriuretic peptide (1023 pg/ml), and positive urinary protein. Chest radiography showed only mild cardiomegaly. ECG showed R-wave elevation and T-wave strain abnormalities, and transthoracic echocardiography showed symmetric hypertrophy of the LV (left atrial dimension: 51 mm, interventricular septum thickness: 18 mm, posterior LV wall thickness: 22 mm, ejection fraction: 68%). CMR was performed with a 3 T MR scanner (Magnetom Skyra, Siemens Medical Solution, Enlargen, Germany). T2WI-STIR with a black-blood technique (Fig. ) showed symmetric hypertrophy of the LV and moderate thickening of the right ventricle. Short- and long-axis cine images showed hypokinetic wall motion of the LV (Fig. ). CMR showed LGE at the mid-myocardium of the mid-lateral through apical segments of LV (Figs. and ). Because of the atypical distribution of the LGE of the LV, coronary angiography was performed and showed normal results. An endomyocardial biopsy was also performed and the specimen demonstrated cytoplasmic vacuolation. Alpha-galactosidase activity in the peripheral blood was deficient, and gene mutation analysis showed a homozygote L19p gene mutation. Therefore, a diagnosis of classical AFD was made. He was treated with enzyme replacement therapy.
|
[[48.0, 'year']]
|
M
|
{'14643276': 1, '25106696': 1, '23564562': 1, '17312078': 1, '19234246': 1, '16755835': 1, '19786638': 1, '30151436': 2}
|
{}
|
2,033 |
6100659-1
| 30,151,445 |
comm/PMC006xxxxxx/PMC6100659.xml
|
Disappearing Inferior Vena Cava in A Pediatric Patient with Down Syndrome and Hereditary Thrombophilia
|
A ten-months-old girl was referred to our clinic with swelling and warmth and red discoloration in the right lower extremity. Regarding the clinical history, she had growth retardation and protein-energy malnutrition.\nOn the color Doppler ultrasound examination, there was generalized thrombus within the great and small saphenous veins, popliteal vein, superficial and deep femoral veins, and common femoral vein. Upon seeing this and noting the visible surface veins both in the right lower extremity and abdomen, an intraabdominal venous color Doppler ultrasound was performed. Bilateral common iliac veins and infrarenal and renal segments of IVC were thrombosed, as well. Suprarenal and intrahepatic segments of IVC were preserved (Figure ). No family history of deep venous thrombosis or IVC agenesis were noted (neither in her parents nor in her two elder brothers). A detailed genetic testing revealed that the patient has Down syndrome (with one extra twenty-first chromosome) and pericentric inversion in the ninth chromosome that p11 and q13 are inversely translocated (47, XX, inv (9p11q13), +21). Patient’s cardiovascular risk analysis panel revealed that she had increased venous thrombosis risk with homozygous MTHFR (A 1298C) polymorphism, HPA 1 (b/b), factor V Leiden (G1691A) heterozygous and ACE I/D genotype (Del/Del); other panel polymorphisms were normal (MTHFR C677T polymorphism was C677C, factor XIII V34L polymorphism was V34LL, PAI- Serpine1 mutation 4G/5G test was 5G/5G, Prothrombin G20210A was 20210GG, Beta Fibrinogen 455A > G polymorphism was 455G > G, APO B R3500Q polymorphism was 3500RR). In addition, the patient’s mother had a 46, XX, inv (9p11q13) karyotype, which represents the normal female with peripheric inversion at the ninth chromosome. Mother had also increased venous thrombosis risk confirmed by heterozygous PAI-SERPINE1 4G/5G, MTHFR (A1298C) heterozygous, ACEI/D Ins/Del, HPA 1 a/b a/b; another panel polymorphisms were normal. She gave birth to two older boys who were phenotypically normal and were not genetically analyzed. Her father had a normal karyotype 46, XY with increased venous thrombosis risk confirmed by homozygous MTHFR (A1298C), HPA 1 a/b a/b, and ACEI/D Ins/Ins; another panel polymorphisms were normal.\nAfter initial visit, the patient was lost to follow-up. Six months later she was referred from the emergency unit with similar symptoms to our clinic. This time, on the color Doppler ultrasonography, in addition to the thrombotic venous structures observed previously, the suprarenal segment of her inferior vena cava (IVC) was also thrombosed. A Computed tomography scan (CT) showed thrombosed (disappearing) IVC, the continuous hemiazygous vein draining into the continuous azygous vein, draining of the left renal vein into the intrahepatic segment of IVC, collateral veins in the lower extremities and pelvis, dilated ascending lumbar veins (Figure ). A detailed physical exam revealed that she developed secondary pulmonary hypertension and cardiac murmur.
|
[[10.0, 'month']]
|
F
|
{'12529095': 1, '7466729': 1, '10071172': 1, '11714571': 1, '16681418': 1, '10556190': 1, '15043024': 1, '24967034': 1, '10350299': 1, '18480478': 1, '11564079': 1, '11331855': 1, '16304352': 1, '10835118': 1, '11273066': 1, '25035247': 1, '9550527': 1, '19507668': 1, '12654149': 1, '22530883': 1, '1257455': 1, '30151445': 2}
|
{}
|
2,034 |
6100660-1
| 30,151,475 |
comm/PMC006xxxxxx/PMC6100660.xml
|
MDCT Diagnosis of Symptomatic Incarceration of the Right Ileocecocolic Mesentery Within a Complete 360-Degree Whirl of the Great Omentum: Follow the Vessels!
|
A 74-year-old female was referred to the emergency department with persistent abdominal pain. Five months earlier, she had experienced acute small bowel intestinal obstruction necessitating emergency laparotomy. This occlusion was caused by anterior parietal adherences related to recurrent previous abdominal surgery. Contrast-enhanced MDCT excluded now significant dilatation of the gut but demonstrated an unusual accumulation of abdominal fat incarcerating mesenteric vessels and bowel segments in the midline of the anterior mesogastrium (Figure , white arrows). Careful multiplanar analysis (Figure shows the antero-posterior coronal MPR views, and Figure shows the axial oblique MPR view) revealed the omental nature of the encircling fatty structure through the clear delineation of the encircling omental vessels (white arrows). This 360-degree whirl of the greater omentum was incarcerating the right ileocecocolic mesenteric vessels (white star); the two incarcerated and compressed bowel segments were identified as the terminal ileum and the transverse colon (black arrows). Selective volume-rendering reconstruction confirmed the whirl (Figure ). Despite the fact that there was no critical dilatation nor suffering signs of the gut at the time of MDCT, the risk of occlusion was nevertheless considered important, and it seemed unlikely that this complete omental whirl would resolve spontaneously. This caution justified laparotomy.
|
[[74.0, 'year']]
|
F
|
{'19214367': 1, '30151475': 2}
|
{}
|
2,035 |
6100663-1
| 30,151,452 |
comm/PMC006xxxxxx/PMC6100663.xml
|
A Female Newborn Infant with FATCO Syndrome Variant (Fibular Hypoplasia, Tibial Campomelia, Oligosyndactyly) – A Case Report
|
We report on a case of fibular hypoplasia, tibial campomelia, and oligodactyly in a female neonate of one day old. The patient was born by elective Cesarean section at 39 weeks, 4 days. She was the first pregnancy of a healthy mother. The infant birth weight was 2660 g, the birth length was 48 cm, and the head circumference at birth was 34 cm. There was no history of prenatal complications. There was no relevant family history. The neonate needed to be insufflated shortly after birth with immediate recuperation.\nPhysical examination revealed shortening and anterolateral bowing of the left lower limb at the distal third of the tibia with associated overlying soft tissue dimpling and oligosyndactyly of both feet. Only three toes (the fourth and fifth ray were absent) were found on the left extremity and four toes (the fifth ray was absent) on the right extremity.\nThere was no associated abnormality in the upper limbs. There was no associated facial dysmorphism nor other associated anomalies. Hip ultrasound revealed no congenital hip dysplasia.\nRadiographic examination revealed hypoplasia of the left fibula (Figure ), absence of two rays left and one ray on the right foot (Figure ), and anterolateral bowing and shortening of the left tibia (Figure ). Both femora were normal.
|
[[1.0, 'day']]
|
F
|
{'25386471': 1, '23926365': 1, '23807497': 1, '10529577': 1, '7937589': 1, '26042905': 1, '25144151': 1, '20964118': 1, '12990634': 1, '15754355': 1, '10739276': 1, '7337959': 1, '12868468': 1, '20947407': 1, '21965580': 1, '22628253': 1, '3146293': 1, '32933589': 2, '30151452': 2}
|
{'7493856-1': 1}
|
2,036 |
6100671-1
| 30,151,499 |
comm/PMC006xxxxxx/PMC6100671.xml
|
Bronchial Mucoepidermoid Carcinoma
|
A 12-year-old boy with chronic respiratory complaints, including cough, exercise intolerance, and persistent wheezing, was referred to our hospital because of persistent symptoms under extensive asthma therapy. A standard radiograph of the chest detected very slight hyperinflation of the left lung with increased lung translucency (Figure ). Computed tomography revealed a polypoid mass distally in the left main bronchus with a density around 55 HU and very slightly decreased attenuation of the left lung, probably due to secondary air trapping (Figure ). Bronchoscopy confirmed this finding, and biopsy revealed the mass to be a low-grade mucoepidermoid carcinoma (Figure ). A curative bronchial sleeve resection was performed with partial mediastinal lymphadenectomy. All lymph nodes were normal, and there is no recurrence to this date (one year). Adjuvant chemotherapy was not indicated.
|
[[12.0, 'year']]
|
M
|
{'34113123': 2, '16133240': 1, '30151499': 2}
|
{'8184241-1': 1}
|
2,037 |
6100672-1
| 30,151,470 |
comm/PMC006xxxxxx/PMC6100672.xml
|
Pear-Shaped Lesion of the Fossa of Rosenmüller
|
A 72-year-old man was admitted with persistent temporal headache. Further clinical history, physical examination, and laboratory tests were unremarkable. Nonenhanced computed tomography (CT) of the head (Figure , black arrow) revealed a lesion with nonspecific attenuation in the left fossa of Rosenmüller. For further characterization, magnetic resonance imaging (MR) was performed.\nThe lesion was pear-shaped and well circumscribed. The lesion was slightly hyperintense on T1-weighted images (WI) (Figure , white arrow) and hyperintense on fat-suppressed T2-WI (Figure , white arrow). There was subtle peripheral enhancement after administration of gadolinium contrast (Figure , white arrow). The diagnosis of a retention cyst of Rosenmüller’s fossa was made. As the patient was asymptomatic, watchful waiting was recommended.
|
[[72.0, 'year']]
|
M
|
{'24378893': 1, '30151470': 2}
|
{}
|
2,038 |
6100673-1
| 30,151,500 |
comm/PMC006xxxxxx/PMC6100673.xml
|
Two Rare Cases of Posttraumatic Peripheral Artery Pseudoaneurysm
|
A 43-year-old woman was treated in the emergency room for a painful ankle sprain with marked soft tissue swelling, confirmed by plain radiograph. After resolution of the soft tissue swelling, US examination was ordered for persistent pain and targeted to the periarticular ligaments revealed a partly thrombosed pseudoaneurysm but could not identify its feeding vessel. A magnetic resonance angiography (MRA) was performed and revealed that the feeding vessel was a collateral branch of the anterior tibial artery. Whilst injecting 1 mL of thrombin (Dstat®, Vascular Solutions, Minneapolis, Minnesota) into the pseudoaneurysm under US guidance, the arterial signal disappeared on power Doppler US. As ankle movements were still very limited, the residual hematoma was incised. Acute bleeding necessitated DSA of the lower limb that revealed extravasation of contrast material. After selective catheterization of the feeding vessel, one coil of 2 cm in length and 3 mm in diameter was deployed (MReye®, Cook, Bloomington, Indiana) (Figure ) which led to the complete exclusion of the pseudoaneurysm whilst keeping the anterior tibial artery patent. Two weeks thereafter, the patient recovered complete ankle mobility and her professional activity.
|
[[43.0, 'year']]
|
F
|
{'25415822': 1, '12538327': 1, '9423705': 1, '18587511': 1, '24953919': 1, '23396224': 1, '21769220': 2, '34484525': 1, '14612861': 1, '24293904': 1, '30151500': 2}
|
{'3132373-1': 1}
|
2,039 |
6100674-1
| 30,151,484 |
comm/PMC006xxxxxx/PMC6100674.xml
|
Intratendinous Patellar Ganglion Cyst with Coexistant Osgood Schlatter Disease
|
A 19-year-old boy was sent in by the general practitioner with complaints of persisting tenderness and swelling just below the knee. Conventional radiography of the knee showed fragmentation of the tibial tuberositas pointing towards Osgood Schlatter Disease (Figure ).\nUltrasound examination of the knee with a high frequency linear probe was performed. Findings included fragmentation of the tibial tuberosity, hypoechoic tendon and increased power doppler signal, compatible with Osgood Schlatter disease (Figure ). Additionally, a sharply delineated, elongated anechoic structure with enhanced through transmission occupied the center of the patellar tendon (Figure ). A small pedicle towards the proximal bony fragment of the tibial tuberosity seemed to be present. The diagnosis of an intratendinous patellar ganglion cyst was made, possibly related to a coexistant chronic Osgood-Schlatter disease.\nTo further investigate the etiology of the intratendinous ganglion cyst additional magnetic resonance imaging (MR) was performed (Figure ). This demonstrated swelling and increased signal intensity of the distal patellar tendon on both T2-weighted images (WI) and intermediate/proton density weighted images (PD-WI) with fragmentation of the tibial tuberosity as part of Osgood Schlatter disease. A large intratendinous cyst with high signal intensity on T2- and PD-WI occupied nearly the whole length in the centre of the tendon and terminated into a thin pedicle towards the proximal bony fragment. Additionally, there was mild fluid distension of the deep infrapatellar bursa. The diagnosis of an intratendinous patellar ganglion cyst with a coexistant chronic Osgood-Schlatter disease was confirmed.
|
[[19.0, 'year']]
|
M
|
{'31641563': 2, '30151484': 2}
|
{'6802811-1': 1}
|
2,040 |
6100676-1
| 30,151,471 |
comm/PMC006xxxxxx/PMC6100676.xml
|
Imaging Features of Hypertrophic Olivary Degeneration
|
A 55-year-old female patient consulted the neurologist because of vertigo and tinnitus. Clinical examination revealed an obvious palatal myoclonus. Magnetic resonance imaging (MRI) of the brain was performed, and T2-weighted and fluid-attenuated inversion recovery (FLAIR) images showed focal hyperintensity and expansion of both medullary olives (Figure ). Neither enhancement was seen following contrast administration, nor restriction on diffusion-weighted imaging. Based on the clinical symptoms and radiologic findings, a diagnosis of HOD was made. The etiology for this case remains unknown since no history of infarction, hemorrhage, tumor, or trauma was present.
|
[[55.0, 'year']]
|
F
|
{'19246355': 1, '23486559': 1, '23370897': 1, '8029428': 1, '18217209': 1, '28650218': 1, '24716899': 1, '26073621': 1, '22332198': 1, '1171410': 1, '25332842': 1, '32493244': 2, '29275394': 1, '31019597': 1, '34357': 1, '10580959': 1, '5720756': 1, '7270084': 1, '10871017': 1, '20846979': 1, '30151471': 2}
|
{'6100676-2': 2, '6100676-3': 2, '7268217-1': 1}
|
2,041 |
6100676-2
| 30,151,471 |
comm/PMC006xxxxxx/PMC6100676.xml
|
Imaging Features of Hypertrophic Olivary Degeneration
|
A 57-year-old woman presented with vertigo. An MRI of the brain revealed a mass in the right posterior fossa (Figure ). The tumor was resected and an anatomopathological diagnosis of a medulloblastoma was made. A follow-up MRI obtained five months after surgery revealed a postoperative defect in the vermis immediately posterior to the fourth ventricle and extending to the right dentate nucleus, as well as a new T2-hyperintense lesion in the left inferior olivary nucleus (Figures and ). This lesion did not enhance after contrast administration and showed no restriction on diffusion-weighted imaging.
|
[[57.0, 'year']]
|
F
|
{'19246355': 1, '23486559': 1, '23370897': 1, '8029428': 1, '18217209': 1, '28650218': 1, '24716899': 1, '26073621': 1, '22332198': 1, '1171410': 1, '25332842': 1, '32493244': 2, '29275394': 1, '31019597': 1, '34357': 1, '10580959': 1, '5720756': 1, '7270084': 1, '10871017': 1, '20846979': 1, '30151471': 2}
|
{'6100676-1': 2, '6100676-3': 2, '7268217-1': 1}
|
2,042 |
6100676-3
| 30,151,471 |
comm/PMC006xxxxxx/PMC6100676.xml
|
Imaging Features of Hypertrophic Olivary Degeneration
|
A 43-year-old woman suffered a left pontine hypertensive hemorrhagic stroke (Figure ). On a follow-up MRI performed four months later, irregular T2-hypointensities could be seen in the left dorsal tegmentum of the pons, compatible with hemosiderin and ferritin deposits (Figure ). Furthermore, a nodular T2-hyperintense lesion could be seen in the left anterolateral part of the ventral medulla oblongata, showing no restriction and no enhancement, respectively, on diffusion and postcontrast imaging (Figure ). This lesion was not present on an MRI performed shortly after the hemorrhage but remained completely unchanged on a follow-up MRI performed one month later. Based on the typical location of the lesion, a diagnosis of HOD was made. At the follow-up consultation, the patient declared she intermittently experienced symptoms that could be subscribed to palatal myoclonus. However, clinical examination could not objectify these symptoms.
|
[[43.0, 'year']]
|
F
|
{'19246355': 1, '23486559': 1, '23370897': 1, '8029428': 1, '18217209': 1, '28650218': 1, '24716899': 1, '26073621': 1, '22332198': 1, '1171410': 1, '25332842': 1, '32493244': 2, '29275394': 1, '31019597': 1, '34357': 1, '10580959': 1, '5720756': 1, '7270084': 1, '10871017': 1, '20846979': 1, '30151471': 2}
|
{'6100676-1': 2, '6100676-2': 2, '7268217-1': 1}
|
2,043 |
6100677-1
| 30,151,450 |
comm/PMC006xxxxxx/PMC6100677.xml
|
Diffuse Alveolar Hemorrhage Due to Malignant Arterial Hypertension – an Unusual Manifestation of a Common Disease
|
A 51-year-old Caucasian male presented to the emergency department with a four-day history of dry cough, orthopnea and asthenia. He was a smoker (30 packs/year) but had no other known previous pathologies, in particular arterial hypertension.
|
[[51.0, 'year']]
|
M
|
{'22347941': 1, '19825341': 1, '32728521': 2, '16046511': 1, '10644871': 1, '23074127': 2, '20442117': 1, '21279812': 1, '8915239': 1, '30151450': 2}
|
{'7386058-1': 1, '3481392-1': 1}
|
2,044 |
6100678-1
| 30,151,449 |
comm/PMC006xxxxxx/PMC6100678.xml
|
A Rare Case of Adult Acute Ileocecal Ischemia Related to Henoch-Schönlein Purpura: MDCT Findings
|
A 62-year-old man presented to the emergency department with complaints of colicky abdominal pain and active rectorrhagy. Two days before, these symptoms had been preceded by the apparition of diffuse purpuric spots on the lower limbs and the forearms. One week before, the patient had experienced a viral episode of the nasopharyngeal sphere. At admission, the patient was apyretic and articular symptoms were absent. Physical examination revealed a compressible and painless abdomen. Peristalsis was preserved, and laboratory blood tests were normal except a mildly elevated IgA level. There were only subtle urinary signs of glomerular damage with microscopic hematuria, mild proteinuria, and mixed cellular urinary casts.\nRectosigmoidoscopy was normal except for rare bloodstains. Gastroscopy revealed diffuse duodenal small necrotic ulcers.\nContrast-enhanced multidetector-row CT (Figure ) demonstrated homogenous circumferential bowel thickening of a rather long segment of the ileum terminal. The typical “target sign” (or stratified pattern) was present with hypodense edema of the submucosa contrasting with hyperemia or hyperperfusion of the mucosa. Engorgement of the ileocecal mesenteric vessels with typical comb sign was also present. Hypodense thickening of the cecum and proximal ascending colonic wall was also clearly present, and the demarcation between the thickened and normal colonic wall appeared very sharp on conventional CT views (Figure ) and virtual endoscopic views (Figure ). A small amount of ascite was also found in the pelvic floor and in the perihepatic space. Skin biopsy revealed typical signs of leukocytoclastic vasculitis (Figure ).\nThe final diagnosis of Henoch-Schönlein purpura with gastrointestinal involvement was proposed, and the patient was successfully treated with an association of corticosteroids and cyclophosphamide. Gastrointestinal symptoms resolved within two days, and there was no recurrence of symptoms.
|
[[62.0, 'year']]
|
M
|
{'21619657': 2, '23122016': 1, '22707542': 1, '21958439': 1, '12356974': 1, '22442741': 1, '11961015': 1, '23343144': 2, '24407923': 1, '23097737': 2, '17975696': 1, '22563183': 1, '30151449': 2}
|
{'3125277-1': 1, '3125277-2': 1, '3558347-1': 1, '3477656-1': 1}
|
2,045 |
6100686-1
| 30,151,501 |
comm/PMC006xxxxxx/PMC6100686.xml
|
Ultrasound Diagnosis and Follow-Up of Neonate Renal Candidiasis
|
A 4.5-month-old girl was admitted to the emergency room for loss of consciousness. Her past nine days were marked by cough and apathy. She was born at 41 weeks with a weight of 3.5 kg and her past history was unremarkable. Physical examination was strictly normal and the patient was looking good, with only a mild cough. The diagnosis of respiratory syncytial virus infection was made by Polymerase Chain Reaction. The rest of the blood analysis was strictly normal, with no inflammatory syndrome. In response to a rapid decrease of arterial oxygen saturation in the emergency room, the baby was transferred to intensive care, intubated and her bladder catheterized to monitor liquid excretion. Broad-spectrum antibiotherapy was started to prevent bacterial surinfection. After three days of intubation, the patient presented oliguria and acute renal failure with transient peaks of elevated blood pressure (120/65 mmHg, treated with diuretics) and fever (38.6°C). Blood culture and lumbar puncture detected neither bacteria nor fungal agent. Meanwhile, pyuria was detected and Candida Albicans was present in urinary cultures above the threshold of 100,000 colony-forming units per milliliter. A treatment by intravenous Fluconazole was started. The subsequent immune check-up detected no anomaly, and a renal ultrasound was requested.\nIt showed a right nephromegaly with hyperechoic parenchyma. There were five parenchymal anechoic rounded formations with septations and internal echoes. Some of them were connected to the pelvi-calyceal system through a thin meatus. Pelvi-caliceal wall was thickened and the cavities contained rounded hyperechoic nodules suggesting fungus balls, with mild dilatation of some calices, and hyperechoic formations with fork shape suggesting moulded image of papillae (Figure ). Because of the right urinary tract obstruction (Figure ) an the potential risk of subsequent renal failure, the question of open-kidney surgery was discussed. Considering the risk for the kidney long-term growth after surgery, we decided for a conservative treatment, which consisted of 3 months of Fluconazole.\nFollow-up ultrasound examinations showed a favorable evolution, with shrinking of the abscesses and increasing acoustic shadowing of the echoic material in the calices suggesting calcification (Figure ). Iterative urinary culture showed decrease in pyuria. The baby suffered then two nephritic colic episodes due to elimination of calcified fragments, requiring pain management, respectively at the age of 5.5 and 6 months, confirmed by ultrasonography. There has been no reinfection yet, 6 months after the release from the hospital.
|
[[4.5, 'month']]
|
F
|
{'21498838': 1, '20513207': 1, '34162849': 1, '21695474': 1, '19930662': 1, '15883715': 1, '24457108': 1, '30151501': 2}
|
{}
|
2,046 |
6100695-1
| 30,151,448 |
comm/PMC006xxxxxx/PMC6100695.xml
|
Short Occult Retractile Fibrous Scar Causing Exclusive Retrograde Stenosis of the Sigmoid Colon: An Incidental Diagnosis Nineteen Years After a Single Episode of Colonic Diverticulitis
|
A 69-year-old man was referred to our Medical Imaging Department to undergo a virtual colonoscopy (VR). The patient had no specific abdominal complaint except mild chronic diarrhea worsened by metformin. He was referred to explain a positive fecal occult blood test. A conventional rectoscopy was normal, and a sigmoidoscopy was interrupted because of pain due to a spastic diverticular sigmoid. As he was taking clopidrogel (Plavix) for ischemic heart disease, there was a relative contraindication to perform a total optical colonoscopy (OC).\nAlmost immediately after starting the automated low-pressure colonic insufflation with carbon dioxide, the insufflator (with a maximal pressure set at 25 mm Hg) automatically stopped repeatedly, suggesting that there was a colonic stenosis or obstacle.\nA complete cut off of the inflated colon was seen on a CT topogram at the level of the sigmoid and descending colonic junction (Figure ). The virtual colonoscopy was immediately converted into a conventional non-contrast-enhanced abdominal CT and completed by secondary contrast-enhanced acquisition.\nA short contrast-enhancing “scar-like” intra- and extraparietal structure was found infiltrating the posterior colonic wall at the level of the sigmoid and descending colonic junction (Figure ). This curvilinear retractile “scar-like” tissue had developed multiple adherences with the retroperitoneum and the left iliac fossa and seemed to be stapling the colon on the retroperitoneum.\nThere was no obstruction, subocclusion, nor fecal stasis upstream, thereby suggesting a purely retrograde and unidirectional functional stenosis.\nAdditional ultrasound (Figure ) study showed a perfectly empty descending colon with a normal mucosal relief, but with a thickening of the muscle layer. At the junction of the sigmoid and descending colon, ultrasound demonstrated a centripetal retractile convergence of the muscle layers to an intraparietal very hyperechoic and very attenuating scar.\nThe complete retrograde and unidirectional stenosis was confirmed by classical colonic opacification obtained the next day after CT. Only a small amount of hydrosoluble contrast could pass through the stenosis.\nRetrospective anamnesis of the patient revealed a very old history of a single acute colonic diverticulitis episode 19 years before.\nAfter a discussion with the multidisciplinary staff, a celioscopic resection of the stenotic segment was proposed to protect the patient from a prograde occlusion. The celioscopic resection was difficult due to retroperitoneal and left ureteral adherences, so a classical laparotomy became necessary. The postoperative period was uneventful.\nGross anatomy (Figure ) of the resected colonic segment confirmed a short stricture constituted by corbelling fibrosis infiltrating the colonic wall of a diverticular segment. Histology showed typical fibrosis with discrete chronic inflammatory infiltrates and lymphoid clusters. Rare micro-abscesses related to chronic diverticulitis were also found.\nFour months later, the patient was readdressed to the gastroenterologic staff to complete the study of the proximal colon which had not been studied. In the meantime, clopidrogel (Plavix) could be interrupted, and an optic colonoscopy was proposed to the patient. A small adenocarcinoma of the caecum was demonstrated – which was not visible on the CT – and a ceolioscopic right hemicolectomy was performed.
|
[[69.0, 'year']]
|
M
|
{'18647926': 1, '22347935': 1, '24163654': 2, '25492999': 1, '23669306': 1, '21876861': 1, '30151448': 2}
|
{'3806696-1': 1}
|
2,047 |
6100697-1
| 30,131,978 |
comm/PMC006xxxxxx/PMC6100697.xml
|
Ultrasound-Guided Morcellation During Holmium Laser Enucleation of the Prostate
|
The patient is a 66-year-old Caucasian man with a history of an enlarged prostate and urinary retention with a prostate volume of 158 cc on pelvic ultrasonography. After informed consent was obtained, HoLEP was performed using a 550-μm end-firing laser fiber and a 100-W holmium laser (Lumenis, Inc., Tel Aviv, Israel). Laser settings were 2 J and 20 to 40 Hz, translating into 40 to 80 W of power. Enucleation was performed by making a transverse laser incision just proximal to the verumontanum to identify the appropriate prostatic capsule plane. With minimal median lobe tissue present, a 6 o'clock incision was made connecting the bladder neck with the initial transverse incision. The enlarged left and right lateral lobes were then enucleated in the standard manner as described previously. Transurethral morcellation was initiated using the 26F outer sheath with the Wolf Piranha Scope (12° nephroscope) and the Piranha morcellator (Richard Wolf, Knittlingen, Germany) at the manufacturer's recommended settings of 1500 rpm.\nUpon placement of the nephroscope into the bladder, it became apparent that the lens was damaged resulting in an extremely poor cystoscopic image (). No replacement nephroscope was readily available. To safely complete the procedure, it was decided to utilize a 3.5-MHz convex abdominal transducer (Hitachi Prosound Alpha 7; Hitachi Aloka Medical America, Wallingford, CT) under B-mode ultrasound to view the bladder and guide morcellation ().\nIn the sagittal plane, the enucleated adenoma could be seen in the dependent portion of the distended bladder with both the nephroscope and Piranha morcellator just entering the bladder neck (). Guided by the assistant holding the ultrasound probe and controlling the view, the operator aimed the morcellator tip in the direction of the dependently resting enucleated adenoma, and the suction pedal was applied until the tissue was seen to be engaged into the morcellator blade. The nephroscope and morcellator hand piece were then tilted anteriorly toward the center of the bladder and the morcellation pedal was activated, safely removing the adenoma away from the walls of the bladder (). A final inspection with both ultrasound and a functional cystoscope lens confirmed the absence of any remaining adenoma pieces within the prostatic fossa and bladder. The patient was safely discharged from the hospital the next day and experienced an uneventful postoperative recovery. Pathology analysis demonstrated a specimen weight of 69 g of BPH. A defective water seal was identified as the source of the defective lens.
|
[[66.0, 'year']]
|
M
|
{'25781490': 1, '18086107': 1, '12837423': 1, '17997021': 1, '30131978': 2}
|
{}
|
2,048 |
6100715-1
| 30,124,173 |
comm/PMC006xxxxxx/PMC6100715.xml
|
The challenges of treating tracheobronchitis in a laryngectomee due to nontypeable Haemophilus influenzae: a case report
|
A 76-year-old Caucasian man who underwent laryngectomy 10 years earlier, presented with fever (38.9 °C; 102.0 °F), increased sputum production, and purulent conjunctivitis. These symptoms emerged gradually over a period of 48 hours. He noted increasing difficulty in coughing out his sputum that became brownish and viscous. He had been wearing a heat and moisture exchanger (HME) filter that covered his stoma and spoke through a tracheoesophageal voice prosthesis. The symptoms started a day after a very cold weather spell with temperatures of −7 to −1 °C (19–31 °F). He had to remove his HME on several occasions for extended periods of time to enable him to breathe when he walked outside his home.\nHis past medical history included hypopharyngeal squamous cell carcinoma which was treated with intensity-modulated radiotherapy (IMRT) 12 years earlier. A recurrence of the cancer 2 years later required laryngectomy. He had no signs of tumor recurrence since then. He also suffered from paroxysmal hypertension, diverticulitis, and migraines.\nHe was vaccinated with the current Influenza virus vaccine 3 month earlier. He had also received a pneumococcal polysaccharide vaccine (PPSV23) 2 years earlier.\nHe was in mild respiratory distress especially when coughing. He had coughing spells and expectorated green-brown dry and viscous sputum. A physical examination revealed bilateral purulent conjunctivitis and auscultation of his lungs revealed coarse rhonchi and no crepitations. No lymphadenopathy was noted. The results of the rest of the physical and neurological examinations were within normal limits. A chest X-ray was normal.\nSputum and conjunctival culture grew heavy growth of beta-lactamase-producing nontypeable Haemophilus influenzae (NTHi) that was susceptible to levofloxacin and amoxicillin- clavulanate. A FilmArray® Respiratory Panel 2 (RP2) polymerase chain reaction (PCR) system test did not detect 14 viruses (adenovirus, coronavirus HKU1, coronavirus NL63, coronavirus 229E, coronavirus OC43, human rhinovirus/enterovirus, human metapneumovirus, influenza A, influenza B, parainfluenza virus 1, parainfluenza virus 2, parainfluenza virus 3, parainfluenza virus 4, respiratory syncytial virus) and four bacteria (Bordetella pertussis, Bordetella parapertussis, Chlamydophila pneumoniae, Mycoplasma pneumoniae).\nHe was treated with orally administered levofloxacin 500 mg/day, ciprofloxacin eye drops, acetaminophen, and guaifenesin. Humidification of his trachea and the airway was maintained by repeated insertions of 3–5 cc respiratory saline into the stoma at least once an hour and by breathing humidified air.\nThe main challenge was to maintain a patent airway as the mucus was very dry and viscous and tended to stick to the walls of his trachea and the stoma. The mucus had to be repeatedly expectorated by vigorous coughing and by manual removal from the upper part of his trachea and stoma.\nHe experienced repeated episodes of sustained elevated blood pressure (up to 210/110) and tachycardia (112/minute). This was managed by administration of clonidine 0.1 mg as needed (1–2/day).\nHis fever started to decline 48 hours after antimicrobial therapy was started. The conjunctivitis improved within 36 hours. The sputum production declined and became less viscous over time, but persisted for 5 days.\nAntimicrobial therapy was discontinued after 7 days.\nHis condition improved and he had a complete recovery in 7 days. He was seen in the clinic every 2 months and showed no recurrence of his infection for the following 8 months. He received vaccination for H. influenzae B and Prevnar 13® (pneumococcal conjugate vaccine; PCV13) 4 weeks after his recovery.
|
[[76.0, 'year']]
|
M
|
{'19644780': 1, '3739687': 1, '5517953': 1, '18367021': 1, '14239534': 1, '22070637': 1, '5508709': 1, '2282704': 1, '477429': 1, '21094183': 1, '9061728': 1, '24554391': 1, '30124173': 2}
|
{}
|
2,049 |
6100716-1
| 30,151,016 |
comm/PMC006xxxxxx/PMC6100716.xml
|
Unintentional injection to the bone with a pediatric epinephrine auto-injector
|
MS is a 10-year-old female patient diagnosed with multiple food allergies and anaphylaxis (Table ). MS has a family history of atopy (both parents). MS’s index allergic event was at 9 months of age when she presented with urticaria after contacting milk and cheese. By the age of 5, MS had been diagnosed with milk, peanut, and tree nut allergies based on clinical history, skin prick testing, serum-specific IgE testing, and oral food challenge (OFC). Also, she has dust mite and pet allergies.\nSince early in life, she was prescribed a pediatric EAI (EpiPen Jr®; 0.15 mg) in case of an allergic emergency. The first use of her prescribed EAI for MS was at age 6, and she has had 2 subsequent allergic emergencies requiring the use of her EAI as of the date of this report (Table ). At 6 years old, her height was 117 cm, weight was 17.7 kg, BMI was 12.9, and her STBD was 10.7 mm by ultrasound of the right mid-anterolateral thigh. At 7 years old, around her second event requiring the EpiPen Jr®, her height was 122 cm, weight was 25 kg, and her STBD was not recorded. After this event, and during her observation period in the hospital, MS complained of pain immediately in her right thigh at the injection site. X-ray and ultrasound results were negative. It is believed that MS suffered an unintentional bone injection with her EAI based on clinical presentation following the allergic emergency. At 9 years old, her height was 141 cm, weight was 30 kg, and her STBD was 12.1 mm. In 2017, MS was evaluated again for pain and discomfort in her right thigh.\nThe indication for the EpiPen Jr® is for children between 15 and 30 kg and this device has a needle length of 12.7 mm. MS and her parents were made aware that use of her prescribed EAI could cause an unintentional injection to the bone using the standard injection technique with compression. It was suggested that, prior to injection, the vastus lateralis muscle be squeezed as to avoid full compression while using her EAI because of the high risk of unintentional bone injection.\nThis case of possible bone injection was reported to Health Canada.
|
[[10.0, 'year']]
|
F
|
{'26452720': 1, '19441598': 1, '31993272': 2, '25110478': 1, '27271769': 1, '33666759': 1, '20159254': 1, '18694903': 1, '28483294': 1, '26949403': 1, '30151016': 2}
|
{'6970458-1': 1}
|
2,050 |
6100721-1
| 30,122,151 |
comm/PMC006xxxxxx/PMC6100721.xml
|
Conventional cardiopulmonary resuscitation-induced refractory cardiac arrest due to latent left ventricular outflow tract obstruction due to a sigmoid septum: a case report
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A 73-year-old Asian woman with an underlying anxiety disorder, functional headache, and hypertension was prescribed escitalopram and lorazepam when she presented with progressively worsening headaches to her primary care doctor. Her symptoms did not improve with the medications, and she was unable to eat well and required bed rest. She was transported to our hospital 4 days later after developing chest and back pain with altered consciousness. She was a housekeeper, had no allergies, and had no alcohol or tobacco smoking history. On arrival, her Glasgow Coma Scale score was 3/15 (E1V1M1); both pupils were approximately 4 mm in diameter and reactive. Her blood pressure was too low to be measured, her carotid artery pulse was palpable, her heart rate was 112 beats/minute, and her respiratory rate was 30 breaths/minute. Her conjunctiva was pale. An auscultation of breath sounds did not reveal upper and lower airway obstructions and was within normal limits. Her abdomen was soft and flat without tenderness. She had no skin abnormalities (such as rash). Both legs had no edema. Echocardiography on arrival was performed as point of care ultrasound and revealed a hypercontractile left ventricle with an eliminated left ventricular cavity and a collapsed inferior vena cava without right ventricular dilation. There was no pericardial effusion or obvious large regurgitant jet observed on color Doppler. In response, we immediately inserted a peripheral venous catheter and began introducing fluid resuscitation; however, she developed PEA. Conventional CPR according to the adult advanced cardiovascular life support guidelines (including adrenaline) was initiated and a return of spontaneous circulation (ROSC) occurred. However, her blood pressure was unstable and PEA returned, prompting repeated CPR with immediate administration of fluids and three adrenaline injections. Venoarterial extracorporeal membrane oxygenation (VA-ECMO) was initiated for refractory PEA. Whole-body contrast-enhanced computed tomography was unremarkable, and the admission laboratory results were also unremarkable, except for anemia (Table ). Her hemoglobin level decreased from 7.1 g/dL to 3.5 g/dL 1 hour later without obvious signs of gastrointestinal hemorrhage. Therefore, 8 units of packed red blood cells were transfused for 1 day, after which her hemodynamic status stabilized. She was in a coma without sedatives; thus, targeted temperature management at 34 °C was initiated on admission to an intensive care unit. Echocardiography in the intensive care unit showed a thickened interventricular septum (which was 12.8 mm), prolonged anterior mitral valve, and contact between the bodies of the anterior and posterior mitral valves, suggesting that the left ventricular obstruction could have potentially occurred through this redundant anterior mitral valve. VA-ECMO was terminated on day 3, and after stabilizing her hemodynamics, transthoracic echocardiography showed a sigmoid septum with normal left ventricular function (ejection fraction, 75%) (Fig. ). On day 26, dobutamine-infused (30 μg/kg per minute) Doppler echocardiography revealed a significant outflow gradient (236 mmHg) accompanied with chest pain (Fig. ) and intermittent systolic anterior motion (SAM) of the mitral valve; continuous monitoring during Doppler echocardiography showed a Brockenbrough–Braunwald sign (Fig. ), which is a fall of arterial blood pressure after premature ventricular contraction; these findings confirmed a diagnosis of latent LVOTO due to a sigmoid septum. The significant LVOTO was not dependent on SAM but might have occurred due to the greatly thickened interventricular septum. As a result, carvedilol was initiated with gradual increment up to 10 mg/day on day 35. In addition, verapamil (120 mg/day) was administered on day 29. A follow-up dobutamine-infused Doppler echocardiography on day 40 showed a reduction of the outflow gradient to 14 mmHg, indicating a successful medical therapy.\nThe worsening anemia that was identified at admission was suspected to be hemolytic anemia (HA) based on results of the blood test. The results of the laboratory examination, including total bilirubin, direct bilirubin, lactate dehydrogenase, reticulocyte count, and haptoglobin, and a direct Coombs test on day 1 are presented in Table . Her drug lymphocyte stimulation test was positive, and agglutination occurred when her serum reacted with lorazepam. Therefore, lorazepam-induced immunological HA was diagnosed. Her anemia improved following discontinuation of lorazepam. Her hemoglobin level was 11.9 g/dL on day 64, and she was eventually discharged on day 68 without any sequelae.
|
[[73.0, 'year']]
|
F
|
{'26702321': 1, '21801200': 1, '28921420': 1, '16754630': 1, '25173338': 1, '26472995': 1, '27559948': 1, '18657666': 1, '12540642': 1, '4672681': 1, '12420671': 1, '30122151': 2}
|
{}
|
2,051 |
6101150-1
| 30,186,991 |
comm/PMC006xxxxxx/PMC6101150.xml
|
First report of Vulvovaginitis due to Cryptococcus magnus in Iran
|
A 23-year-old married female patient presented to one of the hospitals of Damavand city, Tehran, Iran, due to severe itching and vaginal irritation. Vaginal examination revealed thick, curdle-like, white-colored discharge, edema, and intense pruritus of the vulva. The vagina and labia were erythematous. She was using an intra-uterine device (IUD) as a contraceptive method.\nDue to the suspected diagnosis of vulvovaginal candidiasis, fresh samples of vaginal discharge were sent for mycological examination to the Division of Mycology, School of Medicine, Shahid Beheshti University of Tehran, Iran. Vaginal discharge was sampled by using a speculum and sterile swab. The swab was transported to the laboratory into normal saline. Two specimens were obtained under sterile conditions, one for microscopic examination and the other for fungal culture. A slide was prepared for Methylene blue staining. The vaginal swab was inoculated on Sabouraud Dextrose Agar (SDA; Merck, Germany) [] and incubated at 30°C for 24 h. The produced cream-colored colonies were slightly mucoid, smooth, highly glossy, and slim in texture that were indistinguishable from Candida spp. colony. After three days, the cream color changed to pink ().\nMicroscopic examination of the culture after 48 h showed round to oval yeast, single or pairs of cells without true hyphae or pseudohyphae and without capsule in Indian ink ().\nGenomic DNA was extracted from culture using glass bead method [6]. Then, the ITS regions of rDNA gene of isolates was amplified by the universal fungal primers, ITS1 (5´-TCCGTAGGTGAACCTGCGG-3´) and ITS4 (5´-TCCTCCGCTTATTGATATGC-3´) []. The PCR product was applied for the accurate identification of isolate (Bioneer, Korea). For confirmation of species identity, the obtained sequences were compared with similar sequences in the open access NCBI database (http://blast.ncbi.nlm.nih.gov/Blast.cgi). Alignment of the obtained sequence in BLAST revealed a 100% identity with the type strain of Filobasidium magnum, which is indicated with sequence ID: MG786767.1 and high homology (99%) with Cryptococcus magnus with sequence ID: GU237052.1. The sequences were in GenBank under accession number ‘‘MG786767-1.’’\nAntifungal susceptibility tests were performed by broth micro dilution method as described in Clinical and Laboratory Standards Institute [8] guidelines, document M27-S3 []. C. parapsilosis type strain (ATCC 22019) was used for quality control in all antifungal susceptibility tests. Tests were performed in 96-well round-bottom microtiter plates. Drug concentration ranges were 0.03 to 64 μg/ml for itraconazole (ITC), fluconazole (FLC), ketoconazole (KTC), and amphotericin B (AMB). Cell suspensions were prepared in RPMI 1640 medium (Invitrogen, USA) and were adjusted to give a final inoculum concentration of about 0.5 × 103 to 2.5 × 103 cfu/ml. The plates were incubated at 35°C for 48 h. Minimum inhibitory concentration (MIC) was then determined and compared with a drug-free control. All the tests were performed in duplicate [, ].\nThe MIC values for ITC, KTC, AMB, and FLC were 0.031 μg/ml, 0.031 μg/ml, 0.062 μg/ml, and 0.062 μg/ml respectively, revealing the sensitivity of the mentioned causative agent. The patient received treatment with topical ketoconazole ointment, but there were no signs of recovery after seven days. Then, the patient was finally treated successfully using 200 mg daily of oral ketoconazole in 10 days. No further clinical signs of vaginal infection were observed after six months. Relapse of the infection was not revealed in two, four, and six-months follow up of the patient. No clinical manifestations were shown at the involved site.\nThe Ethics Committee of Shahid Beheshti University of Medical Sciences in Iran approved this study (ethics committee code: IR.SBMU.MSPPP.REC.1395.3).
|
[[23.0, 'year']]
|
F
|
{'10074502': 1, '34663233': 1, '3679221': 1, '18032039': 1, '19351253': 1, '27141494': 1, '15180152': 1, '20513171': 1, '31766661': 1, '31750814': 1, '20979444': 1, '33917243': 1, '8748273': 1, '397620': 1, '15774599': 1, '3895072': 1, '16984867': 1, '30186991': 2}
|
{}
|
2,052 |
6101440-1
| 30,131,922 |
comm/PMC006xxxxxx/PMC6101440.xml
|
Management of Biliary Stricture Following Emergent Pancreaticoduodenectomy for Trauma: Report of Two Cases
|
Case 1: An 18-year-old male sustained a single gunshot wound to the abdomen. Exploratory laparotomy demonstrated the following injuries. Liver laceration was found in segment five, it was controlled with two sutures on a blunt needle and hemostatic matrix. The colon was found to have avulsion of the mesentery with obvious ischemia to the hepatic flexure, secondary to transection of the middle colic vessels. It was managed with right hemicolectomy and end ileostomy. Duodenum was found to have an entrance and exit wound involving the ampulla of Vater and distal common bile duct. He underwent PD with choledochojejunostomy, pancreaticojejunostomy, and gastrojejunostomy at the index operation.\nHis post-operative course was complicated by a high-grade obstruction at the biliary anastomosis (Figure ). Serial attempts at percutaneous cholangioplasty and stenting (Figure ) were unsuccessful, which was demonstrated by persistently elevated total serum bilirubin levels (>2.0mg/dL). Therefore, long-term percutaneous transhepatic drainage (PTD) was performed. After several months of catheter decompression, a subsequent attempt at cholangioplasty was again unsuccessful. The patient then underwent operative revision of the anastomosis to hepaticojejunostomy. He had no procedural complications and no evidence of restricturing at three-month follow-up.
|
[[18.0, 'year']]
|
M
|
{'24841125': 1, '17929105': 1, '26130436': 1, '16632990': 1, '23823615': 1, '14644281': 1, '8222749': 1, '30131922': 2}
|
{'6101440-2': 2}
|
2,053 |
6101440-2
| 30,131,922 |
comm/PMC006xxxxxx/PMC6101440.xml
|
Management of Biliary Stricture Following Emergent Pancreaticoduodenectomy for Trauma: Report of Two Cases
|
Case 2: A 16-year-old male sustained multiple gunshots and presented to the trauma bay in hemorrhagic shock. He was taken immediately for emergency laparotomy and injuries identified were injury to two segments of the small bowel, injury to the inferior vena cava (IVC), grade four injury to the right kidney, and destructive injury to the head of the pancreas. Right nephrectomy, IVC ligation, small bowel resection, and PD without reconstruction were performed at first operation. At planned re-exploration on postoperative day two, biliary continuity was accomplished with hepaticojejunostomy.\nThe patient had a complicated post-operative hospital stay, including ventilator-acquired pneumonia and hemodialysis requirement. However, he was discharged home in good health after 68 days. Three years later, the patient developed symptomatic stricture of the hepaticojejunostomy. ERCP was attempted but without success in reaching the biliary limb. The stricture was managed by interventional radiology using percutaneous transhepatic catheterization with serial balloon dilation. The transhepatic catheter was removed after six months, and the patient has no signs of obstructive jaundice six months later.
|
[[16.0, 'year']]
|
M
|
{'24841125': 1, '17929105': 1, '26130436': 1, '16632990': 1, '23823615': 1, '14644281': 1, '8222749': 1, '30131922': 2}
|
{'6101440-1': 2}
|
2,054 |
6101442-1
| 30,131,933 |
comm/PMC006xxxxxx/PMC6101442.xml
|
Intracranial Calcification Masquerading as Hemorrhage in a Patient with Multiple Myeloma Presenting with Facial Neuropathy
|
A 75-year-old Caucasian male presented to the emergency room with the chief complaint of left-sided facial weakness. He noticed the weakness while brushing his teeth, and also noted slurred speech. He denied eye pain, tearing or redness, hearing loss, difficulty with swallowing, and weakness or numbness in his extremities. He was able to understand and express his words without any difficulty. He denied any headache, gait problems, falls or recent illness, and prior history of stroke or seizures. Past medical history was positive for hypertension, hyperlipidemia, diabetes mellitus, and multiple myeloma (MM). He was on chemotherapy with ixazomib, acyclovir prophylaxis, and a daily aspirin. Vital signs were unremarkable. Physical examination was significant for lower facial muscle weakness with no difficulty in closing the left eye. His National Institutes of Health (NIH) stroke scale was two for facial weakness and dysarthria.\nHis blood work was remarkable for mild anemia and normal serum calcium. Coagulation workup was unremarkable. A non-contrast computerized tomography (CT) of the head showed acute intraparenchymal hemorrhage in the right parietal region with global cerebral atrophy (Figure -), (repeat CT of the brain four weeks later showed the same hyperdensity; see Figure ).\nHowever, CT angiogram of the head and neck was unremarkable. On day two, he was unable to close his left eye with Bell’s phenomenon. The differential diagnosis considered were lower motor neuron (LMN) facial palsy from multiple myeloma or diabetes mellitus or focal seizure from acute right parietal intracerebral hemorrhage. Magnetic resonance imaging (MRI) of the brain showed hyperintensity in T1-weighted sequence (Figure ), no significant post-contrast enhancement (Figure ), blooming artifact in the susceptibility weighted imaging (SWI) (Figure ), and hyperintensity in T2-weighted fluid attenuation and inversion recovery (FLAIR) test (Figure ) consistent with possible right parietal hemorrhage or calcification.\nVaricella zoster antibody test was negative. Monoclonal protein analysis showed an atypical restricted band in the lambda region consistent with monoclonal gammopathy. Given the LMN type of facial weakness, we provisionally diagnosed him with Bell’s palsy. Focal seizure was clinically ruled out as a possibility due to persistent facial weakness with no fluctuation. We started him on valacyclovir 1000 mg three times daily for seven days with a subsequent switch to his home oral acyclovir chemoprophylaxis for multiple myeloma (400 mg by mouth twice daily) and oral prednisone taper. At the four weeks follow-up appointment, his symptoms improved to a mild residual weakness of the left lower face, but he was able to close his eyes completely. Follow-up CT of the brain showed the same hyperdensity in the right parietal region consistent with intracerebral calcification without surrounding edema (Figure ).
|
[[75.0, 'year']]
|
M
|
{'24384965': 1, '18332230': 1, '3246115': 1, '2051036': 1, '3587557': 1, '27902730': 1, '8273615': 1, '28627953': 1, '19124139': 1, '20031303': 1, '17522337': 1, '26602603': 1, '1786668': 1, '24126366': 1, '23210572': 1, '24385728': 2, '16026744': 1, '25972938': 2, '17577791': 1, '30131933': 2}
|
{'4421944-1': 1, '3781618-1': 1}
|
2,055 |
6101451-1
| 30,131,916 |
comm/PMC006xxxxxx/PMC6101451.xml
|
Malignant Melanoma Metastasizes to Colonic Polyp
|
A 74-year-old Caucasian male had a past medical history of hypertension and gout. He was also diagnosed with melanoma of left ear at left medial antihelix seven years ago, and it was stage IIB and treated with wide local excision and sentinel lymph node excision. Two years later, he developed recurrent melanoma of left ear, and it was staged IIIB treated with left aurilectomy. He underwent colon cancer screening. His stool was positive for blood. He underwent colonoscopy and was found to have three polyps. One polyp was 1 cm in ascending colon, 1 cm polyp in the sigmoid colon, and 4.5 cm polyp in sigmoid colon. Differential diagnosis was benign polyp, and primary colon cancer.\nBiopsy displayed malignant melanoma in the largest polyp in sigmoid colon with negative margins. Tumor cells were positive for melanin A and negative for MCK. Histopathology confirmed malignant melanoma in sigmoid colonic polyp (Figures , ). Molecular analysis showed NRAS Q61R mutation (NRAS is in the Ras family of oncogenes), B2M copy number loss. Other two polyps showed tubular adenoma. All polyps were resected. His previous colonoscopy 12 years ago was normal. Endoscopy did not reveal any polyp in the stomach or small intestine.\nPositron emission tomography or computed tomography (PET/CT) exhibited increased fludeoxyglucose avidity in right adrenal gland, gallbladder, and in right orbital apex avidity. It also showed hyper-metabolic ac nodule in the left orbital apex, and no recurrence at the left auricular region. Hyper-metabolic activity was seen in gallbladder of the size of 1.57 cm and right adrenal of 1.8 x 1.2 cm. Magnetic resonance imaging of the brain showed no evidence of metastases.\nThe patient was started on pembrolizumab. He was closely followed up with the oncologist. Repeated PET/CT displayed stable activity in right adrenal gland, gallbladder, and right orbital apex. The patient was tolerating immunotherapy well, and he has no new complaint during follow-up three months later.
|
[[74.0, 'year']]
|
M
|
{'28533659': 1, '26616020': 1, '17663525': 1, '12682534': 1, '23553262': 1, '20658527': 1, '30131916': 2}
|
{}
|
2,056 |
6101456-1
| 30,131,928 |
comm/PMC006xxxxxx/PMC6101456.xml
|
Craniotomy Improves Traumatic Optic Neuropathy
|
A 46-year-old gentleman who was well pre-morbidly was admitted to our neurosurgery department after allegedly sustaining a fall from about three meters' height while attempting to climb a tree. He landed head down on his left frontotemporal region against a rock. Immediately after the impact, he sustained loss of consciousness. He complained of severe blurring of vision when he regained consciousness five minutes later. It was associated with pain over his left eye. He was brought to the hospital six hours later.\nAt the time of presentation, his Glasgow Coma Scale (GCS) was 15. The visual acuity was 6/18 in the right eye and 6/60 in the left eye. A grade II relative afferent pupillary defect (RAPD) was well demonstrated in the left eye. Ocular motilities were full over the right eye. However, clinically there was a marked restriction of ocular movement in all gazes over the left eye. Light brightness and red desaturation of the left eye were reduced compared to the right eye. Intraocular pressures were 13 mmHg and 19 mmHg in the right and left eye respectively. Examination of the ocular adnexa revealed a periorbital ecchymosis and severe chemosis over the left eye. Anterior segment evaluation of both eyes was normal. There was no hyphema, iris sphincter tears or penetrating injury to the cornea, conjunctiva, or sclera of either eye. Bilateral fundoscopy showed normal optic disc and macular.\nAn emergency computed tomography (CT) scan of brain and orbit was performed and showed a left frontotemporoparietal extradural hemorrhage with multiple comminuted fractures in the left frontotemporoparietal bone and greater wing of sphenoid fracture with a bony spur abutting and impinging the left lateral rectus and indirectly the optic nerve on the same side (Figure ).\nA diagnosis of the left frontotemporoparietal skull fracture with left eye traumatic optic neuropathy (TON) was made. Being co-managed by neurosurgical team, a left craniotomy, elevation of depressed frontotemporoparietal skull fracture, and evacuation of clots was done 12 hours post-trauma (Figure ). Intraoperatively, it was noted that the bony impingement was relieved once the depressed skull fracture was elevated. Hence, no further orbital exploration was done.\nThe surgery went well and was uneventful. However, the patient was not started on systemic corticosteroid in view of the intracranial bleed. Two days post-operation, his visual acuity improved to 6/6 for both eyes and the RAPD was absent. The other optic nerve function test was also normal. There was also marked improvement in his extra-ocular motility clinically. During discharge, the condition was stable. He was referred to his hometown hospital for continuation of the treatment. The follow-up six months post-operatively reveals a stable visual acuity and visual fields.
|
[[46.0, 'year']]
|
M
|
{'12059868': 1, '2381671': 1, '26052483': 1, '2725887': 1, '7470234': 1, '8066541': 1, '5490277': 1, '15534597': 1, '7099563': 1, '32431973': 2, '3434336': 1, '10406604': 1, '30131928': 2}
|
{'7233501-1': 1}
|
2,057 |
6101457-1
| 30,131,932 |
comm/PMC006xxxxxx/PMC6101457.xml
|
Symptomatic Meckel’s Cave Metastasis from Castration-resistant Prostate Cancer Treated with Gamma Knife Radiosurgery
|
The patient was a 64-year-old male with a history of diffusely metastatic castration-resistant prostate cancer. The disease was initially discovered due to an elevated prostate-specific antigen (PSA) of 4-5 in 2005 with two negative prostate biopsies. His PSA level went up to 9.0 and eventually to 78.4. Magnetic resonance imaging (MRI) at that time revealed a large prostate with the disease in the left pelvic lymph node, extracapsular extension, and a left hip pathologic fracture. A pelvic lymph node biopsy revealed prostate adenocarcinoma in June 2016. The patient was started on triptorelin in June 2016, followed by leuprolide acetate, bicalutamide, and denosumab soon after. Palliative radiation therapy to the left hip and femur and open reduction internal fixation were performed. In spite of this, his PSA continued to rise in December 2016 and a positron emission tomography/computed tomography (PET/CT) scan revealed diffuse osseous disease in the axial and appendicular skeleton and pelvic lymphadenopathy. Casodex was withdrawn, and the patient was started on abiraterone and prednisone in April 2017. Unfortunately, he developed a new osseous right femoral lesion which was treated with palliative radiation therapy. A PET/CT scan revealed further progressive osseous disease and pelvic lymphadenopathy. Abiraterone was stopped and docetaxel was initiated in addition to prednisone in September 2017. A bone marrow biopsy revealed extensive involvement of metastatic prostate cancer. Denosumab was stopped and enzalutamide was started in December 2017. In January 2018, enzalutamide was stopped due to intolerance.\nHe presented to us one year and seven months after his pathologic diagnosis for treatment of a single lesion measuring 1.4 x 1.0 x 1.3 cm in the Meckel’s cave contiguous with the left cranial nerve V with some extension into the prepontine cistern. This was consistent with being metastatic cancer on radiologic appearance as illustrated in Figure . The patient developed left forehead and cheek numbness two weeks prior to presenting to our clinic. This led to difficulty with eating secondary to numbness. Objectively, there was numbness in the left-sided ophthalmic branch of the cranial nerve V. His other medical problems included well-controlled diabetes type 2, hypertension, depression, and various complications of his cancer treatment which impaired his functional status including leg numbness since his deep vein thrombosis (DVT) status post inferior vena cava (IVC) filter placement, cancer-related bone pain on oxycodone, fatigue, tingling and numbness in his hands, pancytopenia and osteonecrosis of the jaw. Given that this patient had widespread castration-resistant prostate cancer with a metastatic lesion causing cranial nerve dysfunction, he had a very poor prognosis. Treatment with radiotherapy was initiated without a pathologic confirmation to produce the most rapid symptomatic relief without morbidity and possible mortality associated with biopsy and surgical resection.\nA radiation therapy dose of 22 Gy was given to the 50% isodose line via 17 shots, delivered via Leksell Gamma Knife produced by Elekta (Stockholm, Sweden) to the gross tumor volume (GTV) of 2.11 cc with palliative intent. The treatment plan is shown in Figure . Tumor coverage was 100%. Maximum dose was 44 Gy. The patient’s head was immobilized using a Gamma Knife Perfexion (Elekta, Stockholm, Sweden) head frame with metal pins. Constraints for all organs at risk were met. There were no complications from the procedure.\nOn a one-month follow-up, the patient’s facial sensation has improved, leading to a better ability to eat. No additional cranial nerve dysfunction or other neurologic deficits were noted. No side effects attributable to Gamma Knife radiosurgery were observed. The patient decided to stop undergoing systemic chemotherapy soon after his last follow-up visit with us stating that chemotherapy caused fatigue and that the infusion center visits took up too much of his time. The patient elected to go home on hospice care. Unfortunately, the patient died three months after the Gamma Knife procedure. No new neurologic deficits or Gamma Knife side effect were recorded.
|
[[64.0, 'year']]
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M
|
{'25434942': 1, '12872358': 1, '34430094': 2, '32995454': 1, '16215817': 1, '20728984': 1, '29040711': 1, '20436844': 1, '33718819': 1, '29296364': 1, '25510811': 1, '26294996': 2, '30131932': 2}
|
{'8372691-1': 1, '4534606-1': 1}
|
2,058 |
6101459-1
| 30,131,915 |
comm/PMC006xxxxxx/PMC6101459.xml
|
Not Your Usual Suspect: Clear Cell Renal Cell Carcinoma Presenting as Ulcerative Esophagitis
|
An 82-year-old Caucasian male presented with dark tarry stools for two days, progressive dysphagia to solid food for several weeks and significant unintentional weight loss. His past medical history was significant for hypertension, diverticulosis and right-sided renal cell cancer for which he underwent nephrectomy 13 years ago. He denied family history of gastrointestinal (GI) malignancies. He also denied use of non-steroidal anti-inflammatory drugs, antiplatelet or anticoagulants, smoking, and drinking. Physical examination was unremarkable for hepatosplenomegaly, lymphadenopathy, and blood in the rectal vault. Laboratory data showed a hemoglobin of 12.5 g/dL, with normal platelet count and international normalized ratio (INR). His stools were positive for occult blood. Esophagogastroduodenoscopy (EGD) revealed a fragile mid esophageal mass and antral erosive gastritis which were both biopsied. Colonoscopy showed diverticulosis without stigmata of active GI bleed. Computed tomography (CT) scan of the chest showed a solid esophageal mass in lower esophagus measuring 5 x 4 x 7 cm3 (Figures -).\nIt also revealed a right upper lobe lung mass (Figure ) for which the patient underwent a CT-guided needle biopsy procedure.\nThe histopathology report of esophageal mass revealed an erosive and ulcerated esophageal mucosa with underlying metastatic renal cell cancer of clear cell subtype (Figures -).\nSubsequently, pulmonary nodule was also confirmed as metastatic renal cell cancer. The patient was started on palliative radiotherapy and was discharged. On completion of radiotherapy two months later, his dysphagia had resolved. The patient is currently on chemotherapy with Sunitinib.
|
[[82.0, 'year']]
|
M
|
{'7615361': 1, '3761436': 1, '9438004': 1, '1195458': 1, '25075797': 1, '19434703': 1, '3325678': 1, '34544382': 2, '25620904': 2, '33977239': 2, '9626229': 1, '30131915': 2}
|
{'8088885-1': 1, '8454032-1': 1, '4297612-1': 1}
|
2,059 |
6101460-1
| 30,131,920 |
comm/PMC006xxxxxx/PMC6101460.xml
|
Amyand’s Hernia: A Rare Surgical Pathology of the Appendix
|
A 24-year-old female presented to our surgical outpatient department with the complaint of an asymptomatic swelling in the right inguinal region for the past two years. Her clinical predicament subsequently worsened with the onset of a sharp stabbing pain in her right inguinal region, with associated nausea and vomiting for two days. She also provided a history of a low-grade fever. There was no history of abdominal distention and constipation. Initial assessment found the patient to be alert, well-oriented and in no apparent distress. Her heart rate was 98 beats per minute with a blood pressure of 130/75 mm Hg, a respiratory rate of 16 per minute and a temperature of 99.4°F. An abdominal exam revealed no scar-mark of a previous cesarean section. She was found to have a non-distended abdomen with tenderness in the right inguinal region. A 5 cm x 7 cm irreducible mass with normal overlying skin was noted in the right inguinal region with an expansile cough reflex. All other hernial orifices were intact. Normal bowel sounds were perceptible on auscultation. A digital rectal exam revealed an empty rectal vault. Per our clinical exam, the patient was diagnosed as a usual case of a right-sided inguinal hernia. She was admitted and scheduled for an open herniorrhaphy. The details of her pre-operative investigations are described in Table .\nIntraoperatively, a 10-cm incision was made in the right inguinal region and the hernial sac was approached. Upon opening the sac, the appendix was discovered within the hernial pouch. On gross examination, the appendix was enlarged, edematous and approximately 10 cm in length. Figure shows our intra-operative findings.\nConsequently, an appendectomy was performed followed by a tension-free darn repair. The postoperative period was uneventful and our patient has had a favorable clinical outcome to date.
|
[[24.0, 'year']]
|
F
|
{'22879848': 1, '18186392': 1, '22548145': 1, '19626272': 1, '20740297': 1, '24963899': 2, '18214637': 1, '21292218': 1, '30131920': 2}
|
{'3813824-1': 1}
|
2,060 |
6101461-1
| 30,131,931 |
comm/PMC006xxxxxx/PMC6101461.xml
|
Hemophagocytic Lymphohistiocytosis Complicating Systemic Sarcoidosis
|
A 36-year-old female presented with fever, weight loss, enlarged right axillary lymph node, and bilateral pulmonary infiltrates. The axillary lymph node biopsy (Figure ) revealed noncaseating granulomas typical for sarcoidosis. The patient was started on steroids and showed only mild improvement in symptoms.\nOver the next few months, she exhibited gradually increasing leukopenia and thrombocytopenia [white blood cell (WBC) count 1.5-4 × 109/l and platelet count 45-100 × 109/l]. A bone marrow biopsy was performed, and it confirmed the presence of noncaseating sarcoid granulomas. The patient was maintained on steroids, but no improvement in cytopenia was noted.\nOne year after diagnosis, she presented again with fever, fatigue, and hepatosplenomegaly. Laboratory workup revealed the following: WBC count 0.1 × 109/l, hemoglobin 5.5 g/dl, platelet count 9 × 109/l, total bilirubin 1.4 g/dl, aspartate aminotransferase (AST) 151 IU/l, alanine aminotransferase (ALT) 125 IU/l, lactate dehydrogenase (LDH) 317 U/l, alkaline phosphatase (ALP) 423 IU/l, and ferritin 67,590 ng/ml. The patient was treated with antibiotics but was persistently febrile. Blood cultures and viral and fungal studies were negative. Given worsening pancytopenia, very high ferritin and liver dysfunction, MAS was suspected. The fasting triglyceride level was 292 mg/dl, and the D-dimer level was 1001 ng/dl. However, the fibrinogen levels were normal. The sCD25 level was 10,440 pg/ml (ref < 1000 pg/ml) and the natural killer (NK)-cell activity was 4 LU30 (normal 7-125 LU30). A bone marrow biopsy (Figure ) demonstrated hypocellular marrow with normal hematopoiesis replaced by proliferation of histiocytes and vague granulomas. Grocott-Gomori's methenamine silver (GMS) stain and acid-fast bacilli stain (AFB), CD1a, S100, and CD23 were negative.\nMagnetic resonance imaging (MRI) of the brain revealed diffuse pachymeningeal enhancement. Despite the absence of hemophagocytosis, she met the remainder of the criteria for HLH. The patient did not respond to a trial of intravenous immunoglobulin (IVIG) and 1 g/d methylprednisolone. She developed encephalopathy and status epilepticus and was transferred to another facility for escalated care. She died shortly after the transfer.
|
[[36.0, 'year']]
|
F
|
{'12051388': 1, '7892057': 1, '24782338': 1, '19932759': 1, '22464018': 1, '16937360': 1, '23147060': 1, '3981309': 1, '18782855': 1, '21828139': 1, '23271259': 1, '18854090': 1, '14558048': 1, '8980272': 1, '32517812': 1, '31431835': 2, '23104659': 1, '32315294': 1, '21257627': 1, '30131931': 2}
|
{'6695236-1': 1}
|
2,061 |
6101463-1
| 30,131,925 |
comm/PMC006xxxxxx/PMC6101463.xml
|
Ranolazine-induced Elevation of Creatinine Kinase in the Absence of Statin Usage
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A 33-year-old female with sickle cell trait, anxiety, miscarriages (twice), late-onset Raynaud’s phenomenon, and fibromyalgia, initially presented with chest pain and elevated troponin level. Her local physician found a negative cardiac workup, and subsequently she was initiated on ranolazine for treatment of suspected coronary vasospasm.\nShe presented to a local hospital for evaluation of intermittent and increasing non-exertional chest pain and mild shortness of breath about four weeks after hysterectomy. On admission, she was noted to have an elevated troponin I level at 0.28 (normal <0.02), which downtrended to 0.26. She had a cardiac evaluation with a technetium-99m sestamibi stress test that revealed no evidence of ischemia. Computed tomography (CT) with contrast showed no evidence of pulmonary consolidation or pulmonary embolism. She was diagnosed with suspected coronary vasospasm. Her chest pain resolved on ranolazine 500 mg twice daily, however, within one week, she developed generalized myalgia. Follow-up labs revealed creatinine kinase (CK) levels to be 4551 U/L (range 26-308). Aldolase elevated at 32.4 U/L (range 3.3-10.3). Other pertinent labs included an elevated aspartate aminotransaminase of 101 U/L, normal alanine aminotransaminase, positive antinuclear antibody (ANA) (1:160, homogenous), and erythrocyte sedimentation rate (ESR) at 1 mm/hr. The ranolazine was held with the improvement of myalgia symptoms. Repeat lab testing two weeks later was notable for CK of 76 U/L. Evaluation by neuromuscular and rheumatologist confirmed undifferentiated connective tissue disease based on positive ANA, late-onset Raynaud’s, alopecia, and no signs to suggest an autoimmune inflammatory myositis.\nHer serology was negative for anti-double-stranded DNA, anti-Jo-1, anti-Scl-70, anti-Smith, anti-SS-A, anti-SS-B, and anti-cyclic citrullinated peptide (CCP). Other workup included normal C3, C4, comprehensive metabolic panel (CMP), complete blood count (CBC), ESR, C-reactive protein (CRP), anti-cardiolipin panel, anti-B2glycoprotein, dilute Russell viper venom time (dRVVT), and comprehensive Oklahoma Medical Research Foundation (OMRF) myositis antibody panel. She was evaluated by a neuromuscular team. Cardiac and lower extremity magnetic resonance imaging (MRI) showed no evidence of inflammation. Electromyography (EMG) with nerve conduction study (NCS) and left thigh muscle biopsy also did not reveal evidence of inflammatory myopathy.\nAt last follow-up, the patient had no recurrence of myalgias 10 months after discontinuing ranolazine. CK and aldolase have remained within normal limits at 82-138 and 5.8-7.4 (aldolase range 3.3-10.3), respectively.
|
[[33.0, 'year']]
|
F
|
{'20966146': 1, '17349881': 1, '25466697': 1, '23492463': 1, '19099014': 1, '19389561': 1, '15778423': 1, '30131925': 2}
|
{}
|
2,062 |
6101464-1
| 30,131,924 |
comm/PMC006xxxxxx/PMC6101464.xml
|
Mycobacterium Kansasii Infection and Microscopic Polyangiitis: An Unexpected Association
|
A 27-year-old man was admitted to our hospital with a two-week history of hemoptysis, shortness of breath, and fever. He reported fatigue, night sweats, bilateral knee pain, and a rash on his back and chest. Two months prior to this admission, the patient developed acute onset of nonproductive cough associated with generalized weakness and muscle pain. For his musculoskeletal symptoms, the patient was prescribed prednisone 20 mg daily for five days by his primary care physician without improvement in his symptoms.\nAt the time of admission, his blood pressure was 130/69 mmHg, heart rate was 99 bpm, temperature was 37.8°C (100°F), and respiratory rate was 17 breaths per minute. He was found to have bilateral diffuse rales on chest auscultation and a morbilliform rash on his back and upper chest. Laboratory studies showed his white blood cell count was 13.2 × 103/ml, erythrocyte sedimentation rate was 122 mm/hour (reference rate, <20 mm/hour), hemoglobin was 10.4 g/dl, serum creatinine was 1.48 mg/dl (reference range, 0.6–1.1 mg/dl), and glomerular filtration rate was 57 ml/min/1.73 m2 (reference rate, > 90 ml/min). Urinalysis showed proteinuria and hematuria with few red blood cell casts. A radiograph of the chest demonstrated diffuse nodular reticular interstitial opacities and right upper lobe cavitation (Figure ).\nThe patient was admitted to the intensive care unit with respiratory failure, and he was intubated. A computed tomography scan of the chest revealed a 4.7-cm right upper lobe cavitary lesion and multiple bilateral nodules in a miliary pattern throughout the lungs with mediastinal lymphadenopathy (Figure ).\nGiven the clinical features and imaging findings, we considered an infection with mycobacterium tuberculosis as the main cause of his symptoms. Therefore, empirical treatment with rifampin (600 mg oral daily), ethambutol (1200 mg oral daily), isoniazid (300 mg oral daily), and pyridoxine (50 mg daily) was initiated. The patient underwent bronchoscopy, the findings of which were unremarkable and acid-fast bacilli (AFB) smear and cultures were sent. In addition, pulmonary-renal syndrome was included in our differential diagnosis based on hemoptysis, hematuria, and proteinuria. Thus, immunologic studies were obtained, and the p-ANCA was positive, with a titer of 1:160 (negative, < 1:20) as well as the anti-myeloperoxidase (MPO) antibody with a titer of 150 U/mL (negative, < 9). Antinuclear antibody, proteinase-3 antibody, and glomerular basement protein antibody were not detected. The results of the QuantiFERON-TB gold test was indeterminate, human immunodeficiency virus (HIV) antigen and antibody test results were negative, and coccidioidomycosis antibodies IgM and IgG test results were normal. Further evaluation with renal biopsy demonstrated crescentic and necrotizing glomerulonephritis (Figure ) with mesangial immune complex deposits and 25% tubulointerstitial fibrosis. Given the hemoptysis, cavitary lung lesion, renal failure due to necrotizing glomerulonephritis, elevated anti-MPO antibody levels, the absence of upper respiratory system symptoms, and granulomas on renal biopsy, the patient was diagnosed with MPA and treatment with prednisone 60 mg daily was initiated. Due to concerns for an active mycobacterial infection, the patient was not treated with intravenous (IV) corticosteroids and/or immunosuppressive agents like rituximab or cyclophosphamide. His symptoms were slowly improving, and the patient was extubated. Two weeks later, multiple sputum AFB stains (Figure ) and cultures were found to be positive for M. kansasii, which confirmed our suspicion of mycobacterial infection, and we continued the anti-mycobacterial regimen. Considering a serious lethal infectious process and the patient’s clinical improvement, the prednisone was tapered to 30 mg daily, and additional immunosuppressive treatment was deferred until the patient received at least eight weeks of consolidative antimycobacterial therapy. The patient’s symptoms continued to improve, and he was discharged after four weeks of hospitalization.\nUnfortunately, the patient stopped the anti-mycobacterial regimen and prednisone two weeks after he was discharged due to nausea and vomiting. One week later, he experienced recurrent episodes of hemoptysis and shortness of breath, and he was readmitted to the hospital where he was intubated due to acute hypoxic respiratory failure and diffuse alveolar hemorrhage. Renal function and acidosis worsened, and continuous renal replacement therapy was initiated. The working diagnosis was active MPA with coexistent M. kansasii infection. He was started on an anti-mycobacterial treatment, plasmapheresis, IV methylprednisolone 1000 mg daily for three days and then to 60 mg daily, and IV cyclophosphamide 850 mg was given once. Unfortunately, the patient developed shock and multi-organ failure; he was placed on multiple vasopressors and antibiotics without response, and seven days after this admission, he died.
|
[[27.0, 'year']]
|
M
|
{'8783725': 1, '8608642': 1, '17277290': 1, '21605158': 1, '22089093': 1, '9839771': 1, '26927756': 1, '2453802': 1, '16677376': 1, '30131924': 2}
|
{}
|
2,063 |
6101465-1
| 30,131,930 |
comm/PMC006xxxxxx/PMC6101465.xml
|
Thyrotoxic Periodic Paralysis and Cardiomyopathy in a Patient with Graves’ Disease
|
A 34-year-old Hispanic male, diagnosed with Graves’ Disease three years prior to presentation, non-compliant with his medications, presented to the emergency room (ER) with complaints of generalized weakness, palpitations, chest pain and multiple episodes of nausea and vomiting. The patient had been in his usual state of health till a day before admission. Vitals showed his blood pressure to be 137/83 mmHg and heart rate to be 119 beats per minute. Physical exam was significant for proptosis, a systolic flow murmur and upper and lower extremity weakness graded with a three out of five on the strength scale. Blood work showed a potassium of 1.8 millimoles per liter (mmol/l), thyroid stimulating hormone (TSH) 0.02 micro international units/milliliters (mcIU/ml), Free Triiodothyronine (T3) 25.14 picograms/milliliters (pg/ml) and Free Thyroxine (T4) 5.23 nanograms/deciliter (ng/dl). Cardiac troponin was 0.04 nanograms/milliliter (ng/ml). Electrocardiogram showed the patient to be in atrial flutter. In the ER, Propranolol was administered, along with Propylthiouracil and Hydrocortisone to prevent thyroid storm. Morphine was given to manage the pain and Ondansetron for the nausea and vomiting. A central line was placed through the Internal Jugular vein for rapid Potassium repletion. He developed rebound hyperkalemia with a potassium as high as 6.9 mmol/l. The patient was given calcium gluconate, insulin and sodium polystyrene. He was stabilized and admitted to the medical intensive care unit (MICU) for further management. In the MICU, the patient was switched from Propylthiouracil to Methimazole. Hydrocortisone was continued. He had an elevation in his cardiac troponin to 1.52 ng/ml, however, it trended down after the patient was hemodynamically stabilized. Echocardiogram revealed mild to moderately dilated left ventricle, mild to moderately dilated left atrium, severely decreased left ventricular systolic function and an ejection fraction of 26-30%. The patient was diagnosed with cardiomyopathy secondary to thyrotoxicosis. Management was continued with anti-thyroid drugs and Propranolol. On day two, the patient improved clinically, his weakness abated, he did not complain of any chest pain and he did not have any episodes of nausea and vomiting. Physical exam showed an increase in the upper and lower extremity muscle strength to five out of five. The patient's potassium was down to 4.2 mmol/l and thyroid function tests were repeated which showed the TSH, Free T3 and Free T4 trending down. The patient was downgraded to the regular medicine floor and discharged on day nine with Methimazole, Propranolol and Lisinopril, with an outpatient follow-up appointment.
|
[[34.0, 'year']]
|
M
|
{'28638574': 2, '26792255': 1, '17207725': 1, '26623197': 2, '17693226': 1, '885993': 1, '25803030': 1, '32968579': 2, '11081259': 1, '10090117': 1, '15476566': 1, '26834286': 1, '17127140': 1, '22316449': 1, '30131930': 2}
|
{'7505608-1': 1, '5473192-1': 1, '4641601-1': 1, '4641601-2': 1}
|
2,064 |
6101466-1
| 30,131,923 |
comm/PMC006xxxxxx/PMC6101466.xml
|
A Rare Case of Bilateral Adrenal Hemorrhage
|
A 47-year-old male with no known comorbidities was started on a course of oral prednisone (60 mg once daily) following a routine diagnosis of bilateral anterior uveitis, with a consequential improvement in his visual acuity. In the ensuing two weeks, he developed generalized weakness and fatigue, which hindered his ability to walk without assistance. This prompted his visit to our emergency department. In a detailed interview, he did not complain of any chest pain, dyspnea, altered bowel habits, previous syncopal episodes, headaches, dizziness, or prior substance abuse.\nInitial assessment disclosed a patient with bilateral periorbital puffiness, who was visibly lethargic but alert and well-oriented, with a Glasgow Coma Scale (GCS) score of 15/15. His heart rate was 80 beats per minute with a blood pressure of 70/50 mm Hg, a respiratory rate of 20 per minute and a temperature of 98.6°F. An extensive neurological exam revealed 4/5 power in all muscle groups, intact perception to pain, touch, and proprioception, an absence of cerebellar signs or impaired plantar reflexes. An ophthalmological examination revealed normal visual acuity, pupillary reflexes, extraocular movements and fundoscopic examination.\nIn lieu of the severe hypotension, the patient was admitted to the medical floor and started on a combination of intravenous fluids, norepinephrine, hydrocortisone (100 mg every eight hours) as well as tazobactam/piperacillin (4.5 g every eight hours) to treat for any underlying sepsis. His initial laboratory investigations are shown in Table , and Table shows the trend of laboratory investigations over a period of a next few days.\nThe patient underwent an extensive workup to determine the etiology of his generalized weakness and hypotension. An initial diagnosis of septic shock was ruled out following normal blood and urine cultures. A secondary explanation for the elevated total leukocyte count (TLC) with neutrophilia was attributed to the patient’s previous oral prednisone prescription which was supplemented with hydrocortisone injections in the hospital. Due to the previous history of uveitis, and a mild elevation of angiotensin-converting enzyme (ACE) in the blood, we suspected sarcoidosis as a possible cause of his condition, which was further supplemented by the findings on chest x-ray (CXR), which revealed bilateral hilar and perihilar interstitial prominences with bilateral nodular opacities in the middle and lower lung zones (Figure ).\nWe ruled out this possibility owing to the patient’s hasty deterioration and lack of response to the corticosteroid therapy. The patient’s antinuclear antibody (ANA) was negative, and an antineuronal profile ruled out Lambert-Eaton syndrome, myasthenia gravis, and other autoimmune polyneuropathies. Echocardiography revealed an ejection fraction of 60%, which ruled out cardiogenic shock.\nA presumptive diagnosis of Addison crisis was made due to the history of steroid use. Further evaluation to support this diagnosis showed an evening serum cortisol of 59 µg/dL, which was still inappropriately low (considering the patient’s clinical predicament). The adrenocorticotropic hormone (ACTH) level was found to be low (4.17 pg/mL) as well. This was followed by a contrast-enhanced computed tomography (CT) scan of the chest, abdomen, and pelvis, which revealed an enlarged right adrenal gland with a heterogeneous hyperdense area. A smaller heterogeneous lesion was present in the lateral limb of the left adrenal gland (Figure , Figure ).\nA resultant diagnosis of an adrenal crisis was made owing to the clinical presentation, inappropriately low cortisol level in a hypotensive patient and the presence of bilateral adrenal hemorrhage. An ACTH stimulation test was not performed due to the persistently low blood pressure. An intravenous hydrocortisone drip was initiated at a rate of 200 mg per 24 hours to aggressively manage the adrenal crisis secondary to bilateral adrenal hemorrhage (BAH).\nIt is important to note that our patient did not have the classical features of adrenal insufficiency. Serum sodium and potassium levels were mildly low, which was consistent with our vigorous fluid resuscitation; low ACTH levels could be justified by the prior prednisone therapy, which could have been further augmented by the administration of hydrocortisone. Another possible differential diagnosis was panhypopituitarism (due to low thyroid stimulating hormone [TSH] and low ACTH levels); however, normal prolactin levels along with the evidence of BAH made the diagnosis less likely. Low TSH, triiodothyronine (T3), and thyroxine (T4) could also be explained by euthyroid sick syndrome, as these levels were obtained when the patient was critically ill.\nFurther inquiries to determine the causality of BAH ruled out sepsis, owing to a lack of growth in blood and urine cultures. Negative lupus anticoagulant and negative anticardiolipin antibody ruled out antiphospholipid syndrome. Our patient did not have a history of abdominal trauma or recent surgeries. Abdominal CT scan negated the existence of a previous adrenal cyst or signs of previous visceral harm. The patient did not have a history of anticoagulant use, and a coagulation profile ruled out any bleeding diathesis. It was hypothesized that BAH in an otherwise healthy male could have been due to the previous steroid intake. However, no consensus was reached on the etiology of the BAH.\nOn the third day of admission, the patient was transferred to the intensive care unit (ICU) to seek further therapy for persistently low blood pressure. His condition worsened despite vigorous intravenous resuscitation and vasopressor therapy. He subsequently developed a fever of 101°F with an altered mental status (GCS of 12/15) in the ICU and was therefore intubated. On the fourth day of admission, he developed bradycardia, which ultimately disintegrated into to an asystolic rhythm. A cardiopulmonary resuscitation (CPR) was performed for 25 minutes, which did not revive the patient, and care was ultimately withdrawn.
|
[[47.0, 'year']]
|
M
|
{'26760044': 1, '10464802': 1, '26673817': 2, '23458363': 1, '31684918': 2, '25973281': 2, '27855238': 1, '32682452': 2, '32257478': 2, '3980555': 1, '28828107': 1, '25437659': 1, '30131923': 2}
|
{'7470557-1': 1, '6829824-1': 1, '7106905-1': 1, '4417992-1': 1, '4641559-1': 1}
|
2,065 |
6101468-1
| 30,131,918 |
comm/PMC006xxxxxx/PMC6101468.xml
|
Exploring the Excluded Stomach: A Case Series of Novel Endoscopic Techniques to Diagnose Gastric Cancer in the Excluded Stomach After Roux-en-Y Gastric Bypass Surgery
|
A 40-year-old female with RYGB surgery performed 13 years ago for morbid obesity presented with epigastric pain and weight loss. She was recently diagnosed with bilateral metastatic signet cell carcinoma to the ovaries for which she was on chemotherapy. Her family history is significant for gastric cancer in her maternal aunt. CT imaging of the abdomen was unable to reveal the primary source of the tumor. Upper and lower GI endoscopies were unrevealing for malignancy with the upper endoscopy failing to examine the excluded stomach due to the limited length of the scope. The excluded stomach was subsequently approached using ADBE via the afferent limb of the Roux-en-Y bypass. A large infiltrative ulcerated circumferential mass was found in the prepyloric region and antrum of the stomach (Figure ).\nBiopsies were negative for H. pylori infection and revealed invasive signet cell gastric adenocarcinoma (Figure ) that likely had metastasized to the ovaries.\nMolecular analysis showed a human epidermal growth factor receptor 2 (HER2)-negative tumor. The patient is currently undergoing chemotherapy for Stage IV gastric cancer with fluoropyrimidine, plus oxaliplatin (FOLFOX).
|
[[40.0, 'year']]
|
F
|
{'11868296': 1, '15826480': 1, '31001760': 1, '18350638': 1, '17938306': 1, '34977263': 1, '12184547': 1, '23025966': 1, '25651787': 1, '12448395': 1, '23639638': 1, '17938307': 1, '3565686': 1, '25238176': 1, '18280327': 1, '9287934': 1, '21034896': 1, '15014179': 1, '30131918': 2}
|
{'6101468-2': 2}
|
2,066 |
6101468-2
| 30,131,918 |
comm/PMC006xxxxxx/PMC6101468.xml
|
Exploring the Excluded Stomach: A Case Series of Novel Endoscopic Techniques to Diagnose Gastric Cancer in the Excluded Stomach After Roux-en-Y Gastric Bypass Surgery
|
A 50-year-old female with RYGB surgery performed six years previously presented with epigastric pain, nausea, and recurrent gastrointestinal bleeding of nine months duration. Multiple upper and lower GI endoscopies, as well as a video capsule endoscopy, failed to identify the source of her recurrent bleeding. A CT scan of the abdomen showed an obstructing enhancing soft tissue mass at the pylorus measuring approximately 5.5 x 4.5 cm (Figure , arrow) with marked fluid-filled distention of the gastric remnant and normal appearance of the RYGB. It also revealed a small soft tissue nodule anterior to the gastric antrum suspicious for peritoneal metastatic disease.\nPositron emission tomography (PET)/CT images demonstrated marked hypermetabolism within the gastric pylorus mass; however, no evidence of fluorodeoxyglucose (FDG)-avid metastatic disease was identified (Figure ).\nSubsequently, an endoscopic ultrasound (EUS) via the gastric pouch showed diffuse wall thickening of the excluded stomach at the antrum, as well as two enlarged, hypoechoic, and well-defined lymph nodes in the gastrohepatic ligament (Figure ).\nFine needle aspiration (FNA) of the lymph nodes and the gastric wall of the excluded stomach revealed poorly differentiated gastric adenocarcinoma (Figure ).\nThe biopsy was negative for H. pylori infection. Molecular analysis showed a HER2-negative tumor. Staging laparoscopy confirmed peritoneal implants. The patient is currently undergoing chemotherapy for Stage IV gastric cancer with capecitabine, plus oxaliplatin (CAPOX).
|
[[50.0, 'year']]
|
F
|
{'11868296': 1, '15826480': 1, '31001760': 1, '18350638': 1, '17938306': 1, '34977263': 1, '12184547': 1, '23025966': 1, '25651787': 1, '12448395': 1, '23639638': 1, '17938307': 1, '3565686': 1, '25238176': 1, '18280327': 1, '9287934': 1, '21034896': 1, '15014179': 1, '30131918': 2}
|
{'6101468-1': 2}
|
2,067 |
6101469-1
| 30,131,913 |
comm/PMC006xxxxxx/PMC6101469.xml
|
Rare Metastatic Sites of a Lung Adenocarcinoma
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A 78-year-old non-smoker Chinese female presented with a six-month duration of progressive breathlessness. This was associated with cough, poor appetite and weight loss over the last one month. She had reduced air entry on the right chest with stony dullness on percussion. Chest radiograph showed a right moderate effusion. Thoracocentesis drained milky fluid which was biochemically in keeping with chylothorax (pH 7.7; triglycerides, 3.18 mmol/l; total cholesterol, 2.44 mmol/l; lactate dehydrogenase, 632 U/L; protein, 43 g/l and glucose, 6.2 mmol/l). The fluid had no malignant cells or pathogens. Blood biochemistry showed obstructive liver function (alkaline liver phosphatase, 899 U/L; alanine aminotransferase, 51 U/L; aspartate aminotransferase, 79 U/L and total bilirubin, 14 umol/l). Computed tomography (CT) scan revealed a right lower lobe lung mass with a right pleural effusion (Figure ), rectum thickening, prominent common bile duct and a moderate left hydronephrosis with soft tissue non-opacification in the left mid-ureter. Magnetic resonance cholangiopancreatography (MRCP) (Figure ) showed suspicion of a common bile duct stricture with biliary tree dilatation and an abrupt change in calibre at the distal common bile duct without any stone or soft tissue mass seen in the biliary and pancreatic region. In view of the radiological and clinical findings, main differential diagnosis was metastatic lung cancer to multiple extra-thoracic sites versus multiple synchronous primary oncological malignancies.\nCT-guided core needle biopsy of the lung mass revealed pulmonary adenocarcinoma with diffuse strong nuclear immunohistochemical staining for thyroid transcription factor-1 (TTF-1) (Figure ). Epidermal growth factor receptor mutational analysis was negative. Colonoscopy showed a circumferential rectal tumor with biopsies (Figure -) proving adenocarcinoma in keeping with lung metastasis (positive immunohistochemical staining for TTF-1; negative for caudal-related homeobox 2 (CDX2)). Endoscopic retrograde cholangiopancreatography showed a short distal common bile duct obstruction by a periampullary tumor extending to the duodenal margins (Figure ). Biliary stent was inserted with successful good drainage. Cytobrushing and biopsies (Figure ) revealed poorly-differentiated adenocarcinoma of lung origin (positive immunohistochemical staining for TTF-1, Napsin-A, cytokeratin (CK)7, CK19, mucicarmine 1; negative for CK20, chromogranin, synaptophysin and carbonic anhydrase 19-9). Invasive biopsy was not performed for the ureter lesion but impression at a multi-disciplinary tumor board discussion was that it was clinical-radiologically in keeping with a synchronous metastatic lung lesion.
|
[[78.0, 'year']]
|
F
|
{'21541230': 2, '33369224': 1, '28105072': 1, '23963996': 1, '29197379': 1, '29084394': 1, '17410025': 1, '24691919': 1, '23106585': 1, '30131913': 2}
|
{'3085393-1': 1}
|
2,068 |
6101515-1
| 30,151,218 |
comm/PMC006xxxxxx/PMC6101515.xml
|
Gastric xanthelasma associated with hyperplastic polyp and mucosal erosions: report of an unusual case and literature review
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A 78-year-old male presented with symptoms of chronic anemia. His physical examination showed bleeding per rectum. Blood investigations revealed iron deficiency anemia. The cause of anemia was fully investigated including CT abdomen/pelvis, upper and lower GI endoscopy. Gastrointestinal malignancy was excluded. Colonoscopy showed anal hemorrhoids. His anemia was secondary to chronic blood loss from anal hemorrhoids. Interestingly, esophagogastroduodenoscopy showed an incidental findings including yellow-white gastric lesion at the gastric fundus measuring 0.7 cm and a pedunculated gastric polyp at the antrum measuring 1.0 cm (Fig. a). Histological examination of the gastric biopsy specimens revealed an inflamed and hyperplastic polyp at the antrum (Fig. d and e). The fundus showed that the mucosal lamina propria contained chronic inflammatory infiltrate and clusters of oval shaped cells with abundant, foamy cytoplasm consistent with the diagnosis of GX (Fig. b and c). Biopsy from the surrounding area of the GX lesion showed a significant amount of acute on chronic inflammatory cells infiltration suggestive of severe gastritis with mucosal erosions and intestinal metaplasia (Fig. e) associated with a small number of H. pylori-like organisms. There was no evidence of glandular dysplasia or malignancy in the sections examined. The gastric lesions did not seem to be contributing to his anemia and therefore was not resected. The anemia was resolved after ligation of anal hemorrhoids and 3 months course of oral iron supplement.
|
[[78.0, 'year']]
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M
|
{'24165503': 1, '15064997': 1, '19037727': 1, '1753432': 1, '31988882': 2, '26117951': 1, '24761501': 1, '14562385': 1, '10365893': 1, '27250981': 1, '24372908': 1, '8893228': 1, '23020998': 1, '2705875': 1, '30151218': 2}
|
{'6966225-1': 1, '6966225-2': 1}
|
2,069 |
6101516-1
| 27,103,737 |
comm/PMC006xxxxxx/PMC6101516.xml
|
Spontaneous rupture of intrahepatic pseudocyst into the inferior vena cava
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A 58-year-old male, a chronic alcoholic, presented to us with mild-to-moderate abdominal pain in the epigastric region, with presence of fever for the previous 10 days, for which he was admitted in our institute for further evaluation and management. Ultrasonography (USG) of the abdomen was done in the emergency setting, revealing chronic liver parenchymal disease with mild ascites and multiple collections in the abdomen, one of which was in the caudate lobe of the liver (). The patient showed elevated serum amylase (674 U/L) and serum lipase (4897 U/L). Thereafter contrast-enhanced computed tomography (CT) of the whole abdomen was carried out. The patient’s CT scan confirmed multiple collections in the abdomen. The unusual thing was a large intrahepatic collection in the caudate lobe, approximately 3.7 x 4.8 x 5.8 cm. The caudate lobe collection in its superior aspect was communicating with the IVC through a narrow tract approximately 5 mm in thickness and extending superiorly as far as the right atrium with an average attenuation value of 15–30 HU (). Apart from the intraluminal IVC extension, the caudate lobe collection was also seen extending and communicating inferiorly with the peripancreatic collection near the head of the pancreas. The collection showed few internal septations. Collections were also seen in the lesser sac, mesentery and perigastric region.\nThe patient was managed conservatively. On the day following screening ultrasound, there was a significant reduction in the size of the caudate lobe collection. The patient had no fever or signs of septicaemia, so conservative management was continued and the patient was discharged after 5 days.
|
[[58.0, 'year']]
|
M
|
{'8591628': 1, '7553473': 1, '33652518': 2, '26224684': 1, '20209844': 1, '34754856': 2, '19561436': 1, '20103016': 1, '30279257': 1, '25500342': 1, '22563287': 1, '23100216': 1, '27103737': 2}
|
{'8505190-1': 1, '8554436-1': 1}
|
2,070 |
6102433-1
| 30,131,650 |
comm/PMC006xxxxxx/PMC6102433.xml
|
Foreign Body causing Displacement of Immature Fractured Apical Root Fragment: An Unusual Case Report
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A 12-year-old boy presented to the Department of Pedo-dontics with a complaint of broken front tooth and pus discharge. He gave a history of fall while playing 1 year back. Clinical examination revealed Ellis class III fracture of maxillary right lateral incisor (12) (). The tooth was tender to percussion and there was grade I mobility. Radiographic examination revealed displaced fractured root apex with periapical radiolucency ().\nInitially, while exploring the canal, a wooden green stick was found in the canal firmly stuck to the apex. He gave the history of putting the sticks in the canal since the fracture to counter irritation. Retrieval of that stick was tried using ultrasonic, H-Files, and ProTaper files, but all in vain. So, it was decided to treat it surgically. Labial mucoperiosteal flap was raised and bone cutting was done by surgical bur (). The displaced fractured immature root apex was removed along with the wooden stick () and the retrograde filling was done using zirconium-reinforced glass ionomer cement ().
|
[[12.0, 'year']]
|
M
|
{'11556566': 1, '19841551': 1, '20215673': 1, '4150618': 1, '269345': 1, '10635138': 1, '30131650': 2}
|
{}
|
2,071 |
6102434-1
| 30,131,649 |
comm/PMC006xxxxxx/PMC6102434.xml
|
Squamous Papilloma on Hard Palate: Case Report and Literature Review
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A 10-year-old girl reported with the chief complaint of growth of soft tissue mass on the palate that was present since 1 month. History regarding the growth revealed that it first started as painless slow growing soft tissue mass that gradually enlarged and associated with discomfort and occasional pain on eating and interference while biting. Past medical, dental, and personal history were noncontributory.\nGeneral and extraoral examination of the patient did not reveal any significant findings. Intraoral examination revealed a lesion on anteriormost part of hard palate. The lesion was a pale, pink colored, pedunculated growth with finger-like projections of soft tissue present on right side of the rugae area of hard palate just adjacent to incisive papilla. It was approximately 1.5 cm in size, circumscribed, and not associated with bleeding ( and ).\nBased on these clinical features, the growth was provisionally diagnosed as papilloma. Surgical excision of the growth was done with a 1 mm margin to the depth of submucosa under local anesthesia. After excisional biopsy, specimen was fixed and stained with hematoxylin and eosin for histological analysis.\nHistological examination revealed papillary projections of parakeratinized stratified squamous epithelium of variable thickness with localized areas showing mild basilar hyperplasia with few koilocytes and enclosing connective tissue cores ( and ). The connective tissue is fibrocellular in nature with moderate vascularity. Histological features are suggestive of SP.
|
[[10.0, 'year']]
|
F
|
{'17432786': 1, '24262405': 1, '19776503': 1, '32133247': 2, '30131649': 2}
|
{'7034761-1': 1}
|
2,072 |
6102438-1
| 30,131,652 |
comm/PMC006xxxxxx/PMC6102438.xml
|
Pedodontic Considerations in a Child with Attention Deficit Hyperactivity Disorder: Literature Review and a Case Report
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A 14-year-old male child diagnosed with ADHD presented to the Department of Pedodontics and Preventive Dentistry at DA Pandu Memorial RV Dental College, with the chief complaint of broken tooth in upper front region since 2 years ( and ). Patient gave a history of root canal treatment done on the same tooth 2 years back.\nPatient was diagnosed with ADHD (primarily hyperactive subtype) when he was 6 years old and was on medications Sizodon (Risperidone). He was unable to speak in sentences, unable to understand most of the things, and often got aggressive outbursts. Medical history revealed that the child was hospitalized 10 months back due to typhoid and there was increased frequency of micturition. There was a history of delayed milestones. Family history was insignificant except for the fact that the mother experienced high caries rate. Child had a habit of keeping food in the mouth for prolonged period (food pouching) and self-inflicted injuries, such as hitting on wall and banging head. He exhibited endomorphic features. Extraoral examination revealed scar marks on the face and upper limbs (). On intraoral clinical examination, there was no abnormal soft tissue finding. However, there was crown fracture up to gingival third with 21, dental caries with 16, 15, 26, 36, 46, retained 53, deep dentinal caries with 14, 24, 25, 31, and 32, unilateral crossbite on right side, and rotated 11. The patient was advised for orthopantomogram (OPG) (). Pulp vitality tests showed negative results with 24, 31, 32. After meticulous clinical and radiographic examination, following diagnosis was given: Root canal treated and fractured 21; chronic irreversible pulpitis with respect to 24, 31, 32; deep dentinal caries with respect to 14, 25; dental caries with respect to 16, 15, 26, 36, 46; retained 53; unilateral posterior cross-bite; and rotated 11.\nTherefore, the treatment plan was oral prophylaxis, restoration with respect to 16, 15, 26, 36, 46, root canal therapy with respect to 24, 31, 32, core build-up with crown 14, 25, post and core with crown with respect to 21 (after gingivectomy), and extraction of 53. Orthodontic treatment was questionable due to child’s habit of self-inflicting injuries ( and ).\nChild was reasonably cooperative during most of the treatment but turned extremely fidgety and slightly aggressive on few appointments due to skipping of doses of his medication. Although we had an option of treating the child under GA, but using appropriate nonpharma-cological behavior management, such as Tell-Show-Do, positive reinforcement, and breaks/time-outs, treatment was rendered successfully to the patient.\nPatient came for a follow-up after 6 months, and on intraoral examination, he was caries-free and was maintaining oral hygiene properly. On a follow-up after a year, child had lost the acrylic crown on upper front tooth for which composite build-up was done.
|
[[14.0, 'year']]
|
M
|
{'14560871': 1, '20622942': 1, '19568859': 1, '26199709': 1, '19941763': 1, '16055761': 1, '20470335': 1, '14684974': 1, '18254422': 1, '10997239': 1, '24011294': 1, '32440072': 1, '18615170': 1, '9041578': 1, '23019769': 1, '18489658': 1, '15552341': 1, '17541055': 1, '15768947': 1, '19405409': 1, '17403737': 1, '30131652': 2}
|
{}
|
2,073 |
6102439-1
| 30,131,651 |
comm/PMC006xxxxxx/PMC6102439.xml
|
Nonsyndromic Gingival Fibromatosis: A Rare Case Report
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An 8-year-old male child reported to the Department of Pediatric and Preventive Dentistry, Government Dental College and Hospital, Jaipur, Rajasthan, India, with chief complaint of gingival swelling and absence of teeth, which caused damage to his speech, mastication, and esthetics and led to a significant change in his facial profile due to severe gingival enlargement.\nThe patient noticed that the gingival enlargement was simultaneous with deciduous dentition eruption and gradually covered entire dentition. Gingival enlargement covered all teeth anteriorly and posteriorly, and only occlusal surfaces were visible.\nExtraoral examination of patient was done with convex profile, lips incompetency, and enlarged tissue was protruding out of the mouth ().\nIntraoral examination of generalized gingival enlargement including both mandibular and maxillary arches and vestibule was recorded ( and ). The tissue was pink, leathery in consistency, and firm on palpation and covered entire dentition. There were no signs of ulceration on enlarged tissue due to mastication forces.\nA scanty amount of food debris and plaque was present on the posterior teeth, but there were no signs of inflammation present. Due to excessive gingival growth, positions of teeth were difficult to determine. However, the panoramic radiograph showed normal bone height and tooth positioning (). Routine blood investigations were done and values were found within normal limit.\nBased on provisional diagnosis, an incisional biopsy was done and section was evaluated. The patient’s medical history was nonsignificant for any hormonal changes or drug-induced gingival enlargement and exhibited no signs of mental retardation or hypertricho-sis. His parents did not reveal any evidence of gingival overgrowth.\nThe enlarged tissue was excised by the external bevel gingivectomy under general anesthesia arch wise. Periodontal dressing was given and antibiotics were prescribed. Postoperatively, periodontal dressing was placed on the surgical site and was covered with custom-made acrylic stent. Oral hygiene instructions were given. The histological evaluation revealed moderately dense to highly dense collagenous connective tissue with collagen bundles arranged in an irregular manner.\nThe connective tissue was relatively avascular with scanty inflammatory cell infiltrate. The overlying epithelium was hyperplastic with enlarged rete ridges. This was suggestive of gingival fibromatosis (). Postsurgical healing was satisfactory. Patient was recalled after 1 week for periodontal dressing removal and was on follow-up after 2 weeks, and at 1- and 3-month intervals for evaluation.\nPostsurgically, his facial profile improved drastically and the parents were satisfied with the results ( and ).
|
[[8.0, 'year']]
|
M
|
{'11203959': 1, '33776359': 2, '32039068': 2, '13787614': 1, '7800376': 1, '8655871': 1, '14233392': 1, '6415252': 1, '34565352': 2, '11314351': 1, '5792612': 1, '15287422': 1, '8018496': 1, '10863370': 1, '30131651': 2}
|
{'7989762-1': 1, '8474844-1': 1, '6984817-1': 1}
|
2,074 |
6102810-1
| 30,129,425 |
comm/PMC006xxxxxx/PMC6102810.xml
|
“Recurrent multiple cerebral infarctions related to the progression of adenomyosis: a case report”
|
A 44-year-old woman experienced sudden onset of difficulty using her left hand and walking during her menstrual phase. She had a history of adenomyosis and infertility treatment for 18 years, and heavy menstrual bleeding. She complained of headache, abdominal pain, nausea, and had a fever (37.7 °C) at presentation. She is not obese (BMI of 21.5 kg/m2), had no history of taking steroids or contraceptives. Neurologic examination revealed left spatial neglect, left facial hypoalgesia, mild paresis in her left arm, and right pyramidal signs. Brain magnetic resonance imaging (MRI) revealed bilaterally multiple infarctions in the cerebrum and cerebellum, including cortical and subcortical lesions (Fig. ). MR angiography presented severe stenosis in the M2, M3, >and M4 portions of right middle cerebral artery (Fig. ). Contrast computed tomography revealed a splenic infarction (Fig. ). Blood examination revealed normocytic anemia (hemoglobin 10.3 g/dl, mean corpuscular volume 90.5 μm3), thrombocytopenia (112,000 /μl), and low-grade elevation of C-reactive protein (2.9 mg/dl). The serum levels of D-dimer (17.0 μg/ml, normal < 0.5 μg/ml), CA125 (2115 U/ml, normal < 35.0 U/ml), and carbohydrate antigen 19–9 (CA19–9) (1824 U/ml, normal < 37.0 U/ml) were increased. Results of a hypercoagulable panel, including protein C and S, antithrombin Ш level, lupus anticoagulant, and anticardiolipin antibody titers, were within normal limits. Pelvic MRI revealed giant adenomyosis (Fig. ), but no malignancy was detected. Fluorine-18–2-fluoro-2-deoxy-d-glucose (FDG) positron emission tomography revealed FDG accumulation in the adenomyosis, but no malignancy was detected by cervical cytology. The result of continuous electrocardiography monitoring, transesophageal echocardiography with agitated saline injection, carotid ultrasonography, upper gastrointestinal endoscopy, and colonoscopy were normal.\nShe was treated with edaravone (60 mg/day) and anticoagulated with heparin for 2 weeks. Subsequently, she was treated with rivaroxaban (15 mg/day). Her serum levels of D-dimer, CA125, and CA19–9 improved (2.7 μg/ml, 911 U/ml, and 501 U/ml, respectively), and the treatment was continued.\nAt day 31, a day after her menstrual phase started, she complained of numbness in her left lower limb. Brain MRI revealed a new CI in the right cerebrum (Fig. ). The serum levels of D-dimer, CA125, CA19–9 were 2.4 μg/ml, 561 U/ml, 417 U/ml, respectively. We discontinued the rivaroxaban treatment, and started anticoagulant therapy with warfarin. Afterwards, her menstrual bleeding increased, the anemia progressed, and the serum level of D-dimer increased (14.1 μg/ml). She started to receive pseudomenopause treatment with a GnRH agonist for the adenomyosis. Ten days after initiating the GnRH agonist treatment, her serum D-dimer level improved (2.30 μg/ml). She continued the warfarin and GnRH agonist once a month for 6 months, and showed no recurrence of CIs during that time. The serum levels of CA125, CA19–9 improved after 3 months of initiating the therapy (117 U/ml, 224 U/ml, respectively).\nShe presented with transient weakness of her right lower limb and visited our clinic 5 months after her last GnRH agonist therapy, when her irregular menstrual bleeding had continued for a month. Brain MRI revealed new multiple cortical and subcortical infarctions in the left occipital lobe and right parietal lobe (Fig. ). Her serum D-dimer, FDP, CA125, and CA19–9 levels were elevated (22.0 μg/ml, 56.5 μg/ml, 1291.6 U/ml, and 803.2 U/ml, respectively). Anticoagulant therapy with warfarin was well controlled (PT-INR 2.5), and her electrocardiographic findings were normal. We concluded that total hysterectomy would be the most effective therapy for preventing CI recurrence. She underwent total hysterectomy and bilateral salpingo-oophorectomy, which was effective in not only preventing CI recurrence, but also for normalizing the serum D-dimer, FDP, CA125, and CA19–9 levels for the last 2 years.
|
[[44.0, 'year']]
|
F
|
{'16855354': 1, '17496204': 1, '10726623': 1, '15955949': 1, '2432019': 1, '4261794': 1, '27520610': 1, '16479463': 1, '22142777': 1, '26408926': 1, '2664619': 1, '23706331': 1, '32450843': 2, '21277226': 1, '34539994': 1, '21860019': 1, '23001775': 1, '27480069': 1, '7028788': 1, '33430804': 2, '27404454': 1, '23266651': 1, '24794947': 1, '30129425': 2}
|
{'7798234-1': 1, '7249642-1': 1}
|
2,075 |
6102819-1
| 30,126,417 |
comm/PMC006xxxxxx/PMC6102819.xml
|
Full-length genome and molecular characterization of dengue virus serotype 2 isolated from an imported patient from Myanmar
|
In September 2013, a 32-year-old female patient, who came from Myanmar, was clinically diagnosed with dengue fever in Ruli, Yunnan, China. She had dengue-like symptoms including fever, joint pain, myalgia and headache. The patient′s acute serum was positive for NS1 antigen by One Step Dengue nonstructural protein (NS) 1 RapiDipTM InstaTest (Cortez). The patient’s acute serum (2–5 ml) was collected with informed consent and stored at -80 °C until testing.
|
[[32.0, 'year']]
|
F
|
{'2224837': 1, '24465613': 1, '30528666': 1, '16789820': 1, '24132122': 1, '11038328': 1, '9445071': 1, '11717435': 1, '9519821': 1, '28482813': 1, '20339476': 1, '26597450': 1, '15703242': 1, '28414004': 1, '27630156': 1, '23756811': 1, '25885572': 1, '17409078': 1, '17263893': 1, '1556748': 1, '21152061': 1, '22584140': 1, '2174669': 1, '17846036': 1, '10600594': 1, '2665017': 1, '12797969': 1, '23735713': 1, '24016428': 1, '24497032': 1, '33495898': 1, '15665649': 1, '22506599': 1, '15956576': 1, '16818477': 1, '22829749': 1, '10377418': 1, '17272680': 1, '12824337': 1, '24734212': 1, '25375211': 1, '27774277': 1, '15713735': 1, '17553878': 1, '21546353': 1, '25772205': 1, '19653928': 1, '22807683': 1, '23563266': 1, '27812857': 1, '22729802': 1, '21291623': 1, '30126417': 2}
|
{}
|
2,076 |
6102832-1
| 30,126,397 |
comm/PMC006xxxxxx/PMC6102832.xml
|
Suprachoroidal hemorrhage followed by swept-source optical coherence tomography: a case report
|
A 66-year-old woman with reduced vision in her left eye was examined in the Tokyo Medical and Dental University Hospital on June 27, 2015. Her best-corrected visual acuity (BCVA) in her left eye was 20/50, and both eyes were pseudophakic. The refractive error of the left eye was − 1.75 diopters, and the axial length was 25.89 mm. A rhegmatogenous retinal detachment (RRD) was detected by ophthalmoscopy and SS-OCT which extended over the inferotemporal quadrant including macula in her left eye (Fig. ).\nShe underwent pars plana vitrectomy on the same day, and during the intraocular photocoagulation for a retinal tear, a sudden choroidal elevation and vitreous hemorrhage occurred. A suprachoroidal hemorrhage was also observed at the site of the trocar insertion. Although we intended to inject silicone oil into the vitreous cavity, a sufficient amount could not be injected because of an obstruction at the trocar insertion site. The surgery was terminated with a closure of the surgical incision.\nOn postoperative day 1, an elevated lesion was detected in the B-scan ultrasound images that was considered to be the suprachoroidal hemorrhage (Fig. ).\nThe hemolyzed hemorrhage was removed by scleral fenestration on postoperative day 13. During the surgery, a reduction of choroidal elevation was observed. New silicone oil was injected after removing the original silicone oil.\nPostoperatively, the resolution of the suprachoroidal hemorrhage was followed in the SS-OCT images (Fig. ). However, the RRD on the inferior quadrant remained, and a scleral encircling procedure was performed on day 63, and silicone oil was reinjected to tamponade the retina. On day 73 after the RRD surgery, the retina was reattached, and the suprachoroidal hemorrhage was not present in the SS-OCT images.\nAt 3 months after the most recent surgery, the patient’s BCVA is 20/200, and the silicone oil was still present. A future surgery is planned to remove the silicone oil.
|
[[66.0, 'year']]
|
F
|
{'8887392': 1, '11389343': 1, '21763674': 1, '8493013': 1, '4618395': 1, '30126397': 2}
|
{}
|
2,077 |
6102837-1
| 30,126,388 |
comm/PMC006xxxxxx/PMC6102837.xml
|
Nonsurgical periodontal treatment and prosthetic rehabilitation of a renal transplant patient with gingival enlargement: a case report with 2-year follow-up
|
A 51-year-old woman presented with chief complaints of bleeding gums and chewing disability. Her medical history revealed that she had received renal transplantation surgery in 1999 and had remained in a stable condition without graft-versus-host disease ever since. She suffered from hypertension and gout, both of which were being well controlled and followed by treating physicians. Her medications at the time of initial examination including the immunosuppressive regimen (cyclosporine, prednisolone, and mycophenolate mofetil) are listed in Table . The patient was a nonsmoker who did not consume alcohol. She stated that she seldom brushed her teeth and had not flossed for a long time because of serious gum bleeding upon brushing or flossing.\nA facial examination revealed normal appearance without lymph node enlargement or local heat. No temporomandibular joint related symptoms were reported. Normal hard and soft tissue were observed in the patient’s oropharynx, hard and soft palates, floor of the mouth and tongue. An intraoral examination revealed highly inflamed periodontal tissue with heavy plaque and calculus deposition. Fibrotic changes over interdental papillae, facial and also lingual gingivae were noted, especially in the anterior segment (Fig. ). The patient’s upper left and lower left molars were missing. Her anterior teeth were flaring and highly mobile with a diastema of approximately 2.5 mm between the maxillary central incisors. Upon examination, we noted full mouth deep probing pocket depth (up to 15 mm) and profound bleeding. A fistula with suppuration was observed over buccal gingiva of tooth 46 (lower right first molar). Periapical films revealed generalized horizontal bone loss with the supporting bone of less than one half or one third of the root length. Periradicular radiolucency with an angular bony defect extending beyond the apex was observed over the mesial root of tooth 46 (Fig. ).\nThe clinical diagnosis was severe periodontitis and gingival disease modified by medication []. A hopeless prognosis was assigned to tooth 46. After consultation with treating physicians and discussion with the patient, a tentative treatment plan was formed involving cause-related periodontal treatment and extraction of tooth 46. In addition, the immunosuppressive regiment was not altered.\nThe patient was treated in the Department of Periodontics in Taipei Chang Gung Memorial Hospital between July 2014 and January 2015. Dental appointments were coordinated with physician appointments to obtain blood test results before each dental visit. Data were mostly within the normal range except for the occurrence of mild thrombocytopenia (listed in Table ). Prophylactic antibiotics (amoxicillin, 2 g) were prescribed before each appointment []. The treatments included scaling, root planing, oral hygiene instruction, and extraction. Although tooth mobility decreased after multiple visits, we discovered occlusal interference during the patient’s lateral excursion and anterior jaw movement; therefore, occlusal adjustment was incorporated into the treatment plan. Six months after the patient’s initial visit, a marked improvement of her periodontal condition as well as more effective plaque control were observed. The gingivae were considerably less edematous and glazed and without any residual fibrotic appearance (Fig. ). The periodontal probing result revealed some residual but largely decreased periodontal pockets and grade I tooth mobility over the upper and lower anterior teeth and lower right second molar []. In addition, the diastema between the upper incisors closed “spontaneously” after treatment.\nPocket elimination periodontal surgery was initially planned to treat the upper right and lower right second molars; however, nonsurgical treatment was eventually selected as the final treatment plan after the patient rejected surgery and the residual periodontal pocket depth were mostly less than 6 mm with horizontal bone loss pattern (Fig. ) []. After 3 months of follow-up, the patient was referred to our prosthodontic department for oral rehabilitation with removable partial dentures. The dentures were designed with palatal strap, lingual bar, and wrought-wire clasps (Fig. ). The periodontal supportive treatment recall interval was monthly in the first year and every 3 months subsequently []. A clinical examination and periodontal probing after 2 years of follow-up revealed excellent oral hygiene, continuous pocket reduction, and tooth mobility within normal limit for all remaining teeth (Figs. and ). The difference of attachment level gain, probing depth reduction, and change of the distance from cementoenamel junction to gingival margin (CEJ-GM) between anterior (canine to canine) and posterior teeth were shown in Fig. . No recurrence of gingival enlargement was recorded throughout the follow-up period. The diastema between the upper incisors remained closed without centric or lateral occlusal interference (Fig. ). Full mouth periapical and bite-wing radiographs revealed that the alveolar bone level had been maintained from its initial condition (Fig. ). The treating prosthodontist also recalled the patient regularly. The patient reported good chewing function, considerable ease in conducting oral hygiene practices, and overall high satisfaction with the treatment outcomes.
|
[[51.0, 'year']]
|
F
|
{'16677333': 1, '16856895': 1, '15948679': 1, '11495141': 1, '10703661': 1, '10487307': 1, '10534072': 1, '12686921': 1, '10765878': 1, '1732303': 1, '21150873': 1, '32489824': 1, '9029457': 1, '24389563': 1, '15985985': 1, '17474927': 1, '9358363': 1, '9775650': 1, '22362336': 1, '34877332': 2, '15659128': 1, '8841894': 1, '28298458': 1, '10863370': 1, '15766370': 1, '9444600': 1, '7608843': 1, '25853131': 1, '21359247': 1, '4521349': 1, '9497712': 1, '14974825': 1, '12787211': 1, '20854459': 1, '25680368': 1, '15643744': 1, '15562922': 1, '9379336': 1, '29292608': 1, '32557242': 1, '9226390': 1, '11551304': 1, '9118268': 1, '34393408': 2, '30126388': 2}
|
{'8610926-1': 1, '8610926-2': 1, '8610926-3': 1, '8336778-1': 1}
|
2,078 |
6102845-1
| 30,129,424 |
comm/PMC006xxxxxx/PMC6102845.xml
|
Reversible reddish skin color change in a patient with compressive radial neuropathy
|
A 42-year-old male was referred for left wrist drop, finger drop and a tingling sensation over the lateral dorsum of the left hand. The patient reported that he was well until 4 days prior when he was intoxicated and awoke with the symptoms. For 4 days, slight improvement of weakness occurred. He had no history of antecedent trauma, injury, infection, or mononeuropathy. Neurologic examination revealed weakness of the left wrist and finger extension (Medical Research Council grade II). Finger abduction appeared weak, but strength improved when the hand was passively extended to the neutral position. Wrist and finger flexion was intact. On sensory examination, there was a well-demarcated area of hypoesthesia and a tingling sensation over the lateral dorsum of the left hand between the thumb and index finger extending into the proximal phalanges of the 2nd finger. In addition, reddish skin color and slight edema were observed in the same area (Fig. ). There was no definite change in skin temperature and no pain. Reflexes were normal at the biceps and triceps brachii muscles, but the left brachioradialis reflex was absent. Routine blood analysis showed white blood cell count, C-reactive protein level and uric acid level were normal. According to the clinical information and neurologic examination, he was diagnosed with compressive radial neuropathy. After approximately two weeks of observation without specific treatment, the skin color recovered along with a marked improvement of the weakness and aberrant sensation. A nerve conduction study and electromyography were performed 2 weeks after the onset of the symptoms (Table ). On the affected left side, a normal radial compound motor action potential (CMAP) was recorded over the extensor indicis proprius muscle with the forearm and elbow stimulated. When stimulated above the spiral groove, the CMAP was reduced by 34% compared to that of distal stimulations. The contralateral radial motor nerve study and sensory nerve conduction were normal. Electromyography revealed that the left extensor indicis proprius, extensor digitorum communis, extensor carpi radialis and brachioradialis showed increased insertional activity, fibrillation potentials, and positive sharp waves and reduced recruitment pattern.
|
[[42.0, 'year']]
|
M
|
{'8226291': 1, '24125557': 1, '10918257': 1, '21655650': 1, '16421136': 1, '11222458': 1, '30129424': 2}
|
{}
|
2,079 |
6102888-1
| 30,126,414 |
comm/PMC006xxxxxx/PMC6102888.xml
|
Retrolaparoscopic adrenalectomy assisted by three-dimensional reconstructed digital model in a patient with situs inversus totalis
|
A 59-year-old female patient was admitted into our hospital for the abnormal computed tomography (CT) image presentation of right adrenal mass revealed by occasional health examination, accompanied with the complaint of intermittent nausea and blurred vision. She had been diagnosed with SIT when she received the hysterectomy and near-total thyroidectomy for the uterus myoma and thyroid cancer in 2000. Besides, her past medical history also included the diabetes mellitus (type 2) for 6 years and significant hypertension for 5 years, ranging from 150 to 200/90 to 102 mmHg, fluctuated periodically.\nThe patient’s height was 158.0 cm and the body weight was 70.0 kg. The BMI was 28.04 kg/m2, which was well correlated with her significant abdominal obesity. The laboratory tests presented the normal levels of the serum potassium concentration (4.2 mEq/L) and the renin activity (3.8 ng/mL/h). The plasma cortisol and aldosterone (217 pg/mL) concentrations were also within the reference range. Besides, there were no abnormalities found in the levels of the urinary catecholamines (59.2 mcg/24 h) and vanillylmandelic (4.3 mg/24 h) either.\nAs for the medical image examinations, the routine chest X-ray image revealed the dextrocardia; the dual-source 64-slice enhanced CT (LightSpeed VCT, GE Healthcare, USA) scan including arterial phase, venous phase, and excretory phase after intravenous contrast administration confirmed the diagnosis of SIT and presented her round-shaped mass on the right adrenal gland with the size of 10.2 × 9.4 × 7.9 cm (Fig. ).\nIn order to facilitate the surgical orientation and improve the manipulating accuracy, the data from CT images was extracted and the three-dimensional digital model (3D-DM) was reconstructed: The original image data from CT scanning was set in the format of Digital Imaging and Communications in Medicine (DICOM). The copied information was analyzed and reconstructed into the 3D-DM by using a postprocessing software named three-dimensional medical image reconstructing and guiding system (3D-MIRGS, China), which is a multifunctional workstation for the clinical application, whose functions included CT-based image reconstruction, preoperative planning, and intraoperative-assisted navigation []. The retroperitoneal space along with critical anatomic structures including adrenal tumor, the relevant vasculature, the kidney, and the renal collecting system on the affected side were reconstructed and marked by using different colors simultaneously (Fig. ).\nThe morphometric calculation and analysis of the reconstructed 3D-DM provided the surgeons with the valuable anatomic information such as the spatial locations of vital vessels, maximal diameter, and margins of the adrenal mass. The tumor can be shadowed and turned into a transparency, leaving the hollow-shaped crater. A more distinct spatial relationship between the adrenal mass and the nearby structures showed clearly via this intraparenchymal visualization. Based on these data, we tailored a specific surgical plan for this rare case. The surgeons can gain a full comprehension of the regional complexity which is mirrored to the normal anatomy.\nThe retrolaparoscopic adrenalectomy was performed at the Department of Urology. The patient was placed on the operating table in the lateral decubitus position with the affected side upward. The general anesthesia and tracheal intubation were administrated. After padding the pressure points with beanbags and fixing the posture with the optimal table flexion, a longitudinal 1.5 cm incision for 12 mm trocar was made in the posterior axillary line below the 12th rib. In order to minimize the potential irritation to the stability of blood pressure, the retroperitoneal space was dilated in the blunt finger-dissecting style instead of the traditional ballooning way. Another two 12 mm trocars were located at the point of 2 cm above from iliac crest superior border in the mid-axillary line for the laparoscope, and at the point under the subcostal margin in the anterior axillary line for laparoscopic instruments respectively. After the routine insertion of three trocars and the establishment of pneumoperitoneum at a pressure of 10 mmHg, the retroperitoneal fat tissue was removed under the laparoscopic surveillance. Another assisted 5 mm trocar was inserted due to the patient’s obesity. A well-trained full-time surgical technician captured some typical screenshots to illustrate the anatomical landmarks. Then, the semitransparent 3D-DM were superimposed onto these screenshots with appropriate axis and size adjustments. The composite 3D-DM images provided the surgeon with information relative to the inverted anatomy, thereby acting as a kind of assisted navigation for the subsequent manipulations. All these speedy manual image fusions performed synchronously during operation and all the fused images were displayed on a separate screen. Under the assisted navigation of 3D-DM, the Gerota fascia was incised and the adrenal central vein was dissected carefully, following its ligation by using 5 mm Hem-o-lok clips. After that, the mass was excised completely with the careful preservation of normal adrenal tissue and the other adrenal vessels including the adrenal arteries were ligated and scissored up. Then, the retroperitoneal pressure was set down to the level of 5 mmHg and the hemostasis was achieved carefully. Given the size of the tumor mass and the skin elasticity, we extended the incision below the 12th rib along its axis for the total length about 7 cm. The specimen of adrenal tumor was packed into a homemade laparoscopic pouch with a string by graspers and then was withdrawn by holding and pulling the string vigorously. The trocar incisions were carefully closed, and a rubber drainage catheter was left in situ.\nThe operative time was 1 h and 10 min, with no intraoperative complications happened. The estimated blood loss was about 10 mL. The size of resected tumor was 10.0 × 9.1 × 6.8 cm, and no gross extracapsular invasion was found. The final pathological diagnosis was adrenocortical adenoma (Fig. ). The postoperative course was uneventful, and the patient was discharged after 4 days postoperatively. A video demonstrating the operation accompanies this article (Additional file ).
|
[[59.0, 'year']]
|
F
|
{'24862670': 1, '15774004': 2, '10030863': 1, '11468444': 1, '17854150': 1, '24018094': 1, '27251840': 2, '25110602': 1, '25577366': 1, '23256030': 1, '29325527': 1, '11569513': 1, '22563541': 2, '1387700': 1, '30126414': 2}
|
{'5206842-1': 1, '555757-1': 1, '3341483-1': 1}
|
2,080 |
6102897-1
| 30,131,076 |
comm/PMC006xxxxxx/PMC6102897.xml
|
A retrospective case series of segmental zoster paresis of limbs: clinical, electrophysiological and imaging characteristics
|
A 47-year-old man developed severe burning pain and a vesicular eruption in the right shoulder and anterolateral arm. Two days later after the rash, he was not able to elevate his right arm to the shoulder level or bend the forearm at the elbow joint. Additionally, he also presented with numbness in the back of the thumb. Muscle weakness was present in the right deltoid (1/5), infraspinatus (1/5), supraspinatus (1/5) and biceps (2/5), according to the MRC scale. Distal muscle strength was normal. The right biceps reflex was absent. The electrophysiological examination revealed lower amplitude axillary and musculocutaneous CMAPs (12.1 and 7.3 mV, respectively) compared to contralateral sides (25.7 and 18.9 mV, respectively). The sensory nerve conduction studies were normal. Abnormal spontaneous potentials and decreased recruitments of MUAPs were present in the right deltoid, infraspinatus, biceps and C5–6 paraspinal muscles. In conclusion, the electrophysiologic findings were consistent with the incomplete lesions of C5 and C6 nerve roots.\nWithin 3 months follow-up period, he regained the full arm strength without any treatments. Electrophysiologically, the amplitude axillary and musculocutaneous CMAPs (21.1 and 16.6 mV, respectively) were normal. Abnormal spontaneous activities in muscles innervated by C5 and C6 nerve roots disappeared and many polyphasic MUAPs were observed.
|
[[47.0, 'year']]
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M
|
{'24638224': 1, '4673442': 1, '28364009': 1, '21482943': 1, '26829085': 1, '24334599': 1, '10943192': 1, '9270616': 1, '17848871': 1, '12235600': 1, '33145224': 2, '16003688': 1, '34141794': 2, '32664058': 2, '9344310': 1, '4313433': 1, '23999562': 1, '8891477': 1, '27663748': 1, '33766961': 1, '33489582': 2, '23886000': 1, '33814502': 1, '21887512': 1, '26436084': 2, '22715438': 1, '15824336': 1, '23628922': 1, '22499102': 1, '1711192': 1, '24665583': 1, '21339202': 1, '21321495': 1, '9101105': 1, '33150099': 2, '23648986': 1, '27313622': 2, '11293092': 1, '8609933': 1, '30131076': 2}
|
{'6102897-2': 2, '6102897-3': 2, '7360310-1': 1, '7591216-1': 1, '7591216-2': 1, '7603882-1': 1, '4904081-1': 1, '7813428-1': 1, '4581133-1': 1, '8173409-1': 1}
|
2,081 |
6102897-2
| 30,131,076 |
comm/PMC006xxxxxx/PMC6102897.xml
|
A retrospective case series of segmental zoster paresis of limbs: clinical, electrophysiological and imaging characteristics
|
An 87-year-old woman developed burning pain and vesicular rash over the right lateral arm and forearm. Two weeks after rash, she was not able to elevate her right arm to the shoulder level, bend the forearm at the elbow joint or grip tightly. Moderate to severe weakness of C6–8 myotomes was observed, as well as the hypoesthesia over the C6–7 dermatomes. The biceps reflex was absent. The electrophysiological examination revealed decreased motor ampltitudes of axillary, musculocutaneous and median nerve (4.4, 3.6 and 1.4 mV, respectively) and the absence of median and radial nerve SNAPs. The needle EMG revealed many positive sharp waves in the right deltoid, biceps, extensor digitorum communis, abductor pollicis brevis and C6 paraspinal muscles. These findings were consistent with a right incomplete C6–8 radiculoplexopathy. Brachial plexus MRI showed hyperintensity of right brachial plexus especially at the C6–8 nerve roots level. Consequently, clinical one-year follow-up revealed that the patient was still not able to elevate her right arm to the shoulder level. Also, she presented with numbness of the thumb and post-herpetic neuralgia.
|
[[87.0, 'year']]
|
F
|
{'24638224': 1, '4673442': 1, '28364009': 1, '21482943': 1, '26829085': 1, '24334599': 1, '10943192': 1, '9270616': 1, '17848871': 1, '12235600': 1, '33145224': 2, '16003688': 1, '34141794': 2, '32664058': 2, '9344310': 1, '4313433': 1, '23999562': 1, '8891477': 1, '27663748': 1, '33766961': 1, '33489582': 2, '23886000': 1, '33814502': 1, '21887512': 1, '26436084': 2, '22715438': 1, '15824336': 1, '23628922': 1, '22499102': 1, '1711192': 1, '24665583': 1, '21339202': 1, '21321495': 1, '9101105': 1, '33150099': 2, '23648986': 1, '27313622': 2, '11293092': 1, '8609933': 1, '30131076': 2}
|
{'6102897-1': 2, '6102897-3': 2, '7360310-1': 1, '7591216-1': 1, '7591216-2': 1, '7603882-1': 1, '4904081-1': 1, '7813428-1': 1, '4581133-1': 1, '8173409-1': 1}
|
2,082 |
6102897-3
| 30,131,076 |
comm/PMC006xxxxxx/PMC6102897.xml
|
A retrospective case series of segmental zoster paresis of limbs: clinical, electrophysiological and imaging characteristics
|
A 61-year old man developed burning pain and vesicular rash over left thumb, index finger and forearm. Fifteen days after his rash, he noted weakness in his left hand dorsal stretch and grip. There was moderate weakness of muscles in left C6–8 myotomes and hypoesthesia over the thumb. The triceps muscle stretch reflex was absent. The electrophysiological examination revealed decreased amplitude radial CMAPs (4.1 mV) as compared to the contralateral side (11.1 mV) and decreased amplitudes median and radial nerve SNAPs. The needle EMG revealed many positive sharp waves in the left extensor digitorum communis, brachioradialis, abductor pollicis brevis and C7 paraspinal muscles. These findings were consistent with a left median and radial nerve lesions and nerve root lesion. Moreover, brachial plexus MRI showed hyperintensity of distal median and radial nerve. Though, there was no nerve enlargement or T2 hyperintensity of nerve roots. A half-year follow-up revealed that his muscle strength did not recover, and his muscles seemed atrophied. Also, he developed post-herpetic neuralgia.
|
[[61.0, 'year']]
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M
|
{'24638224': 1, '4673442': 1, '28364009': 1, '21482943': 1, '26829085': 1, '24334599': 1, '10943192': 1, '9270616': 1, '17848871': 1, '12235600': 1, '33145224': 2, '16003688': 1, '34141794': 2, '32664058': 2, '9344310': 1, '4313433': 1, '23999562': 1, '8891477': 1, '27663748': 1, '33766961': 1, '33489582': 2, '23886000': 1, '33814502': 1, '21887512': 1, '26436084': 2, '22715438': 1, '15824336': 1, '23628922': 1, '22499102': 1, '1711192': 1, '24665583': 1, '21339202': 1, '21321495': 1, '9101105': 1, '33150099': 2, '23648986': 1, '27313622': 2, '11293092': 1, '8609933': 1, '30131076': 2}
|
{'6102897-1': 2, '6102897-2': 2, '7360310-1': 1, '7591216-1': 1, '7591216-2': 1, '7603882-1': 1, '4904081-1': 1, '7813428-1': 1, '4581133-1': 1, '8173409-1': 1}
|
2,083 |
6102904-1
| 30,126,360 |
comm/PMC006xxxxxx/PMC6102904.xml
|
Successfully treatment by eribulin in visceral crisis: a case of lymphangitic carcinomatosis from metastatic breast cancer
|
In 2010, a 37 year-old black woman had mastectomy and homolateral axillary dissection for invasive carcinoma in her left breast. pTNM stage was pT3 multicentric (53 mm diameter for the biggest) pN2 (seven positive lymph nodes) and no metastasis. Proliferation index was high (Ki-67 = 40%). Immunohistochemistry showed 90% of ER positivity and 60% of PR positivity. No overexpression of HER2 receptors has been found. According to multidisciplinary concertation, the patient was treated with adjuvant chemotherapy with six courses of FEC 100 (LV5FU 500 mg/m2, epirubicin 100 mg/m2, cyclophosphamide 500 mg/m2) every 3 weeks. Thereafter, she was treated by tamoxifen, at a dosage of 20 mg/day, and triptorelin (agonist analog of luteinizing hormone releasing hormone) for 4 years, until February 2014. In February 2014, the clinical exam reported a skin relapse in place of mastectomy scar. A CT scan showed multiple and bilateral pulmonary lesions and left pleural effusion. Chemotherapy with paclitaxel 80 mg/m2 and bevacizumab 10 mg/kg was initiated. Follow up imaging showed a positive partial response, so maintenance with fulvestrant and bevacizumab was initiated in August, 2014.\nIn February 2016, due to further progression in lungs and multiple bones sites, she was treated with exemestane 25 mg and everolimus 10 mg with an initial partial response.\nIn October 2016, she reported a dyspnea with dry cough. Left pleural effusion and non-specific infiltration were observed on the chest x-ray. We evocated first a mTOR inhibitor-associated non-infectious pneumonitis []. According to recommendations for patients with adverse events grade 3, everolimus was interrupted and corticosteroids administered. There was only a slight clinical improvement. The patient was submitted to bronchoscopy which shown a diffuse infiltration of lymphangitic appearance of the superior left trunk. The bronchoalveolar lavage fluid was negative for bacteria, acid-fast bacilli, and fungi. However, many adenocarcinoma cells were observed (Fig. ).\nTherefore, we concluded there was disease progression leading to visceral crisis and eribulin was started on 11.17.2016.\n12.5.2016, a baseline CT scan was performed and revealed infiltration and diffuse nodules distributed throughout the lymphatic vessels confirming lymphangitic carcinomatosis (Fig. ). After only one course of the therapy, that is to say 14 days, a remarkable clinical response on the breathness and cough was noted.\nAfter four courses of eribulin, a CT scan was performed and showed a significant reduction of pulmonary lesions and previously identified micronodules had disappeared (Fig. ). CT scan at 6 months confirmed radiological benefit (Fig. ).\nOverall, this patient benefited of 8,5 months of eribulin with a significant clinical benefit. In August 2017, CT scan showed a major progression disease with several lesions in lung, hepatic and bones. She started a new therapeutic regimen by fluorouracil and vinorelbin with a satisfying efficacy on all target lesions. Progression free survival was 7 months. In March, 2018, the patient had a severe asthenia, dyspnea and diffuse bone pain. Chemotherapy was stopped and she benefited of best supportive care. Death occurred at hospital on 04.24.2018 with an overall survival since diagnostic of 50 months.
|
[[37.0, 'year']]
|
F
|
{'21127197': 1, '18725649': 1, '25938528': 1, '21296855': 1, '26018662': 1, '31593099': 2, '22198425': 1, '17443041': 1, '21376385': 1, '28326833': 1, '28327998': 1, '22689175': 1, '10366939': 1, '8930034': 1, '25653556': 1, '30126360': 2}
|
{'6799856-1': 1}
|
2,084 |
6102914-1
| 30,126,443 |
comm/PMC006xxxxxx/PMC6102914.xml
|
Exceptional mucocutaneous manifestations with amyloid nephropathy: a case report
|
A 52-year-old Korean woman presented to our hospital because of edema and dry mouth. Additional complaints included fatigue, weight loss, and nail dystrophy. She had not had any of these symptoms in her medical history before. She started to complain of dry mouth and nail dystrophy 4 months before admission. During that period she lost 4 kg and felt severe fatigue. Two months before admission, she underwent a health screening in another hospital and received a diagnosis of renal dysfunction and hypothyroidism. There was no fever, rash, Raynaud phenomenon, or articular complaints. She had no medical history, and denied tobacco or alcohol abuse. There was no history of renal disease in her family.\nHer blood pressure was 120/70 mmHg, pulse rate was 62/minute, and her body temperature was 36.8 °C. Her conjunctiva was pale and her oral cavity was dry. Her nails were flattened and revealed onycholysis (Fig. ). A KOH test showed no fungi in her nails. Her thyroid gland was not enlarged and superficial lymph nodes were not palpable. There was no hepatosplenomegaly. No abnormality was present in the urological findings and neurologic examinations.\nLaboratory findings disclosed the following: hemoglobin 69 g/L, erythrocyte sedimentation rate 53 mm/hour, serum protein 88 g/L, albumin 26 g/L, serum creatinine 298.8 umol/L, and creatinine clearance 15 ml/minute according to Cockcroft and Gault formula. Urine sediment contained 0–2 white blood cells (WBC) and 0–2 red blood cells (RBC) per field. Her 24-hour urinary protein excretion was 0.696 g/day. Antinuclear antibodies, antibodies to SSA and SSB, rheumatoid factor, complement fractions, and cryoglobulins were all negative or within the normal range. In a urine protein electrophoresis, the proportion of urine protein was the following: albumin 87.6%, α1-globulin 4.0%, α2-globulin 1.1%, ß-globulin 0%, and γ-globulin 7.3%. Serum and urine protein immunofixation electrophoresis showed no abnormal finding. Serum free light chain of kappa and lambda was increased (0.307 g/L and 0.192 g/L, respectively). Serum immunoglobulin G (IgG) was raised at 38.55 g/L (normal 7.0–17.0), however, IgA and IgM levels were normal (3.04 g/L and 2.45 g/L, respectively).\nA slit lamp examination revealed superficial keratoconjunctival erosion in both eyes. A 99mTc pertechnetate scan of her salivary gland showed normal function. A lip biopsy demonstrated amyloid deposition around her salivary ducts, and atrophy of her salivary duct (Fig. , ). There was no mononuclear infiltration. A renal ultrasound scan showed increased echogenicity and the size of her right kidney and left kidney was 10.32 cm and 9.42 cm, respectively. A renal biopsy was performed. Light microscopy revealed a glomerular and peripheral capillary wall deposition of eosinophilic amorphous hyaline material (Fig. ). The Congo red stain by birefringence under polarized light showed apple-green staining reaction (Fig. ). Under electron microscopy, we observed non-branching, randomly distributed 10 nm-wide fibrils (Fig. ).\nA bone marrow aspiration biopsy reveals hypercellular marrow with 5% plasma cells. She was diagnosed as having AL amyloidosis then started on chemotherapy with cyclophosphamide and steroids. A follow-up at 8 months showed that her renal function remained stable (creatinine 267.85 umol/L) with reduction in free kappa and the lambda light chain (0.119 g/L, 0.154 g/L). The nail dystrophy also improved without other treatment (Fig. ).
|
[[52.0, 'year']]
|
F
|
{'1798223': 1, '5082429': 1, '24434547': 1, '3054024': 1, '8000827': 1, '6606406': 1, '8854150': 1, '3279077': 1, '5579496': 1, '21548513': 1, '1376976': 1, '6492489': 1, '9890691': 1, '8488407': 1, '30126443': 2}
|
{}
|
2,085 |
6102915-1
| 30,126,461 |
comm/PMC006xxxxxx/PMC6102915.xml
|
Robotic low anterior resection plus transanal natural orifice specimen extraction in a patient with situs inversus totalis
|
A 61-year-old man, previously diagnosed as SIT, came to our hospital for 6 months history of hematochezia and altered bowel habit. A diagnosis of rectal cancer was made in view of colonoscopic biopsy which confirmed an irregular circumferential lump of well differentiated adenocarcinoma at 10 cm from the anal verge. And the preoperative chest X-ray image and computed tomography scan revealed a total reversal of abdominal and thoracic organs, proving SIT (Fig. ). The double-contrast barium enema revealed an irregular rectal stenosis, nodulous filling defect and stiffness of involved rectal wall with destruction of mucosa. The magnetic resonance imaging showed the lump invaded through the muscularis propria and the serosa was suspiciously involved, while at least 2 enlarged perirectal lymph nodes were found, while the computed tomography (thorax + abdomen + pelvis) scan showed no distal metastasis (Fig. ). The remaining of the routine blood results were not abnormal, save a slightly decreased haemoglobin and albumin level, 12.9 g/dL and 3.8 g/dL. After obtaining informed consent, Robotic LAR with transanal NOSE was performed.\nPreoperative mechanical bowel preparation was carried out with polyethylene glycol electrolytes powder. Streptomycin and metronidazole were given as antibiotic prophylaxis. The operation was performed under general narcosis while the position of the patient was adjusted to a modified lithotomy position. The patient was placed in the Trendelenburg position at 30 degree and 10-degree tilted right-side-up.\nA 5-port method was adopted: two 12-mm ports for the camera and the assistant respectively, three 8-mm robotic ports. Pneumoperitoneum was established with the Veress needle approach under direct vision and a 12-mm camera port was inserted in 2 cm superior and right lateral to the umbilicus. Laparoscopic exploration of the abdominal cavity confirmed a total transposition of the abdominal organs and no abnormality from the descending to the sigmoid. The mass, in a size of 5*4*4cm3 and locating 2 cm above peritoneal reflection, suspiciously invaded the serosa without significant perirectal lymph node metastasis. The 8-mm port for robotic arm 1 was inserted in the right mid-clavicular line, 4 cm superior to the umbilicus, while the 8-mm port for robotic arm 3 was inserted in the right anterior axillary line, 4 cm inferior to the umbilicus. The third 8-mm trocar for robotic arm 2 was placed in the left lower quadrant (LLQ) that is one-third of the distance from the anterior superior iliac spine to the umbilicus. Harmonic ace curved shears, Prograsp forceps and Fenestrated bipolar forceps were respectively installed in the robotic arms 1, 3, and 2. The 12-mm assistant port was inserted in the right mid-clavicular line, parallel to the umbilicus. A 30-degree camera lens was adopted (Fig. ).\nAfter finishing installation of the various ports, the small intestine was swept to the LUQ to expose the right lower quadrant. The procedure started from incising the peritoneum at the inferior mesenteric artery root by means of Harmonic ace curved shears. The inferior mesenteric vessels were denuded, clipped, and divided. Then the peritoneum of the sigmoid mesentery was incised over the sacral promontory just to the left of midline. With cephalic traction and countertraction to the sigmoid mesentery provided by Fenestrated bipolar forceps and Prograsp forceps, a vascular free plane between the mesentery and the retroperitoneum was developed. After identifying and safeguarding the right ureter, the plane was developed towards the caudal and lateral direction further. Then it was possible to mobilize the descending colon mesentery further. The whole descending colon and sigmoid were mobilized well from the lateral pelvic. Splenic flexure mobilization was also performed.\nThe next step of the procedure was mesorectal dissection. The dissection was started from posterior to the rectum, at the level of the sacral promontory, and the peritoneum was incised along both sides of the rectum down to and around the anterior peritoneal reflection. The proximal line of resection was identified at 14 cm to the superior margin of the tumor, and the proximal end of the specimen was ligated with a special plastic seal, while the distal end of the specimen was ligated at 4 cm to the inferior margin of the tumor. Then the proximal colon and the distal colon were successively transected and divided using Harmonic ace curved shears.\nFor specimen extraction, we used a specially designed bag with an adjustable loop of string which could close the bag. The bag was introduced through the anus, and the specimen was deposited and closed inside the bag. Following carefully dilating the anus until two fingers could be easily reached, the specimen were then grasped and slowly “snaked” out of the bag through the anus. The bag was then removed.\nThe aperture of the proximal colon had been previously estimated and an appropriate stapler was chosen. According to our experience, 31 mm EEA circular stapler allowed the anvil passing and resulted in a very sufficient lumen. The anvil was introduced into the abdominal cavity through the anus and was fixed in the proximal margin of the previously opened proximal colon by purse-string suture, while the redundant tissue around the anvil was cut off to ensure a full exposure of the tissue with staples. Following introducing the CEEA stapler through the anus, the second assistant slowly extruded the spike through the center of the rectal stump and performed a colorectal anastomosis with double-checking the amount of tension. We filled the pelvis with distilled water and injected air in the reconstruct bowel to ensure any leak being repaired in time by means of intracorporeal sutures (Fig. ).\nAfter confirming anastomotic integrity, the whole abdominal cavity, and especially the trocars were watered with distilled water, bromogeramine solution and saline solution successively, and the peritoneal cavity was suctioned dry. And a closed suction drain was placed into the pelvic cavity. After removing the trocars, all port sites were immediately closed with sutures in a subcuticular fashion.\nIn this case, the total operative time was 210 min, while the docking time and the console time was 25 min and 185 min respectively. Estimated blood loss was less than 50 mL. The first flatus and liquid diet happened on the second day after the operation, while solid diet the fifth day. The patient convalesced nicely without any complications and was discharged on the seventh day after the surgery. The postoperative pathological diagnosis revealed a 4x4x0.6 cm3 moderately differentiated adenocarcinoma (T2 N0) with a 1 cm distal and free microscopic circumferential margin. The number of lymph nodes harvested is 13, lymph node retrieval was performed by pathology technicians (Fig. ).
|
[[61.0, 'year']]
|
M
|
{'21471789': 1, '12143842': 1, '24565506': 1, '25278692': 1, '19415395': 1, '26195883': 2, '31830972': 1, '22038650': 1, '10349731': 1, '24282364': 1, '20436720': 2, '26052351': 1, '27901281': 1, '22487647': 1, '31031325': 1, '30126461': 2}
|
{'2858843-1': 1, '4499930-1': 1}
|
2,086 |
6102916-1
| 30,126,374 |
comm/PMC006xxxxxx/PMC6102916.xml
|
PD 1 checkpoint inhibition in solid organ transplants: 2 sides of a coin – case report
|
The patient is a 50 year old male who received a LURT 8 years prior to presentation. He had previously undergone bilateral native nephrectomies 2 months prior to transplant for PKD. His early course was complicated by biopsy-proven acute cellular rejection, vascular type, 5 days after transplant, which was effectively treated with anti-thymocyte globulin and intravenous immunoglobulin. He subsequently went on to enjoy excellent graft function. Initially, he was maintained on standard triple immunosuppression with tacrolimus, mycophenolate mofetil (MMF) and prednisone.\nTwo years prior to presentation, he developed numerous squamous cell carcinomas of the skin treated with resection and radiation. One of these lesions was an invasive poorly differentiated SCC (Bowen’s type) of the left auricle, requiring auriculectomy and reconstruction. Tumor margins were negative. His immunosuppression was reduced by stopping his MMF.\nOne year prior to presentation he developed a parotid mass found to be SCC by fine needle aspiration. It was felt that this was a metastatic lesion from the auricular tumor. At this time, he was switched from a dual immunosuppressive regimen of tacrolimus and prednisone to sirolimus (SRL) and prednisone. He underwent a left parotidectomy and neck dissection with pathology showing invasive keratinizing squamous cell carcinoma, poorly differentiated. The tumor was 4.6 cm with lymphovascular and perineural invasion. Surgical margins were negative, but 5 out of 23 periparotid and cervical LNs were positive for metastasis with focal extranodal extension. He underwent radiation therapy and cetuximab. A surveillance PET CT performed 6 months after treatment revealed 5 bilateral pulmonary nodules, which grew over 2 months from 6 mm to 10 mm. He initiated systemic treatment with carboplatin, paclitaxel and cetuximab with minor improvement initially, followed by disease progression in the lungs and mediastinum after 7 months of treatment. He was then treated with gemcitabine, and imaging after 2 months of therapy revealed tumor growth.\nA complex discussion was then held regarding symptom-focused palliative care or consideration of novel therapies. Next-generation tumor sequencing was performed on his lung biopsy specimen. Although no clear primary tumor driver was found, 16 genetic abnormalities of possible oncogenic effect were demonstrated, including an EGFR amplification event and a ROS1 mutation of uncertain significance. He enrolled in a clinical trial of the ROS1 inhibitor, entrectinib, but had clinical and radiographic progression within 6 weeks. Other clinical trial options were limited by his history of solid organ transplantation.\nWith his young age and active lifestyle, the patient opted to proceed with nivolumab 3 mg per kg therapy, understanding the high risk of alloimmune kidney transplant rejection. In preparation, sirolimus was tapered off and prednisone was tapered to 5 mg daily, after which his allograft function remained stable with a creatinine of 1.4 mg/dL. His sirolimus level prior to discontinuation was 6.9 ng/mL.\nThirteen days after receiving the first dose of nivolumab, he presented with low-grade fevers, oliguria and fluid retention. The physical exam demonstrated an enlarged and tender renal allograft and significant lower extremity and peri-orbital edema. Laboratory testing revealed marked acute kidney injury with a creatinine of 4.4 mg/dL. His sirolimus level was noted to be 1 ng/mL and he was treated empirically for acute rejection with a 3 day methylprednisone pulse but without improvement. A renal biopsy was deferred, as he was not a candidate for T-cell depleting therapy with his active malignancy and hemodialysis was initiated for volume overload and electrolyte disturbances. Given the life-threatening nature of his metastatic SCC, the graft was sacrificed and he continued on nivolumab therapy every 2 weeks. Imaging after 4 weeks demonstrated a partial regression in tumor burden and lymphadenopathy. For continued fevers, hematuria and marked allograft pain, an allograft nephrectomy was performed 2 months after stopping his immunosuppression. Histologic evaluation revealed hemorrhagic infarction with features of acute and chronic vascular rejection (Fig. ).\nNow, he continues treatment with nivolumab and most recent imaging 18 months after treatment initiation shows stable tumor regression. He has been maintained on hemodialysis, but has been able to travel and return to an active lifestyle.
|
[[50.0, 'year']]
|
M
|
{'25891174': 1, '26752406': 1, '1984929': 1, '32043028': 1, '26988410': 1, '31058839': 1, '27592805': 1, '25795410': 1, '28076715': 1, '33291277': 1, '34152556': 1, '26028407': 1, '27718784': 1, '27932166': 1, '22658126': 1, '25482239': 1, '32119110': 1, '25452452': 1, '26951628': 1, '34555935': 1, '26962927': 1, '26952546': 1, '28189378': 1, '32368693': 1, '32043699': 1, '30126374': 2}
|
{}
|
2,087 |
6102931-1
| 30,126,441 |
comm/PMC006xxxxxx/PMC6102931.xml
|
Neural therapy of an athlete’s chronic plantar fasciitis: a case report and review of the literature
|
A 24-year-old white man, a middle-distance runner (800 m) competing at national level (seasonal best/personal best of 1 minute 52 seconds), developed severe left heel pain in the pre-season in March 2013. His maximum perceived pain intensity was 10 cm on a visual analog scale (VAS) that ranged from 0 to 10 cm, with 10 cm expressing the worst perceivable pain; the athlete had to interrupt all running activity, and severe pain was perceived even when walking or standing. He continued training with aqua jogging and cycling. He got personalized hand-crafted orthopedic gel peads. Two months later he was attended by an orthopedic surgeon, who additionally prescribed oral intake of nonsteroidal anti-inflammatory drugs (NSAIDs) for 8 weeks. The athlete could continue his training but was not free from pain. When discontinuing medication in July 2013, pain returned immediately, and perceived pain intensity during walking was 10 cm on a VAS (range 0–10 cm). Eight sessions of ESWT were thus added to his treatment plan, and were conducted at a German Olympic center. He did not feel better after the treatment and reported a high level of frustration. An MRI was performed in January 2014 showing a calcaneal spur, signs of inflammation at the calcaneal tubercle, and structural changes of the plantar fascia, surrounded by a large edema (see Fig. ). In February 2014 he underwent an open plantar fasciotomy. Four weeks later he was allowed to perform the first units of regenerative running. Pain returned after approximately 1 week of training. An X-ray revealed no pathology and he was recommended to continue with soft training sessions. He received a peppering injection that reduced pain for 12 hours, and NSAIDs were re-prescribed. His running performance remained at a remarkably low level in comparison to his non-injured state, despite regular personalized training sessions. He presented himself at our out-patient clinic in July 2014 (for timeline see Fig. ).\nAn examination identified pain to palpation at the medial calcaneal tubercle and along the medial band of the plantar fascia. Thickening and enlargement of the proximal one-third plantar fascia was noted. Full and pain-free range of motion was noted to his ankle and foot. Standing caused moderate (VAS score, 5 cm) pain; walking caused severe (VAS score, 10 cm) pain. Latent myofascial trigger points could be found in the surrounding muscles: gastrocnemius medialis and lateralis, and tibialis posterior. Apart from these symptoms no abnormalities in his medical or family history which may have been relevant to the medical case were reported and he presented himself in a good mental condition. The diagnosis based on these findings was chronic plantar fasciitis (calcaneal spur syndrome).\nHe was treated with neural therapy (that is, injection of < 1 ml procaine 1%, which is a local anesthetic) of the surgical scar and along the surgical puncture channel. He lay in a supine position on a treatment table. Sessions took approximately 5 minutes. In total, three sessions (at baseline, at week 1, and after 4 weeks) were performed.\nAt the first treatment (March 2015), he described a slurping noise, like “if something filled up the pain origin.” Afterwards he could stand pain-free and walking (not running) was subjectively improved. After the third session the pain had been completely eliminated (VAS = 0 cm). He could return to sports at the former level. Since March 2015 no recurrence of the problem could be observed. No adverse events were observed.
|
[[24.0, 'year']]
|
M
|
{'16480459': 1, '26115657': 1, '27402210': 1, '20439021': 1, '16868321': 1, '24559879': 1, '25960898': 2, '27807291': 1, '23827248': 1, '30270815': 1, '12490958': 1, '25056259': 1, '9291553': 1, '24860133': 1, '15989378': 1, '25770572': 1, '16796396': 1, '22326003': 1, '23099290': 1, '21504939': 1, '26913766': 1, '30126441': 2}
|
{'4415660-1': 1}
|
2,088 |
6102942-1
| 30,151,465 |
comm/PMC006xxxxxx/PMC6102942.xml
|
Bilateral Synchronous Stress Fracture of the Tibia in a Young Female Basketball Player
|
An 11-year-old female basketball player was referred to our radiology department with anterolateral pain of both knees over a few weeks to exclude Osgood-Schlatter disease. Previous medical history consisted of Perthes disease of the right hip at the age of 4.\nUltrasound (US) revealed bilateral normal appearance of the tibial tubercle, excluding Osgood-Schlatter disease. Subsequent conventional radiographs of both knees showed sclerotic lines parallel to the growth plates in keeping with synchronous stress fractures of both proximal tibiae (Figures , ). Additional MRI depicted low-intensity fracture lines surrounded by bone marrow oedema, confirming the diagnosis of stress fractures (Figures , , , , , ). On T2-weighted fat-saturated images we observed an extensive high-signal area of bone marrow oedema surrounding fracture lines (Figures , , , ). On T1-weighted images, the oedematous marrow changes have low signal intensity (Figures , ).\nAlthough the conventional radiography in our case was sufficient to allow for the diagnosis of stress fracture, MRI was performed to evaluate the precise extent of the fracture line and surrounding oedema and to exclude any underlying bone marrow disease. Laboratory examination was within normal limits. The patient was treated conservatively by rest. The recovery was uneventful, and the patient was completely pain free after four weeks.
|
[[11.0, 'year']]
|
F
|
{'19809896': 1, '34465684': 2, '24427386': 1, '23396635': 1, '32676251': 2, '7573660': 1, '25805712': 1, '16324973': 1, '30151465': 2}
|
{'7362595-1': 1, '8426658-1': 1}
|
2,089 |
6102943-1
| 30,151,460 |
comm/PMC006xxxxxx/PMC6102943.xml
|
Ultrasonographic Pattern of Testicular Metastasis of Clear Cell Renal Cell Carcinoma with Pathological Correlation
|
A 69-year-old man without relevant medical history presented with a small lump in the right testis. Ultrasound examination revealed a solitary intra-testicular hyperechoic 12 mm tumor with heterogeneous appearance and with multiple small cystic-like areas (Figure ). On colour-Doppler ultrasound, the tumor was hypervascular compared to adjacent parenchyma (Figure ). Dosage of α-fetoprotein, human chorionic gonadotropin and lactate dehydrogenase serum markers was normal. Computed tomography (CT) revealed a hypervascular parenchymal tumor in the right kidney. The patient underwent a right radical nephrectomy as well as a right inguinal orchiectomy. Histopathological and immunohistochemical examination demonstrated a primary renal CCRCC metastasized to the testis (Figure ), staged pT1bN0M1.
|
[[69.0, 'year']]
|
M
|
{'3882978': 1, '11469344': 1, '2672730': 1, '19168021': 1, '20123499': 1, '11796908': 1, '18769334': 1, '5343486': 1, '24678363': 1, '3299487': 1, '5051673': 1, '30151460': 2}
|
{'6102943-2': 2}
|
2,090 |
6102943-2
| 30,151,460 |
comm/PMC006xxxxxx/PMC6102943.xml
|
Ultrasonographic Pattern of Testicular Metastasis of Clear Cell Renal Cell Carcinoma with Pathological Correlation
|
A 77-year-old man presented with painless swelling of the left hemiscrotum. He underwent a partial left nephrectomy for a CCRCC five years earlier and later developed pulmonary metastases. On physical examination, there was a firm left testicular mandarin-sized mass. Scrotal sonography showed a hyperechoic intra-testicular mass (diameter 47 mm) replacing almost the entire left testis. This heterogeneous mass contained multiple small anechoic cystic-like areas (Figure ) and was hypervascular on color-Doppler. Serum tumor markers were within normal limits. The metastatic nature of this testicular mass was confirmed by histological examination of the orchiectomy specimen.
|
[[77.0, 'year']]
|
M
|
{'3882978': 1, '11469344': 1, '2672730': 1, '19168021': 1, '20123499': 1, '11796908': 1, '18769334': 1, '5343486': 1, '24678363': 1, '3299487': 1, '5051673': 1, '30151460': 2}
|
{'6102943-1': 2}
|
2,091 |
6102945-1
| 30,151,457 |
comm/PMC006xxxxxx/PMC6102945.xml
|
Unusual Symptomatic Multipartite Patella Associated with Quadriceps Fat Pad Edema
|
A 29-year-old male, who is a construction worker, presented with a six-month history of bilateral anterior knee pain and underwent an MRI examination at our department. He had no history of major knee trauma. The intensity of his pain was moderate to severe at rest and increased when seated or in a squatting position. On physical examination, there was point tenderness over the suprapatellar region on both sides. No clinical or laboratory findings that supported the presence of inflammation or infection were identified. A standard anteroposterior radiograph and MRI examinations revealed bilateral multipartite patella variation. The MRI also revealed slight bone marrow edema within the main patellar fragment and nonfused bony fragments (Figure ). In addition, the MRI showed QFP edema and inflammation that was characterized by increased signal of the fat pad along with mass effect on the suprapatellar joint recess and contrast enhancement by intravenous contrast administration (Figure ). Surgical treatment was proposed for removing the unstable bony fragments, but the patient refused and received conservative treatment, including oral nonsteroidal anti-inflammatory drugs (NSAIDs) and physical therapy. There was pain reduction at the two- and six-month follow-ups compared to baseline; however, he reported transient pain and discomfort after strenuous activities at the same follow-ups.
|
[[29.0, 'year']]
|
M
|
{'20111951': 1, '25937094': 1, '17151849': 1, '10470905': 1, '15149978': 1, '22488011': 1, '24531356': 1, '25442030': 1, '18607662': 1, '15293677': 1, '16538463': 1, '18664634': 1, '30151457': 2}
|
{}
|
2,092 |
6103389-1
| 30,140,600 |
comm/PMC006xxxxxx/PMC6103389.xml
|
Primary Choroid Plexus Papilloma over Sellar Region Mimicking with Craniopharyngioma: A Case Report and Literature Review
|
This 43-year-old male without systemic disease complained of blurred vision progressively for almost six months. Bilateral visual field defects were found under visual field examination. The patient’s high cortical functions were intact. Cranial nerve function was also normal, except for bilateral lower temporal hemiapnosia. Anatomical MRI revealed a mass lesion over sellar and suprasellar regions with heterogeneous contrast enhancement, and a cystic component that caused upward compression of the optic chiasm (Figure ). Endocrinological data included pre-operative serum measurements of growth hormone (GH), insulin-like growth factor-1, adrenocorticotropic hormone (ACTH), cortisol, prolactin (PRL), triiodothyronine (T3), thyroxine (T4), free T4, thyrotropin-stimulating hormone (TSH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone, all of which were at normal levels.\nAfter the provisional diagnosis of craniopharyngioma with optic nerve compression, we performed endoscopic trans-sphenoidal surgery (ETS) for tumor removal. We used a standard one-surgeon, two-hand technique via a single nostril, with the endoscope mounted on a pneumatic scope holder. A vertical linear mucosal incision was made with electric cautery near the root of the bony nasal septum. A nasal speculum was placed after dilatation of the space and fracture of the bony nasal septum without destruction of the middle turbinate. Subsequently, posterior septectomy was performed with removal of the anterior portion of the vomer bone using high-speed drills and Kerrison rongeurs. The bony septum inside the sphenoid sinus and the rostrum of sphenoid bone were removed to expose the sella turcica. The floor of the pituitary fossa was removed after confirmation of anatomy via the intraoperative navigation system or lateral skull fluoroscopy. A soft density tumor with some yellowish particles was removed endoscopically with ring curettes over the sellar region. The cystic part of the tumor with old blood content was drained during surgery. The tumor was completely removed with the diaphragm sella intact and without cerebrospinal fluid leakage. The sellar floor was reconstructed using with tissue glue and autologous bone grafts harvested during the approach. The patient had no neurological deficit after surgery. No electrolyte imbalance, diabetes insipitus (DI) sign, or hormone deficiency was noted. The original visual field defect also improved after surgery. Post-operative images indicated no residual or recurrent tumor within the two-year follow-up period (Figure ).\nMicroscopic examination revealed that the tumor was composed of delicate fibrovascular cores covered by a single layer of cuboidal to columnar epithelial cells (Figure ). There are no anaplastic features identified. The tumor cells were immunoreactive for cytokeratin AE1/AE3 and epithelial membrane antigen (EMA), focally positive for S-100, and non-reactive for glial fibrillary acidic protein (GFAP) (Figures -). Immunohistochemical stain with multiple pituitary hormones, including ACTH, PRL, FSH, LH, GH, and TSH, was negative. Based on these results, we diagnosed CPP.
|
[[43.0, 'year']]
|
M
|
{'16609849': 1, '10566636': 1, '14758957': 1, '15200124': 1, '18159143': 1, '9726580': 1, '22716306': 1, '26885287': 2, '20185881': 1, '18224277': 1, '3193190': 1, '21140177': 1, '1383866': 1, '9766271': 1, '28684370': 1, '3572508': 1, '30140600': 2}
|
{'4754588-1': 1}
|
2,093 |
6103391-1
| 30,140,596 |
comm/PMC006xxxxxx/PMC6103391.xml
|
Effect of High-dose Biotin on Thyroid Function Tests: Case Report and Literature Review
|
A 49-year-old woman had a past medical history of MS; she was on post iodine-131 therapy for Graves' disease and was euthyroid after that for three years. In a follow-up visit, her thyroid function tests showed markedly elevated free T4 to 3.2 ng/dl and suppressed thyrotropin (thyroid stimulating hormone, TSH) to 0.08. She was treated with Copaxone (Teva Pharmaceuticals, PA, USA) 40 mg injection three times weekly. A month before this thyroid function test was done, the patient started to have 200 mg of biotin orally daily.\nOn physical examination, the patient’s thyroid gland was found to be normal and had no signs of Graves' disease. Thyroid function tests were repeated. Total triiodothyronine (T3) and free thyroxine (FT4) were both markedly elevated, while TSH was suppressed and the TSH binding-inhibiting antibody test was positive (Table ). This combination of test results was suggestive of Graves’ disease. However, the laboratory data were in striking contrast with the paucity of signs and symptoms observed in the patient.\nThe patient was asked to stop the biotin treatment temporarily; and one week later, repeated thyroid function tests showed completely normal results (Table ). No other change was made to her medication list, and she continued to feel well. Biotin treatment was resumed thereafter.
|
[[49.0, 'year']]
|
F
|
{'27843813': 1, '28231059': 1, '31579637': 2, '28222020': 1, '23089740': 1, '27917400': 1, '2032315': 1, '34840835': 2, '22437752': 1, '33791245': 1, '25787192': 1, '32118725': 1, '30140596': 2}
|
{'6768618-1': 1, '8612797-1': 1}
|
2,094 |
6103392-1
| 30,140,599 |
comm/PMC006xxxxxx/PMC6103392.xml
|
Spindle Cell Carcinoma of the Lung/Pleura: An Incidental Finding
|
A 59-year-old African American male with a medical history of hypertension and abdominal aortic dissection presented to our medical clinic complaining of back pain for one month. He described it as dull, non-radiating, and with no associated motor or sensory weakness. The patient denied shortness of breath, chest pain, productive cough, weight loss, night sweats, or loss of appetite. Physical examination was unremarkable. The patient reported a 10-year pack smoking history. One year prior to the current presentation, he was admitted to our hospital with severe stabbing abdominal pain radiating to the back. Computed tomographic (CT) angiography was done which showed an abdominal aortic dissection extending from thoracic aorta to left common iliac artery that was managed conservatively with tight blood pressure control. The patient admitted to not having any follow-up imaging since discharge from the hospital.\nA CT scan of the abdomen and pelvis was ordered to evaluate the abdominal aortic dissection as the cause of his back pain. The results showed a stable long segment type B dissection of the descending thoracic aorta extending into the left common iliac artery. An incidental finding of a large lobulated pleural-based mass was also seen in the lower lobe of the left lung. A CT scan of the chest with contrast was ordered for better visualization of the mass, which again identified a large lobulated pleural-based mass in the posterior mediastinum measuring 21.5 x 9 x 10.2 cm (Figure ).\nA US-guided biopsy of the lung mass was done which showed a poorly differentiated malignant neoplasm with a predominantly spindle cell pattern and epithelioid features, consistent with spindle cell carcinoma. Immunohistochemical (IHC) analysis was performed, which was positive for programmed death-ligand 1 (PD-L1) with a tumor proportion score (TPS) of 85 - 90% (Figure ).\nA bone scan and magnetic resonance imaging (MRI) of the abdomen and pelvis were done to determine the staging. A bone scan did not reveal any abnormal activity suggestive of osteoblastic metastatic disease. The MRI of the abdomen revealed a 2 cm x 2 cm left adrenal lesion suspicious for metastatic disease. The patient refused to undergo surgical evaluation for resection of the mass, so he was started on chemotherapy. So far, he has received one cycle of Carboplatin with a target area under the curve (AUC) of five, and Pemetrexed, 500 mg/m2. He was also started on Pembrolizumab, 200 mg intravenously (IV) to be given every third week, given the high-grade PD-L1 expression. The patient is scheduled for follow-up with a positron emission tomography (PET)-CT scan after completing his third cycle of chemotherapy.
|
[[59.0, 'year']]
|
M
|
{'16941152': 1, '27745820': 1, '29240878': 1, '28025310': 1, '28614235': 2, '21515338': 1, '20073605': 1, '33154219': 1, '28671973': 1, '26291008': 1, '30140599': 2}
|
{'5478320-1': 1}
|
2,095 |
6103970-1
| 30,134,860 |
comm/PMC006xxxxxx/PMC6103970.xml
|
Multifocal motor neuropathy presenting as a post-infectious complication of dengue: a CASE report
|
A 20 year old Sri Lankan male who was employed as a helper in a grocery, admitted to our unit with weakness of both hands of 1 month’s duration. He was treated for serologically confirmed (Dengue NS1 antigen positive) dengue fever approximately 5 weeks ago at the local hospital and had made an uneventful recovery. He has been given 5 days of inward treatment and the records from the local hospital revealed that he had simple dengue fever with no evidence of fluid leakage.\nFive days after discharge from the hospital he has first noticed the weakness of his right hand when he dropped a glass of water due to poor grip. Weakness was more in the right hand which was his dominant hand and it was slowly progressive over 1 month. At the time of presentation to us he could not write or button on his shirt due the weakness of the hands. Weakness of the left hand was milder than that of the right. The weakness was confined to hands and did not involve forearms or arms. He denied any accompanying numbness, parasthesia or pain.\nOn inquiry he admitted that there was slight weakness of both feet which did not significantly interfere with walking. There was no associated neck/back pain or bladder/bowel incontinence. He did not complain of difficulty in breathing, diplopia, dysphagia, nasal regurgitation, dysarthria or fatigability. He did not give a recent history of trauma to the spine/neck or any preceding diarrheal illness or skin rash.\nHe had no previously diagnosed long term medical ailments and has not undergone any surgical procedures in the past. He was not on any long term medications and he denied smoking, use of alcohol or illicit drugs. He did not give a family history of any progressive neurological conditions.\nOn general examination he had an average built with no pallor, lymphadenopathy or any signs of malnutrition. No skin rashes or hypopigmented patches were noted. There was minimal small muscle wasting of bilateral hands and feet. No muscle fasciculations were noted. Distal upper limb (hand) power was diminished asymmetrically, right hand demonstrating a power of 3 out of 5 and left hand demonstrating a power of 4 out of 5. All fine finger movements including flexion, extension, abduction and adduction were affected with some degree of weakness in wrist extension as well. Bilateral supinator and biceps reflexes were diminished.\nDistal lower limb (feet) power was also diminished but was less pronounced (power grade 4) when compared to the degree of hand weakness. Bilateral foot dorsiflexion was weak. Ankle jerks were elicited with reinforcement whereas the knee jerks were elicited without reinforcement. There was no objective sensory impairment of touch, pain, temperature, vibration and joint position sensations in both upper and lower limbs. Bilateral plantar responses were down going. No palpable nerve thickening identified. No cerebellar signs were demonstrated and his gait showed a minor degree of high stepping due to weak dorsiflexion. Examination of higher functions and cranial nerves including the fundal examination revealed no abnormality.\nExamination of the cardiovascular, respiratory systems and the abdomen was essentially normal.\nFull blood count revealed white blood cell count: 8.5 × 109/L, platelet count: 274 × 109/L, hemoglobin 12 g/dl with normal red cell indices. Blood picture showed normochromic normocytic cells with some reactive lymphocytes suggestive of a recent viral infection. Serum creatinine 80 μmol/l (60 - 110 μmol/l), serum sodium 138 mmol/l (135 - 145 mmol/l), serum potassium 3.8 mmol/l (3.5 - 5 mmol/l), serum magnesium 0.9 mmol/l (0.8–1.1 mmol/l), serum ionized calcium 1.2 mmol/l (1.05–1.30 mmol/l). Liver profile: AST 21u/l (10 - 40u/l), ALT 13u/l (7–56 u/l), ALP 67u/l (100–360 u/l), serum total bilirubin 0.7 mg/dl (0.1–1.2 mg/dl), serum albumin 36 g/l (35 - 50 g/l), serum globulin 32 g/l (20 - 35 g/l). CPK levels were normal. Inflammatory markers: ESR 25 mm/hour and CRP < 6 mg/dl.\nNerve conduction study revealed findings in keeping with multifocal motor neuropathy with conduction blocks involving the distal upper and lower limb peripheral nerves without any conduction abnormalities in the sensory nerves (Fig. ).\nCSF analysis did not show any increase in proteins or cells and the values were within the normal limits. Anti-GM1 IgM antibody test was not carried out due to the high cost of the test and the patient’s unstable financial background. A sural nerve biopsy (a sensory nerve) was carried out and revealed histologically unremarkable nerve fibres and blood vessels with no evidence of inflammation, atrophy or granulomata formation. Recent dengue infection was confirmed with positive dengue IgM and IgG antibodies with enzyme-linked immunosorbent assay (ELISA).\nAs the patient fulfilled criteria, the diagnosis of multifocal motor neuropathy with conduction blocks was confirmed. He was then referred to the neurologist and was started on intravenous immunoglobulin (IVIg) therapy (2 g/kg/day) which was given for 5 days. He showed a mild improvement of his neurological weakness with the treatment and outpatient physiotherapy was arranged. The next immunoglobulin dose was planned to be given after 2 weeks.
|
[[20.0, 'year']]
|
M
|
{'21199100': 1, '34805205': 1, '14722828': 1, '15534279': 1, '22346016': 2, '20739796': 1, '20667861': 1, '15611308': 1, '12429589': 1, '17161468': 1, '29669602': 2, '22019654': 1, '17428969': 1, '29350156': 1, '23907602': 1, '9746040': 1, '29119088': 1, '16924002': 1, '25695919': 1, '16279990': 1, '30134860': 2}
|
{'5907410-1': 1, '5907410-2': 1, '3271466-1': 1}
|
2,096 |
6103999-1
| 30,131,065 |
comm/PMC006xxxxxx/PMC6103999.xml
|
Diagnostic difficulties of primary angiosarcoma of the breast: a case report
|
A 56-year-old Arabian woman presented to our institution with a palpable right breast mass (Fig. ). Two months prior to presentation she complained of a painless right breast lump that quickly increased in size with bluish coloration of overlying skin. She had no personal or family history of cancer, breast surgery, or breast irradiation. A physical examination revealed a 5 cm ill-defined painless mass that overlapped two upper quadrants. The mass was firm and fixed to the skin which was bluish without ulceration. There was no nipple retraction, no axillary lymphadenopathy, and no signs of lymphedema. A mammography showed no evidence of spiculation. No suspicious calcifications were seen. A needle core biopsy was performed and showed anastomosing round-to-oval spaces which contained erythrocytes. Lining cells had thin, elongated but hyperchromatic nuclei, which sometimes protruded into the luminal spaces. The neoplastic vascular channels invaded adipose tissue. Immunohistochemical stains performed on the core biopsy revealed membranous reactivity of the tumor cells for CD31-related antigen and CD34-related antigen. These findings were initially interpreted as a benign vascular tumor. However, as the mass measured 5 cm, the diagnosis of angiosarcoma was more appropriate. A mastectomy without axillary dissection was performed since angiosarcoma was suspected. At gross examination, the tumor appeared ill-defined, spongy, and soft (Fig. ). A microscopic examination revealed vascular channels lined by atypical endothelial cells with hyperchromatic, spindle-shaped or round nuclei (Fig. ). There were mild to moderately scattered pleomorphic cells, and scattered mitotic figures (Fig. ). Other sections showed papillary formations, solid foci of spindle cells, and hemorrhagic necrosis (Figs. and ). The margins of the tumor were infiltrative (Fig. ). The diagnosis of primary intermediately differentiated angiosarcoma of the breast (grade II) was made. No distant metastases were found. She was lost to follow-up and further treatment after mastectomy until she developed local tumor progression 4 months later.
|
[[56.0, 'year']]
|
F
|
{'12829679': 1, '15692416': 1, '19433291': 1, '7199829': 1, '23466684': 1, '3179927': 1, '19410492': 1, '27510467': 1, '25521258': 1, '12791356': 1, '22305554': 1, '7190060': 1, '30131065': 2}
|
{}
|
2,097 |
6104166-1
| 30,159,305 |
comm/PMC006xxxxxx/PMC6104166.xml
|
Perineal Groove: Report of Two Cases and Review of the Literature
|
This infant was born to Asian parents. The baby's mother was a 34-year-old woman, and her father was a 32-year-old man. The mother was gravida 2 and para 1 (G2P1) with good prenatal care. Their first baby was induced owing to intrauterine fetal death, and the details were unknown. There was no family history of congenital abnormalities on either side of the family, and the parents were not consanguineous. The mother also had no history of tobacco, alcohol, or substance abuse. The mother's antenatal examination was uneventful except for gestational diabetes. During pregnancy, the mother's blood glucose was maintained between 6.1 mmol/l and 8.1 mmol/l without any drug treatment. The infant's gestational age was 37 weeks and 3 days. The newborn was delivered by vaginal delivery and her birth weight (BW) was 4910 g. Apgar scores were 6 and 8 at 1 and 5 min, respectively. Owing to dyspnea 2 h after the birth, the neonate also received further examination in the NICU. On examination, a perineal defect was noted. The groove extended vertically downward from the base of the vaginal fourchette to the anterior rim of the anus at the 12 o'clock position. The perineal groove was a moist red sulcus that was ~1 cm long, 0.1 cm wide and 0.1 cm deep. There were no signs of malformation, bleeding, fistula, secretions, or infection noted in the genital area (Figure ). During admission, the infant had normal excretory functions. Her vital signs were as follows: temperature of 36.5°C; heart rate of 110 beats/min; respiratory rate of 65 breaths/min; and blood pressure of 75/39 mmHg. The newborn was diagnosed with asphyxia neonatorum, neonatal wet lung disease, fetal macrosomia, cephalohematoma of newborn, PDA, myocardial injury, and congenital perineal groove and as a neonate of a diabetic mother after further examinations. This diagnosis of perineal groove was also based on clinical examination. The neonate was discharged home with her parents at 9 days of life when all her conditions improved. Both patients in case one and case two were advised to undergo follow-up examinations.
|
[[34.0, 'year']]
|
M
|
{'28103464': 1, '21242201': 1, '24026394': 1, '14504889': 1, '21138469': 1, '19753644': 1, '25556416': 1, '25697324': 1, '26729785': 1, '21514189': 1, '34926162': 1, '4072431': 1, '24941754': 1, '3712197': 1, '6632394': 1, '34104451': 2, '33815912': 1, '16516615': 1, '29023894': 1, '26929866': 1, '5242147': 1, '34449719': 2, '16025272': 1, '30159305': 2}
|
{'8396188-1': 1, '8396188-2': 1, '8396188-3': 1, '8396188-4': 1, '8170287-1': 1}
|
2,098 |
6104203-1
| 30,151,399 |
comm/PMC006xxxxxx/PMC6104203.xml
|
Focal Epileptiform Discharges Can Mimic Electrode Artifacts When Recorded on the Scalp Near a Skull Defect
|
Patient 1 is a 23-year-old man who presented in convulsive status epilepticus. He suffered traumatic brain injury and had a right frontal craniectomy 5 months prior to admission; bone flap replacement was delayed due to hospital-acquired infection. Computed tomography (CT) head showed the expected skull defect and old lesions (: CT head). Since lorazepam, levetiracetam, and lacosamide did not abort the seizures, he was intubated and propofol was started. EEG monitoring showed high-amplitude waves with phase reversals in FP2-F4 and F4-C4 F4. Because these waves did not show a clear-cut “physiological field”—even when display sensitivity was increased from 7 to 3 µV/mm—they were thought to be F4 electrode artifacts (: EEG1). Carefully cleaning the scalp, replacing the electrodes, and keeping electrode impedances between 2 and 5 kΩ failed to eliminate the “electrode artifacts.” Switching to a transverse bipolar and a referential montage did not help clarify the issue. Thus, 4 electrodes were removed from the left side of the head (spare electrodes were not within reach) and attached to 10-10 locations around F4 (AF4, FC4, F2, F6). An extended montage was then constructed (: EEG2). This simple maneuver proved that what appeared as F4 electrode artifacts were actually focal epileptiform discharges with an exceptionally “compact” electric field, that is, voltage drop was rapid at short distances from the peak.
|
[[23.0, 'year']]
|
M
|
{'16751720': 1, '18053144': 1, '13810779': 1, '12195981': 1, '1304564': 1, '21872525': 1, '13885270': 1, '2187021': 1, '19925193': 1, '90597': 1, '30151399': 2}
|
{'6104203-2': 2, '6104203-3': 2}
|
2,099 |
6104203-2
| 30,151,399 |
comm/PMC006xxxxxx/PMC6104203.xml
|
Focal Epileptiform Discharges Can Mimic Electrode Artifacts When Recorded on the Scalp Near a Skull Defect
|
Patient 2 is a 63-year-old woman who arrived in the emergency room in a state of delirium. She was on divalproex and zonisamide for seizure disorder, which started after resection of a frontal meningioma. CT head showed a skull defect overlying a right frontal lobe encephalomalacia (: CT head). In addition to clear-cut epileptiform spikes in T3 and F7, EEG showed phase-reversing sharp and slow waves in Fp2-F4 and F4-C4 with no clear-cut “physiological field”—even when display sensitivity was increased from 7 to 3 µV/mm (: EEG1). As in patient 1, troubleshooting the electrodes and montage reformatting were performed, but we were able to conclude that the F4 potentials are focal epileptiform discharges only when additional 10-10 electrodes were placed on the head (: EEG2). Spare electrodes were immediately available (unlike the first case) obviating the need to remove electrodes already attached to the head. Extending the montage proved that the F4 phase reversals were focal periodic epileptiform discharges. Because of the exceptionally focal scalp electric field, F4 was the only 10-20 electrode detecting a scalp potential. Adding 10-10 electrodes and extending the montage allowed us to “see” a physiological field that was “invisible” when the EEG was recorded from 10-20 electrodes only.
|
[[63.0, 'year']]
|
F
|
{'16751720': 1, '18053144': 1, '13810779': 1, '12195981': 1, '1304564': 1, '21872525': 1, '13885270': 1, '2187021': 1, '19925193': 1, '90597': 1, '30151399': 2}
|
{'6104203-1': 2, '6104203-3': 2}
|
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