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162,800 |
3751027-2
| 23,722,429 |
noncomm/PMC003xxxxxx/PMC3751027.xml
|
Feasibility of remote magnetic navigation for epicardial ablation
|
A 50-year-old male presented with frequent PVCs causing marked exercise intolerance. His Holter recording revealed a high number of monomorphic PVCs (27,000/24 h) with bigeminy. Left ventricular ejection fraction was normal. Neither syncope nor sustained ventricular arrhythmias were documented, and the family history was unremarkable. During the previous invasive EP study an ablation had not been performed due to the absence of an adequate pace-map. Using the MNS to guide the catheter, a perfect 12 out of 12 pace-map was gained from the anterior epicardial aspect of the LVOT (Fig. ).\nDelivery of three RF applications with an average energy of 27 W terminated the arrhythmia and rendered it non-inducible (also with isoproterenol infusion). The successful ablation site was 7 mm away from the left main coronary stem (Fig. ). No acute complications were observed, but in the early post-procedure period the patient developed a self-limiting sterile pericarditis with an insignificant amount of pericardial fluid. At follow-up after 3 months, PVCs were absent and the patient reported an improved physical condition. His prior antiarrhythmic medication was discontinued.
|
[[50.0, 'year']]
|
M
|
{'21841191': 1, '23959847': 1, '20434589': 1, '21744697': 1, '24155102': 1, '19602023': 1, '21508006': 1, '27722835': 1, '22006012': 1, '22653815': 1, '17296855': 1, '15851176': 1, '24710865': 2, '16731472': 1, '21149511': 1, '16847159': 1, '20974761': 1, '26215291': 1, '22719063': 1, '22702255': 1, '22554147': 1, '18955400': 1, '10807445': 1, '19789687': 1, '16784438': 1, '24399322': 1, '23722429': 2}
|
{'3751027-1': 2, '3751027-3': 2, '4016330-1': 1, '4016330-2': 1}
|
162,801 |
3751027-3
| 23,722,429 |
noncomm/PMC003xxxxxx/PMC3751027.xml
|
Feasibility of remote magnetic navigation for epicardial ablation
|
A 29-year-old male with frequent palpitations underwent three unsuccessful RF ablation procedures of a left-sided accessory pathway. Mapping ablation catheters were introduced epicardially and retrogradely in the left ventricle. After 39 unsuccessful ablation attempts with a mean energy of 27 W, thorough epicardial mapping revealed the earliest atrial retrograde activation site in the left lateral aspect of the mitral annulus.\nA single RF application at the corresponding endocardial site by the retrograde catheter abolished the conduction over the accessory pathway. The post-procedural period was uneventful and he was discharged without antiarrhythmic medication. In his 3-month follow-up he was completely free of arrhythmias.
|
[[29.0, 'year']]
|
M
|
{'21841191': 1, '23959847': 1, '20434589': 1, '21744697': 1, '24155102': 1, '19602023': 1, '21508006': 1, '27722835': 1, '22006012': 1, '22653815': 1, '17296855': 1, '15851176': 1, '24710865': 2, '16731472': 1, '21149511': 1, '16847159': 1, '20974761': 1, '26215291': 1, '22719063': 1, '22702255': 1, '22554147': 1, '18955400': 1, '10807445': 1, '19789687': 1, '16784438': 1, '24399322': 1, '23722429': 2}
|
{'3751027-1': 2, '3751027-2': 2, '4016330-1': 1, '4016330-2': 1}
|
162,802 |
3751031-1
| 23,605,477 |
noncomm/PMC003xxxxxx/PMC3751031.xml
|
Coronary vasospasm induced by painful compression of the brachial artery following coronary angiography
|
A 69-year-old female patient was admitted to our emergency department with complaints of recurrent short-lasting chest pain during the night in the previous 2 weeks. The chest pain typically occurred every night around 3 A.M., lasting for approximately 3 min. Her medical history mentioned hypertension, and a left-sided T1N0M0 breast carcinoma curatively treated with surgery and radiotherapy 14 years earlier. Analysis for coronary artery disease at the age of 53 showed no abnormalities. Her medication included aspirin, thiazide diuretics and a low maintenance dose of nitrates.\nOn the morning of admission, she experienced the same chest pain with radiation to her neck and complaints of sweating. Sublingual nitrates administered at the emergency department relieved her pain to some extent. There were no abnormalities found during physical examination.\nThe electrocardiogram on admission showed sinus rhythm, normal axis and negative T waves in the anterolateral leads (Fig. ). Since troponin-T levels were slightly elevated (0.11 μg/L) she was treated for a non-ST-elevation myocardial infarction (NSTEMI) with clopidogrel, low-molecular-weight heparins, statins, beta-blockers as well as intravenous nitrates in addition to her previous medication. During hospitalisation, the maximum troponin T level was 0.34 μg/L, creatine kinase 335 U/L. Serial electrocardiograms during chest pain showed repolarisation abnormalities indicative for myocardial ischaemia in the anterior and inferior wall leads as well as QTc prolongation of 490 milliseconds, suggesting a proximal left coronary artery and possibly right coronary artery stenosis as well (Fig. ). Diagnostic coronary angiography was performed within 24 h, the next day. Modified Seldinger procedures in both femoral and right radial arteries were complicated by difficult vascular access. Eventually, the right brachial artery was accessed. Coronary angiography revealed a markedly large left anterior descending artery (LAD), together with a non-dominant right coronary artery. Minor wall abnormalities in both the right and the left coronary artery were found, with no signs of significant coronary stenosis (Fig. ). After removing the arterial sheath, haemostasis was accomplished by manual compression of the brachial artery, followed by a pressure bandage for 4 h.\nThirty minutes after removal of the arterial sheath, the lower right arm turned white and became cold and painful, due to arterial occlusion. The pressure bandage was carefully removed. Shortly thereafter, she again experienced chest pain. The electrocardiogram showed sinus bradycardia with marked ST elevation in the precordial leads as well as in the inferior wall leads (Fig. ). Considering the anatomy of the LAD running over the apex towards the inferior wall, this pattern was consistent with a proximal LAD occlusion, or with a combined LAD and right coronary artery (RCA) spasm. This leaves coronary vasospasm as the only possible explanation of her symptoms. No arrhythmias were seen. Intravenous nitroglycerin was immediately administered resolving her symptoms, and the electrocardiogram showed marked T-wave inversion as was seen previously (Fig. ). She was treated with a calcium antagonist accordingly and was free of symptoms during outpatient follow-up.
|
[[69.0, 'year']]
|
F
|
{'19433770': 1, '21487750': 1, '8613613': 1, '32399339': 2, '8890823': 1, '4415644': 1, '21211685': 1, '10862603': 1, '23605477': 2}
|
{'7212713-1': 1}
|
162,803 |
3751282-1
| 23,990,850 |
noncomm/PMC003xxxxxx/PMC3751282.xml
|
Small intestinal obstruction resulting from ischemic enteritis: a case report
|
A 69-year-old male was admitted to our institution because of a sudden onset of vomiting and abdominal distention in April 2012. His general history did not include smoking or alcohol consumption; however, his medical history included a femoral head fracture, which was treated with an artificial femoral head when he was 60 years old, and congestive heart failure, which improved with diuretic administration in November 2011.\nHis past history also included an episode of ischaemic colitis which presented with severe left-sided abdominal pain. Abdominal radiography and computed tomography revealed no abnormal findings, although colonoscopy revealed longitudinal ulcers in the descending colon (Fig. a). These findings led to a diagnosis of ischaemic colitis. Capsule endoscopy revealed circumferential ulcers in the distal small intestine (Fig. b) and single-balloon enteroscopy confirmed the same in the distal ileum (Fig. c). Ischaemic enteritis was suspected and the patient was prescribed a treatment that included fasting and blood transfusion. Thereafter, his symptom improved rapidly.\nOn admission, the patient’s blood pressure was 103/54 mmHg, heart rate was 72 beats/min, body temperature was 36.3 °C and oxygen saturation was 97 % in room air. On clinical examination, his weight was 51 kg, height was 166 cm and body mass index was 18.5 kg/m2. Inspection of the palpebral conjunctiva revealed evidence of mild anaemia, whereas a chest auscultation revealed no abnormal findings and physical examination revealed no oedema or cyanosis. The patient’s abdomen was markedly distended and reduced peristalsis was evident with mild tenderness over abdominal region. There were no palpable masses or signs of peritoneal irritation.\nBlood chemistry revealed a normal white blood cell count (7000 cells/μL), mild anaemia (red blood cell count, 321 × 104/μL; haemoglobin, 9.2 g/dL), elevated C-reactive protein level (4.8 mg/dL), mild hypoproteinaemia (5.5 g/dL), mild hypoalbuminaemia (2.4 g/dL), mildly elevated serum creatine level (1.36 mg/dL), mildly elevated blood urea nitrogen level (25.6 mg/dL), hyponatraemia (128 mEq/L) and an elevated glucose level (144 mg/dL; Table ). Tuberculin and several stool culture tests were negative. On admission, plain abdominal radiography revealed dilated small intestinal loops (Fig. a). Plain abdominal computed tomography revealed extensively dilated small intestinal loops, a calibre change around the ileal end and an absence of ascites (Fig. b, c). Therefore, small intestinal obstruction was diagnosed and a transnasal ileus tube was placed (Fig. a). During decompression of the small intestinal obstruction using the ileus tube, the patient was fasting and was treated with total parenteral nutrition. The ileus tube was progressively moved along the small intestine until it reached the distal ileum on post-admission day 4. The injected contrast medium revealed a stricture in the distal ileum (Fig. b). Transanal single-balloon enteroscopy performed to inspect the stricture revealed a circumferential and afferent tubular ulcer in the distal ileum, 5 cm from the ileocecal valve (Fig. a); gastrofluorography confirmed the stricture (Fig. b), which was dilated using balloon catheters on several occasions but could not be improved.\nDespite treatment, the patient’s nutritional status deteriorated and his anaemia progressed, with the latter necessitating a blood transfusion. Consequently, we decided to perform surgery on post-admission day 37.\nOperative findings revealed several strictures in the distal ileum (Fig. a). In total, 42 cm of the ileum, including the known stricture, was resected. Several circumferential ulcers with clear margins were detected in the ileum at 5–28 cm from the ileocecal valve (Fig. b). Histological findings revealed the following (Fig. a–c): stenotic portions of the ileum formed ulcers of grade Ul-II with an intact muscularis mucosa, the ileal lumen was covered with fibrin and fibrous connective tissue, an inflammatory cell infiltrate was present in all layers, particularly lymphocytes and eosinophils, dilatation and congestion of capillary vessels was observed in the submucosa and haemosiderin staining revealed sideroferous cells in the submucosal layers. Considering these findings, ischaemic enteritis was confirmed in the resected specimen.\nThe patient’s post-operative course was uneventful. Oral intake was initiated and the patient experienced no recurrence of small intestinal obstruction or symptom of abdominal pain.
|
[[69.0, 'year']]
|
M
|
{'1426849': 1, '33954155': 1, '7021332': 1, '18094205': 1, '19452586': 1, '8323918': 1, '5047519': 1, '34616258': 2, '9873959': 1, '22791732': 1, '26884740': 2, '13968597': 1, '32742131': 1, '29089826': 1, '29491303': 1, '5906128': 1, '23990850': 2}
|
{'8454243-1': 1, '4754528-1': 1}
|
162,804 |
3751332-1
| 23,990,851 |
noncomm/PMC003xxxxxx/PMC3751332.xml
|
Usefulness of contrast-enhanced ultrasonography in the diagnosis of ruptured hepatocellular carcinoma
|
The patient was a 61-year-old male. He had no relevant medical or family history, but he was a heavy drinker who consumed >2 L of beer every day. He visited a nearby hospital for a chief complaint of general malaise and was diagnosed with multiple HCCs caused by alcohol-related cirrhosis. Approximately 1 month after the first visit, he was admitted to our hospital for rapid development of abdominal fullness. Physical findings at admission showed blood pressure 148/98 mmHg, pulse rate 64 bpm, ascites retention, and a palpable fist-sized tumor in the epigastric region. Blood tests upon admission showed Hb 10.4 g/dl (normal 14.0–17.0 g/dl), AST 55 U/l (normal 12–35 U/l), ALT 35 U/l (normal 6–31 U/l),γ-GTP 283 U/l (normal 9–58 U/l), T-Bil 4.9 mg/dl (normal 0.1–1.0 mg/dl) and PT % 68 % (normal ≥70 %), suggesting mild anemia and increased hepatobiliary enzymes. Hepatic function was evaluated as C (10 points) in the Child–Pugh classification. Tumor markers were high, as shown by the levels of AFP and PIVKA II of 27.4 ng/ml (normal 0.0–15.0 ng/ml) and 567 mAU/ml (normal <40 mAU/ml), respectively. HBV and HCV were negative and renal function was normal. Hemorrhagic ascites was found in abdominal paracentesis and the case was diagnosed as ruptured HCC.\nAbdominal CECT showed a large HCC with a maximum diameter of 15 cm in S7/8 of the liver and multiple HCCs in both lobes (Fig. ). The attenuation value of the ascites was as high as 30 Hounsfield units, but no clear extravasation was found in the arterial and equilibrium phase, and thus the bleeding site could not be identified. Abdominal ultrasonography also showed multiple tumors in both lobes and ascites with high echo density (Fig. a). However, even with these data the bleeding site was unclear, and CEUS was performed for the large HCC in S7/8 as the region of interest. The ultrasound equipment used in this examination was SSA-790A (Toshiba Medical Systems, Tokyo, Japan) with a convex probe (PVT-375BT, 3.75-MHz center frequency). The imaging mode used was wideband harmonic imaging (pulse subtraction) with transmission/reception frequencies of 1.8 and 3.5 MHz, respectively. The mechanical index for acoustic output was set to 0.2; the dynamic range was set to 60–65 dB. A intravenous bolus injection of Sonazoid (0.5 ml) was administered via a left cubital venous line followed by 10 ml normal saline flush. Observation in the arterial phase showed no clear leakage of contrast agent from this tumor, but punctate high-intensity echoes of Sonazoid microbubbles were observed in ascites. In particular, extremely high-intensity echoes of Sonazoid microbubbles were present in ascites surrounding the tumor, close to the S5 gallbladder bed. The tumor was imaged again using the re-injection method [] with Sonazoid in the post-vascular phase and leakage of the contrast agent from the tumor into the abdominal cavity was observed, indicating that this was the site of bleeding (Fig. b).\nAbdominal angiography was urgently performed. Imaging of the celiac artery and hepatic artery showed no clear extravasation. However, since the tumor on the gallbladder bed was suspected as the bleeding site based on CEUS, selective cannulation of the cystic artery was performed (Fig. a). The artery was imaged using carbon dioxide (CO2), which is a highly sensitive method for evaluation of blood flow []. Leakage of CO2 out of the vessel was apparent, confirming that the bleeding site was the tumor in S5, which was fed by the cystic artery (Fig. b). TAE was conducted using a gelatin sponge (Gelpart; Astellas Pharma, Tokyo, Japan) with a particle size of 1 mm, and the clinical course after TAE was favorable with arrest of bleeding.
|
[[61.0, 'year']]
|
M
|
{'27278293': 1, '1846058': 1, '10715337': 1, '1851653': 1, '8689200': 1, '31024207': 1, '15359472': 1, '28815352': 1, '1317090': 1, '27278014': 1, '6297703': 1, '18172704': 1, '32691111': 1, '19092266': 1, '23990851': 2}
|
{}
|
162,805 |
3751343-1
| 23,990,849 |
noncomm/PMC003xxxxxx/PMC3751343.xml
|
Superior mesenteric vein thrombosis as a complication of acute appendicitis : report of a case
|
A 45-year-old man whose BMI was 23.2 kg/m2 visited our outpatient clinic primarily due to fever and abdominal pain. Although mild pain was noted in the right lower abdominal region, there was no other symptom including rebound tenderness, and the patient was prescribed drugs and allowed to go home. After 2 days, pain of the right lower abdomen was slightly alleviated, but a fever above 39 °C persisted. The patient consulted the emergency outpatient clinic of our hospital. Blood tests showed high values indicating inflammatory reaction, and abdominal ultrasonography and contrast-enhanced CT showed enlargement of the appendix. The patient was immediately admitted.\nOn admission, the body temperature was 39.0 °C, the abdomen was flat, pain in the right lower abdominal region was mild, and no rebound tenderness was noted. On the blood tests at the outpatient visit 2 days before, the WBC was 8,300/μl, and CRP was 7.5 mg/dl, but they were exacerbated to 11,000/μl and 34.13 mg/dl, respectively. Also, the platelet count was reduced to 75,000/μl, and liver dysfunction was suggested by increases in the AST 71 IU/l, ALT 58 IU/l, T-Bil 2.5 mg/dl, and LDH 303 IU/l. Abdominal contrast-enhanced CT showed increased radiodensity of the enlarged appendix and surrounding adipose tissue (Fig. ).\nAfter admission, as abdominal findings were unremarkable despite of fever and blood test results. Decreases in the platelet count, mild increases in the transaminase levels, and increases in the total bilirubin level were noted. We suspected other diseases, for example, viral infection and blood disease as a cause of inflammation. We initially planned to manage the acute appendicitis conservatively with the possibility of taking into consideration of emergency surgery.\nDetailed examinations were performed. Blood cultures were negative. Tests for viral infections such as cytomegalovirus and EB virus infections were negative, and for fungal infection was negative too. As an empiric treatment, meropenem (MEPM) was administered at 0.5 g × 3/day. The fever, high inflammatory reaction, and liver dysfunction were temporarily alleviated, but the WBC and fever elevated again on the 5th hospital day. Abdominal contrast-enhanced CT was performed again, and the result showed no remarkable changes in appendicitis. However, a vine-like low-density area along the ileocolic vein (ICV) and defects in the lumen of the SMV and dendritic low-density area of the portal vein in S5 of the liver were recognized (Fig. ). We suspected the occurrence of SMVT and PVT induced by inflammation extending from protracted appendicitis. We carried out appendectomy by laparotomy on emergency.\nIntraoperatively, the appendix adhered to the surrounding tissues but could be detached. The mesoappendix was markedly thickened, and there were findings suggestive of abscess formation in the mesoappendix. No sign of edema, congestion, or necrosis was noted in the large intestine, small intestine, and mesentery. Therefore, only an appendectomy was performed.\nHistopathological examinations indicated the diagnosis of phlegmonous or gangrenous appendicitis. Abscesses were noted in the mesoappendix, and fibrinoid necrosis was observed in the vascular wall, particularly the venous wall, in the mesoappendix. No clear thrombus, suppurating thrombus, or biofilm was found in the blood vessels.\nThe postoperative course was uneventful, and improvements were observed in inflammatory reaction, platelet count, transaminase levels, and total bilirubin level. Postoperatively, heparin administration was started at 16,000 U/day, and heparin was substituted for warfarin with the resumption of oral nutrition. On the 7th postoperative day, regression and alleviation of SMVT and PVT were confirmed by abdominal contrast-enhanced CT.\nOn abdominal contrast-enhanced CT on the 48th postoperative day, no sign of recurrence of SMVT or PVT was noted, but the SMV was atrophied (Fig. ). Oral warfarin administration was discontinued half a year after surgery. The blood AT III activity, protein C antigen and activity levels, and antinuclear antibody level were measured after surgery. As these parameters were all within the normal range, abnormality of the congealing fibrinogenolysis system was excluded.
|
[[45.0, 'year']]
|
M
|
{'26081450': 1, '10960436': 1, '18680244': 1, '10372847': 1, '3563882': 1, '26091450': 2, '31770213': 2, '7554738': 1, '14745623': 1, '23990849': 2}
|
{'6890307-1': 1, '4616561-1': 1}
|
162,806 |
3751378-1
| 23,983,486 |
noncomm/PMC003xxxxxx/PMC3751378.xml
|
Spontaneous bacterial peritonitis with a very high leukocyte count in ascitic fluid caused by Haemophilus influenzae
|
A 64-year-old Jewish male of Indian origin was hospitalized in our department, with a 5-day history of fever (39°C), cough, and fatigue. He denied abdominal pain, vomiting, diarrhea, or other symptoms.\nHis medical history was significant for alcoholic cirrhosis with portal hypertension, splenomegaly, hypersplenism, and ascites. Furthermore, he had diabetes mellitus type 2 (hemoglobin A1c of 7%) and hypertension for years.\nHis medications included propranolol, lactulose, Aldospirone, omeprazole, and metformin.\nOn physical examination the patient was alert without encephalopathy or jaundice. The following characteristics of chronic liver disease were present: spider angiomas on his chest, hepatomegaly, splenomegaly, ascites, caput medusa, and pedal edema. His abdomen was swollen with tenderness in the right upper quadrant.\nLaboratory tests showed a total bilirubin level of 1.76 mg/dL (normal range, 0.21–1 mg/dL); alanine aminotransferase level of 20 U/L (normal values, <40 U/L); aspartate aminotransferase level of 24 U/L (normal values, <40 U/L); alkaline phosphatase level of 147 U/L (normal range, 30–150 U/L); γ-glutamyl transpeptidase level of 73 U/L (normal range, 5–60 U/L); albumin level of 1.3 g/dL; prothrombin time of 15 seconds (international normalized ratio, 1.4); creatinine 2.7 mg/dL. His Model for End-Stage Liver Disease score on admission was 22. Complete blood count showed leukocytosis, 14,000 cells/μL, with 85% neutrophils, hemoglobin 7.1 g/dL, and platelets 100,000 cells/μL.\nChest X-ray showed mild right pleural effusion with no pulmonary infiltrates, and his abdominal ultrasonograph showed moderate ascites and hepatosplenomegaly. Blood, urine, and pleural fluid cultures were negative.\nAbdominal paracentesis was done and revealed 134,800 leukocytes/mm3 (100% neutrophils), a serum-ascites albumin gradient of 1.4; levels of lactate dehydrogenase, amylase, and triglycerides were not elevated, and the level of glucose was within normal limits. The unusually high peritoneal fluid leukocyte count raised the suspicion of secondary peritonitis.\nThe patient underwent computed tomography of the abdomen with oral contrast, and no evidence of perforation or abdominal abscess was found.\nA peritoneal fluid culture was positive for H. influenzae, and the patient was treated with ceftriaxone. Abdominal paracentesis was repeated 48 hours after beginning antibiotic treatment and showed a significant decrease of leukocyte count to 3,000/mm3. After hospitalization for 2 weeks the patient improved significantly; his fever resolved, and the patient felt better and was discharged. Three days later, the patient readmitted with septic shock due to Escherichia coli and methicillin-resistant Staphylococcus aureus. Unfortunately, despite antibiotic therapy, the patient died.
|
[[64.0, 'year']]
|
M
|
{'4938274': 1, '15740502': 1, '3137057': 1, '16757647': 1, '6372107': 1, '1438675': 1, '15385716': 1, '1446855': 1, '23983486': 2}
|
{}
|
162,807 |
3751382-1
| 23,983,487 |
noncomm/PMC003xxxxxx/PMC3751382.xml
|
Metformin-induced mixed hepatocellular and cholestatic hepatic injury: case report and literature review
|
A 78-year-old Jewish male patient was hospitalized in our department with a 10-day history of fatigue, nausea, vomiting, diarrhea, anorexia, and abdominal pain. He had also had pruritus and jaundice for 8 days. DM-2 had been recently diagnosed and metformin 850 mg/day had been initiated 2 weeks before presentation to the hospital. The patient reported no alcohol use, smoking, previous liver disease, family history of liver diseases, blood transfusion, exposure to toxins, or cholelithiasis. One month before initiation of metformin treatment, the patient had been given a 13-day amoxicillin-clavulanate (Augmentin) treatment for acute parotitis. His past medical history was significant for hypertension, gout, hyperlipidemia, and diverticulosis. His other medications included aspirin (75 mg/day), pravastatin (20 mg/day), amlodipine (5 mg/day), atenolol (100 mg/day), candesartan (16 mg/day), and hydrochlorothiazide (12.5 mg/day).\nOn physical examination, the patient was alert, with prominent jaundice. No stigmata of chronic liver disease were present. There was no pedal edema or ascites. His weight was 82 kg, his height 172 cm, and his body mass index 27.7 kg/m2. The laboratory findings are summarized in . The level of lactic acid was normal. Creatinine, urea, and electrolytes were normal. The levels of glucose during hospitalization were between 120–180 mg/dL. Results of serologic tests were negative for the following: hepatitis B surface antigen; anti-hepatitis B core Immunoglobolin M (IgM); anti-hepatitis A virus IgM; anti-hepatitis C virus antibody; anti-Cytomegalovirus IgM; anti-Epstein–Barr virus IgM; anti-nuclear antibodies; anti-smooth-muscle antibodies; anti-mitochondrial antibodies; and anti-neutrophil cytoplasmic antibodies. Serum ferritin and ceruloplasmin levels were also normal. C-reactive protein level was 9.97 mg/L (normal range: 0–5 mg/L). Complete blood count was normal. An ultrasound and a computerized tomography (CT) scan of the abdomen revealed no abnormalities.\nOn admission, metformin and pravastatin were discontinued immediately. After 1 week, the patient described significant subjective improvement and the level of bilirubin, alanine transaminase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALKP), and γ-glutamyl transpeptidase (GGT) began to decline gradually. After 9 days of hospitalization, the patient’s laboratory results were as follows: total bilirubin, 16.9 mg/dL; direct bilirubin, 12.4 mg/dL; ALT, 308 U/L; AST, 77 U/L; ALKP, 809 U/L; and GGT, 876 U/L. The patient was discharged for outpatient follow-up. Two months following discharge, all hepatobiliary laboratory abnormalities resolved. Thereafter, pravastatin therapy was readministered, and no changes in bilirubin, ALT, AST, ALKP, or GGT levels were observed.
|
[[78.0, 'year']]
|
M
|
{'12016548': 1, '28353605': 1, '11467664': 1, '25180107': 2, '17206072': 1, '17006920': 1, '20647417': 1, '31531370': 1, '27551311': 1, '9303497': 1, '9626034': 1, '31871510': 1, '25676019': 1, '16503324': 1, '28925884': 1, '7249508': 1, '12093242': 1, '27659300': 1, '34228716': 1, '9742977': 1, '14561576': 1, '710026': 1, '9078205': 1, '31907698': 1, '28405790': 1, '14996697': 1, '7623903': 1, '10656221': 1, '23983487': 2}
|
{'4142286-1': 1}
|
162,808 |
3751385-1
| 23,983,485 |
noncomm/PMC003xxxxxx/PMC3751385.xml
|
Cannabinoid hyperemesis syndrome with extreme hydrophilia
|
A 47-year-old African American male with a history of epilepsy and drug addiction presented to the hospital with a seizure complicated by nausea, vomiting, and severe abdominal pain. He was known to be diabetic, hypertensive, and addicted to marijuana for 30 years. He smoked two to three “blunts” (cigar hollowed out and filled with marijuana) most days and occasionally up to eight blunts daily. The drug was last taken on the day of his admission.\nHis examination was unremarkable except for heart rate of 92 bpm, blood pressure of 174/98 mmHg, and mild epigastric tenderness. His laboratory and radiological tests were within normal limits, except for blood sugar of 217 mg/dL and positive urine drug screen for marijuana and opiates. The patient refused electroencephalography.\nHe immediately went to the bathroom and remained under a hot shower with the exception of two 15-minute breaks for the rest of the day. He believed that a warm shower could relieve his nausea and vomiting. He stated that it made him feel better than medication. Intravenous ondansetron was of limited benefit. It was difficult to persuade him to exit the shower for the rounds and physical examination. Receiving medication and eating were problems because of this compulsive showering. The same event of entrenching himself in the shower had happened 2 months prior to his hospitalization for a grand mal seizure. Abstinence from marijuana during the hospital stay made the patient’s nausea, vomiting, and obsessive warm showering resolve after 3 days. He was discharged after 4 seizure-free days and referred for drug rehabilitation.
|
[[47.0, 'year']]
|
M
|
{'26791124': 1, '15919107': 1, '31241817': 1, '24872901': 2, '19291829': 1, '19066071': 1, '21886087': 1, '21057076': 1, '22305024': 1, '18397936': 1, '12617697': 1, '34676325': 1, '15652378': 1, '19121257': 1, '15479672': 1, '28000146': 1, '23983485': 2}
|
{'4020538-1': 1}
|
162,809 |
3752471-1
| 23,984,229 |
noncomm/PMC003xxxxxx/PMC3752471.xml
|
Cutaneous metastasis from carcinoma of lung
|
A 65-year-old male who was a chronic smoker for the last 30 years presented with generalized weakness, breathlessness, occasional hemoptysis, and multiple cutaneous nodules (8 in number) all over the body since two months. The nodules were present over the chest (2), abdomen (1), back (2), face (1), and both the extremities (2). They were of varying sizes, ranging from 2 to 6 cm and were firm, nontender, and mobile. Some of them were infected []. Systemic examination was normal except for the presence of occasional crepitations and rhonchi. A clinical diagnosis of chronic obstructive pulmonary disease (COPD) with cutaneous lymphoma or soft tissue tumor was made.\nHematological investigations revealed the following:\nHb (hemoglobin): 14.4 gm%; TLC (total leukocyte count): 19,100/cmm; DLC (differential leukocyte count): P87L10E0M03.\nESR (erythrocyte sedimentation rate): 28 mm at the end of one hour.\nSputum examination was negative for malignant cells.\nChest X-ray (CXR) and computed tomography (CT) showed neoplastic right lung and bronchial mass with secondary cavitation.\nExcision biopsy of the noninfected nodule from the back was done and the specimen was received by the department of pathology.\nOn gross examination, it was an irregular tissue measuring 6×3.5×1 cm with a nodule 3 cm in diameter which was surrounded by adipose tissue and muscle.\nThe cut section of the nodule was grayish white and firm in consistency.\nThe histopathological sections from the nodule showed metastatic deposits from squamous cell carcinoma, moderately differentiated (grade II) [Figures and ].
|
[[65.0, 'year']]
|
M
|
{'25969680': 2, '25788997': 2, '34405061': 2, '17642936': 1, '19624979': 1, '33005713': 1, '28861332': 1, '33672554': 2, '8552539': 1, '18853075': 1, '23984229': 2}
|
{'4356377-1': 1, '4427150-1': 1, '4427150-2': 1, '7923794-1': 1, '8352797-1': 1}
|
162,810 |
3752472-1
| 23,984,230 |
noncomm/PMC003xxxxxx/PMC3752472.xml
|
Primary cutaneous leiomyosarcoma: A rare malignant neoplasm
|
A 70-year-old male patient presented with a painful nodule in the right leg, which had been progressively increasing in size for 4 months. On palpation, an irregular, firm, tender exophytic swelling, measuring 5 cm × 5 cm, with overlying skin showing ulceration was noted on the lateral aspect of the lower one third of the right leg []. Inguinal lymph nodes were not palpable. His past history was significant of a trauma and subsequent non-healing ulcer formation at the same site in the right leg.\nSystemic examination and investigations, including complete blood count, fasting blood sugar level, liver function test and renal function test, were within normal limits. Hepatitis B virus surface antigen and human immunodeficiency virus enzyme-linked immunosorbent assay were non-reactive.\nA clinical diagnosis of squamous cell carcinoma was considered and fine needle aspiration cytology of the swelling was requested.\nFine needle aspiration cytology of the same was reported as a spindle cell neoplasm with suspicion of malignancy. The swelling was excised with a 5 cm resection margin and submitted for histopathological examination [].\nGross inspection revealed a grey brown, irregular, nodular soft tissue mass, measuring 5 cm × 5 cm × 2.5 cm and partly covered with skin. The cut surface of the mass was greyish white, solid, homogenous and fleshy [].\nLight microscopy revealed a poorly delineated dermal neoplasm extending into the underlying subcutis. The neoplasm was composed of bundles of elongated spindle cells arranged in interlacing fascicles, with intensely pink, fibrillary cytoplasm and pleomorphic nuclei with coarse irregularly dispersed chromatin. Mitosis, including atypical, amounting to 22 mitotic figures per 10 high power fields and multinucleate tumor giant cells, was evident. Focal necrosis was noted at the edges. The overlying epidermis was thinned out with areas of ulceration [].\nA provisional diagnosis of spindle cell malignant neoplasm of the skin, which typically includes a host of diagnostic possibility, namely fibrosarcoma, leiomyosarcoma, malignant peripheral nerve sheath tumor, monophasic synovial sarcoma, malignant fibrous histiocytoma and spindle cell variant of squamous cell carcinoma, was considered and immunohistochemistry was advised for confirmation.\nOn immunohistochemistry, tumor cells showed strong immunopositivity for vimentin, muscle-specific actin (MSA), smooth muscle actin (SMA), caldesmon and desmin and negative for pancytokeratin, Epithelial Membrane Antigen (EMA), myogenin, CD34 and S-100 protein [].\nBased on the immunophenotypic features, a final diagnosis of PCL was rendered. The patient is currently on periodic follow-up since 1 year and no recurrence or metastasis has been identified so far.
|
[[70.0, 'year']]
|
M
|
{'33959460': 2, '8915854': 1, '34840749': 2, '27990398': 1, '34799385': 2, '9298873': 1, '10469099': 1, '10394436': 1, '4457785': 1, '28913324': 2, '7459804': 1, '23984230': 2}
|
{'8606708-1': 1, '8606758-1': 1, '5556898-1': 1, '8093099-1': 1}
|
162,811 |
3752473-1
| 23,984,231 |
noncomm/PMC003xxxxxx/PMC3752473.xml
|
Dowling-Degos disease and hidradenitis suppurativa: Co occurrence or association?
|
A 44-year-old female patient presented with multiple painful, tender nodular lesions and plaques with multiple sinuses discharging pus involving the buttocks, inner aspect of upper thigh, perianal region and both upper legs since the past 4 years but which aggravated since 1 month. The patient had similar lesions on and off since the past 17 years. There was no history of similar lesions in any family members. Two years back, she was diagnosed as a case of scrofuloderma and had received anti-tubercular treatment for 6 months. The patient frequently took systemic antibiotics for the skin lesions with only temporary relief.\nCutaneous examination revealed multiple tender nodules and plaques with multiple sinuses discharging pus involving the buttocks, inner aspect of upper thigh, anogenital region [Figures and ] and both upper legs. Few plaques over the leg revealed crusting []. Post inflammatory atrophic scarring was seen over the lower abdomen and inner aspect of the right thigh []. Bilateral tender inguinal lymphadenopathy was present. The patient also had asymptomatic, multiple, symmetrical, dark brown pigmented macules over the axillae [Figures and ] and groins. Scattered comedo-like lesions (dark dot follicles) were seen over the abdomen, thighs [], back and upper extremity. The patient had multiple discrete pitted scars over the face [], back and axillae.\nInvestigations revealed normal blood counts, liver and renal function tests, but the erythrocyte sedimentation rate was raised. Blood glucose levels were normal. Mantoux test was negative. Pus for gram staining and culture sensitivity revealed gram positive Staphylococcus aureus. Enzyme-linked immunosorbent assay test for human immunodeficiency virus-1 and 2 was negative. Biopsy from the nodular lesion revealed neutrophilic and histiocytic infiltration around the pilosebaceous apocrine units []. Histopathology from the pigmented lesion revealed irregular epidermis, acanthosis and elongation of rete ridges with increased basal melanin pigmentation [].
|
[[44.0, 'year']]
|
F
|
{'33768038': 2, '11305381': 1, '15550138': 1, '2050858': 1, '9167336': 1, '32831371': 2, '13171638': 1, '9542661': 1, '27900998': 1, '9431718': 1, '23984231': 2}
|
{'7423233-1': 1, '7982026-1': 1}
|
162,812 |
3752474-1
| 23,984,232 |
noncomm/PMC003xxxxxx/PMC3752474.xml
|
Facial plexiform neurofibromatosis: A surgical challenge
|
A 29-year-old female patient presented to us with a history of overhanging folds of loose skin affecting the right side of her face and right forearm []. The swelling appeared during childhood and progressed slowly. She complained of occasional pain and itching on the affected part. The patient initially sought treatment elsewhere, about 10 years back, when excision of forearm swelling was carried out, but the swelling recurred. She came to us now with complaints of inability to open her right eye and sought improvement in her facial appearance.\nOn physical examination, the face was disfigured due to overhanging folds of skin affecting the temporal, orbital and cheek areas. She was unable to open her right eye due to the overhanging folds affecting both eyelids, and the eye was pulled inferiorly. Vision acuity of the right eye was however not affected. Café au lait macules (some measuring over 15 mm) as well as several freckles were observed in the axillary, back and chest regions. She had multiple neurofibromas over her forehead, neck and trunk regions. She also had a similar swelling and an old healed scar over the right forearm.\nReconstructive surgical procedure in the form of subtotal excision of tumor and re-draping of the facial skin was performed. Operative findings revealed grossly thickened subcutaneous nerves and neo-vessels in the tumor mass, which was infiltrating deeply, and no clear tissue planes were identifiable. The neo-vessels were very friable and bled profusely during dissection. Complete excision was not possible; hence, subtotal excision and redraping of skin flap was carried out. Anchoring sutures were applied over the lateral canthal region between the skin flap and the lateral orbital margin to prevent pulling down of eyelids []. The post-operative period was uneventful. However, on review after 6 months, there was partial regrowth of the swelling.
|
[[29.0, 'year']]
|
F
|
{'3082508': 1, '26171111': 1, '17456965': 1, '28166733': 1, '15683544': 1, '11891951': 1, '16103304': 1, '4812027': 1, '34703146': 2, '15638946': 2, '10189917': 1, '9403645': 1, '23984232': 2}
|
{'3752474-2': 2, '546237-1': 1, '8491357-1': 1}
|
162,813 |
3752474-2
| 23,984,232 |
noncomm/PMC003xxxxxx/PMC3752474.xml
|
Facial plexiform neurofibromatosis: A surgical challenge
|
This 18-year-old boy was brought to our out patient department by his parents with a history of progressively increasing swelling over the right side of his face since childhood.\nPhysical examination revealed a huge soft tissue swelling involving the right mandibular region and cheek, extending up to the nasolabial fold pulling down the right angle of the mouth and right eye, partially obstructing the field of vision in his right eye []. He had few neurofibromas over his trunk, axillary freckles and café au lait macules over his back. Magnetic resonance imaging (MRI) of the face excluded any intracranial extension.\nHe was taken up for reconstructive surgery and the swelling was approached through pre-auricular incision extending superiorly into the temporal area. Tumescent fluid infiltration was carried out in the tumor mass to reduce the blood loss. The tumor mass was infiltrating deeply and the tissue planes could not be defined. There was gross thickening of facial nerve in the pre-auricular region as well as its branches. Subtotal excision of tumor mass and readjustment of facial flap was carried out with reasonable post-op correction []. However, 6-monthly review in this case as well showed evidence of some regrowth.
|
[[18.0, 'year']]
|
M
|
{'3082508': 1, '26171111': 1, '17456965': 1, '28166733': 1, '15683544': 1, '11891951': 1, '16103304': 1, '4812027': 1, '34703146': 2, '15638946': 2, '10189917': 1, '9403645': 1, '23984232': 2}
|
{'3752474-1': 2, '546237-1': 1, '8491357-1': 1}
|
162,814 |
3752475-1
| 23,984,233 |
noncomm/PMC003xxxxxx/PMC3752475.xml
|
Extensive and invasive lymphangioma circumscriptum in a young female: A rare case report and review of the literature
|
A 21-year-old female presented to the dermatology out-patient department with multiple hemorrhagic vesicles over the right side of the abdomen, buttock and thighs since birth. Immediately after birth, bluish-colored red plaque was noticed by her mother in the anterior aspect of the right thigh. Gradually, over the next 6 months, multiple water-filled lesions appeared over the whole of the right buttock and right side of the lower abdomen. It was associated with recurrent episodes of pain and fever. At 1 year of age, she was taken to a plastic surgeon and the whole lesion was excised under general anesthesia. After 1 year, the lesions recurred with greater involvement of the thighs, buttocks and right lower abdomen. At 5 years of age, magnetic resonance imaging (MRI) scan showed extensive and deep LC with involvement of deep fascia, muscles of abdomen and buttocks and large vessels, including right iliac and right femoral arteries. The new fluid-filled vesicles appeared over the thighs and legs as well. There was history of episodes of bleeding from the lesion associated with pain. After the MRI scan, she was advised for rest and non-surgical management of the LC as it was deep and extensive.\nExamination revealed a 20 cm X 15 cm-sized large area of hemorrhagic fluid-filled vesicles of varying size from 3 mm to 1 cm over the right lower abdomen and buttocks and extending down toward the right thigh [Figures and ]. Few scattered clusters of vesicles were also seen over the posterior aspect of the right thigh []. The diameter of the right thigh was 6 cm more than that of the left one. Areas of hemorrhage were seen on the lesion. The area was non-tender and there was no rise in local temperature. The fluctuation, compression and cough impulse were absent. No bruit/thrill was present. All other blood investigations like complete blood count, liver function and renal functions were within normal limits.\nHistopathology of a vesicle showed irregular acanthosis of the epidermis, dilated lymphatics lined by endothelial cells in the dermis and containing numerous erythrocytes, macrophages and lymphocytes within the lumen [Figures and ].\nThe patient was referred to the department of plastic surgery for cosmetic debulking of the tumor. She was also reassured regarding the benign nature of the tumor.
|
[[21.0, 'year']]
|
F
|
{'5484713': 1, '27803540': 1, '20043057': 1, '17973881': 1, '18312992': 1, '26287470': 1, '20418997': 1, '33178382': 1, '18177408': 1, '31700851': 2, '17226918': 1, '16792643': 1, '26167062': 2, '23984233': 2}
|
{'6827547-1': 1, '4481748-1': 1}
|
162,815 |
3752476-1
| 23,984,234 |
noncomm/PMC003xxxxxx/PMC3752476.xml
|
Multiple keratoacanthomas developing in healing plaques of Psoriasis
|
A 22-year-old male patient presented with multiple reddish raised scaly lesions all over his body associated with scaling over the scalp for one year. The patient was shopkeeper by profession dealing in stationary items, there was no history of smoking or tobacco intake. Patient had skin type V, and there was no history of diabetes, tuberculosis, or any other immunosuppressive disease. He had applied various emollients and topical steroids with no lasting relief; however, there was no history of tar application or phototherapy. Clinical examination revealed multiple well-circumscribed erythematous indurated scaly plaques on the scalp, bilateral upper and lower limbs, back, and on buttocks. Auspitz sign was positive over the lesions. The diagnosis of psoriasis vulgaris was confirmed by histopathological examination. The Psoriasis Area and Severity Index (PASI) was estimated to be 26.2. After hematological and biochemical investigations, X-ray chest and HIV test, the patient was started on oral methotrexate 15 mg weekly. He significantly improved on this dose, and PASI dropped to 11.5 after three months. The dose was decreased to 7.5 mg weekly, and the patient was maintained on this dose and kept under monthly follow-up.\nFour months later, the patient presented with reddish to hyperpigmented raised nodules over the healing lesions of psoriasis. The nodules were firm and almost all had a central crater.\nHe also reported self resolution of few of the lesions over a period of 6 to 12 weeks without any specific treatment. Examination revealed the presence of multiple well defined dome shaped erythematous to hyperpigmented nodules, ranging in size from 5 to 15 mm, over both legs, especially shins, and a few over the arms and forearms []. The lesions were present on sun exposed as well as on non exposed areas. The nodules were characteristically present over the healing plaques of psoriasis vulgaris. Few post inflammatory hyperpigmented macules and atrophic scars were seen at the sites where previous nodules had healed spontaneously.\nHistopathological examination of the nodules showed a globular growth having a central crater containing keratinous material. The epidermis surrounding the crater was acanthotic and overlapped the crater laterally (“lipping”). Keratinocytes formed islands and cords and had pale eosinophilic cytoplasm []. These features were consistent with keratoacanthoma, and a diagnosis of multiple keratoacanthomas was made.\nThe patient was unwilling to opt for any therapy for the keratoacanthomas in view of spontaneous resolution of few of them. Weekly methotrexate was continued for control of psoriasis. The patient was followed up for the next 6 months, during which time keratoacanthomas continued to appear and some resolved leaving behind scarring. The patient was asked to apply tazarotene gel 0.1% daily over the residual lesions.
|
[[22.0, 'year']]
|
M
|
{'3015051': 1, '7778923': 1, '7364978': 1, '12582383': 1, '6643766': 1, '1810980': 1, '8277007': 1, '14616493': 1, '7000722': 1, '13947459': 1, '479435': 1, '392196': 1, '14021703': 1, '8967780': 1, '2254471': 1, '16092002': 1, '2175166': 1, '7309318': 1, '13781156': 1, '4143536': 1, '1552048': 1, '1528582': 1, '17642609': 1, '23984234': 2}
|
{}
|
162,816 |
3752477-1
| 23,984,235 |
noncomm/PMC003xxxxxx/PMC3752477.xml
|
Necrolytic migratory ulceration
|
A 53-year-old unmarried woman presented to us with history of recurrent episodes of erythematous scaly plaques over face, trunk and extremities of 12-year duration. Since 1 year she noticed vesicles at the margins of such plaques on the lower limbs, which broke down to form erosions and painful ulcers. These ulcers extended peripherally with tendency to heal centrally forming arcuate and annular patterns. Some of the lesions on the leg and hands developed thick waxy scales. She had been treated earlier as a case of psoriasis with no relief. She gave history of diabetes mellitus, weight loss and chronic diarrhea for the past 1 year.\nExamination revealed multiple scaly erythematous plaques of size 1-15 cm over the face, trunk and extremities and multiple annular plaques with thick waxy scales on the thighs, legs, palms and periorbital area []. There were also multiple crusted plaques over the dorsum of both feet and ankles []. This later progressed to multiple arcuate and annular ulcers of size 3-7 cm with irregular borders, marginal vesiculopustules, sloping edges and floor covered with granulation tissue and hemorrhagic crusting over feet and legs []. Additional findings included pallor, angular chelitis and ichthyosis. We investigated the patient with a differential diagnosis of psoriasis, Reiter's disease, pyoderma gangrenosum and acral necrolytic erythema.\nInvestigations showed hemoglobin level of 9.5 gm/dl; total leucocyte count of 13,300 with a differential count of 82% polymorphs and 16% lymphocytes; ESR of 100 mm; low serum zinc and albumin levels; elevated blood sugar levels; and negative HIV, HBsAg, VDRL and HCV serology. Other biochemical parameters were normal. No organism could be isolated despite repeated cultures for bacteria, mycobacteria and fungi. Skin biopsies from the plaque and margin of ulcers showed psoriasiform hyperplasia of the epidermis with focal parakeratosis, dyskeratotic cells and upper epidermal pallor with hydropic degeneration of keratinocytes []. The histopathology was suggestive of the family of necrolytic erythemas, which includes glucagonoma syndrome. But CT scan of the abdomen failed to detect any pancreatic tumors at the time. Due to monetary constraint the patient refused serum glucagon estimation.\nDuring the 3-month hospital stay the patient failed to improve with antibiotics, vitamin supplementation, injection human insulin and general supportive measures. The presence of chronic psoriasiform skin lesions, histologically belonging to the family of necrolytic erythemas[] and coexistent diabetes, made us consider the possibility of undetected glucagonoma. So we treated the patient empirically with oral zinc sulphate 220 mg thrice daily, amino acid infusions and monthly injections of 20 mg octreotide acetate. The skin lesions improved and healed completely in 1 month with residual pigmentary changes and scarring []. On discontinuation of treatment the skin lesions recurred, but responded again to the same line of management. One year later a repeat CT scan showed multiple hypodense lesions in the tail of the pancreas. A diagnostic FNAC from the mass lesion was planned from department of gastroenterology. But prior to the procedure patient developed altered sensorium of one day for which she was readmitted in that department. But her condition progressively worsened and she expired the next day despite resuscitative measures.
|
[[53.0, 'year']]
|
F
|
{'18957496': 1, '25228264': 1, '15657529': 1, '18177818': 1, '21859461': 2, '15655150': 1, '15538929': 1, '23984235': 2}
|
{'3171381-1': 1}
|
162,817 |
3752478-1
| 23,984,236 |
noncomm/PMC003xxxxxx/PMC3752478.xml
|
Granulosis rubra nasi
|
A 27-year-old man presented with erythema over the nose since childhood without sensitivity to sunlight. He was otherwise well and there was no relevant family history. Physical examination showed excessive sweating of the nose, erythema of the nose covered by beads of sweat, and multiple telangiectatic vesicles [Figures and ]. The rest of the physical examination was normal. The skin biopsy showed dilatation of blood vessels, dilated sweat ducts with a discrete mononuclear cell infiltrate surrounding them []. The patient was reassured taking into consideration the benign nature of the disease.
|
[[27.0, 'year']]
|
M
|
{'19991180': 1, '19980361': 1, '29318059': 2, '2279756': 1, '20781078': 1, '8761763': 1, '19496797': 1, '17442081': 1, '19988508': 1, '23984236': 2}
|
{'5727651-1': 1}
|
162,818 |
3752479-1
| 23,984,237 |
noncomm/PMC003xxxxxx/PMC3752479.xml
|
Cavernous lymphangioma: Two case reports
|
A 15-year-old girl reported to our department with the complaint of diffuse, painless swelling of the lower part of the face since birth. On examination the swelling involved the whole of the mandible area. The swelling was soft in consistency, non tender, and non-compressible []. The swelling was present since birth and has not increased in size. Surgical scar was present in the right side of the angle of mandible. Intraoral examination revealed macroglossia with fissured tongue []. Articulation was normal.\nIncisional biopsy from the lesion revealed epidermis, overlying lymph spaces, and sebaceous glands in the fibrocollagenous dermis. Biopsy of the tongue lesion revealed fragments of stratified squamous epithelium enclosing thin walled vascular and lymphatic spaces in a scanty stroma showing lymphoid aggregates []. Hemolymphangioma is another variant with features showing both a vascular and a lymphatic component.\nCT-neck revealed an ill defined heterogeneous lesion with variable degrees of enhancement involving the mental, submental, submandibular, base of tongue, cheek, bilateral para pharyngeal, and masticator spaces with the left side affected more than the right side. Left parotid gland was involved by the lesion and small calcifications noted within the lesion in the left submandibular region. The tongue appeared thickened, especially in the anterior part and showed altered signal intensity [].
|
[[15.0, 'year']]
|
F
|
{'16327140': 1, '27504428': 1, '25624641': 2, '10367920': 1, '19558311': 1, '18533550': 1, '11523862': 1, '10079671': 1, '12491020': 1, '23984237': 2}
|
{'3752479-2': 2, '4296469-1': 1}
|
162,819 |
3752479-2
| 23,984,237 |
noncomm/PMC003xxxxxx/PMC3752479.xml
|
Cavernous lymphangioma: Two case reports
|
A 14-year-old boy came to our OPD with the complaints of painless swelling in the left lower part of the face and macroglossia since birth with on and off history of bleeding from the tongue for the past 6 months. Parents had noticed that the child had a larger lower jaw since birth. The swelling gradually increased in size over the years.\nThere was a history of surgical excision for a similar swelling on the right lower face in the mandibular region which was also present since birth; details of the surgery not known. On clinical examination, a solitary ill-defined swelling measuring roughly 2×3 cm in size was noted in the left chin region []. It was warm, non tender and non compressible. The tongue was grossly enlarged. The dorsum anterior 2/3rd and pos 1/3rd and the lateral surface appears pebbly showing numerous erythematous pinpoint projections []. The tongue also appears lobulated. The midline furrow appears deepened. The movements of the tongue were restricted due to tongue-tie. On palpation, the tongue was firm in consistency and non tender on palpation.\nIncisional biopsy from the lesion revealed stratified squamous epithelium overlying bundles of fibro muscular tissue enclosing lymph spaces consistent with lympangioma [].
|
[[14.0, 'year']]
|
M
|
{'16327140': 1, '27504428': 1, '25624641': 2, '10367920': 1, '19558311': 1, '18533550': 1, '11523862': 1, '10079671': 1, '12491020': 1, '23984237': 2}
|
{'3752479-1': 2, '4296469-1': 1}
|
162,820 |
3752480-1
| 23,984,238 |
noncomm/PMC003xxxxxx/PMC3752480.xml
|
Eruptive vellus hair cyst presenting as asymptomatic follicular papules on extremities
|
A 12-year-old female presented with multiple, asymptomatic skin lesions on flexor aspect of both upper extremities since 6 months. Lesions used to heal with postinflammatory hyperpigmentation. Physical examination revealed discrete, symmetrically distributed, 2-3 mm sized, dome-shaped hyperpigmented follicular papules, few of them with central crust, on flexor aspect of both upper extremities []. There was no family history of similar lesions. Oral and genital examination was normal. Differential diagnosis of eruptive vellus hair cyst, milia was considered.\nBiopsy of the papule showed a mid-dermal cyst lined by flattened squamous epithelium []. The cyst cavity contained abundant laminated keratinous material and varying numbers of transversely and obliquely cut vellus hair shafts []. Thus diagnosis of Eruptive vellus hair cyst was confirmed. We started the patient on topical retinoic acid cream (0.05%) daily at night with complete resolution of lesions, but few lesions recurred after stopping the treatment.
|
[[12.0, 'year']]
|
F
|
{'11860565': 1, '19293527': 1, '17511947': 1, '848982': 1, '7430464': 1, '20166570': 1, '9039182': 1, '19736455': 1, '8746359': 1, '9185910': 1, '23984238': 2}
|
{}
|
162,821 |
3752481-1
| 23,984,239 |
noncomm/PMC003xxxxxx/PMC3752481.xml
|
Phacomatosis cesioflammea with Klippel Trenaunay syndrome: A rare association
|
A 30-year-old male presented with extensive vascular changes on the trunk and limbs and pigmentary changes on the face. Cutaneous examination showed extensive nevus flammeus affecting almost the entire back, crossing the midline and extending to the buttocks and left lower limb [Figure and ]. Similar discrete lesions were present over the flanks and lateral aspect of the chest []. There was bilateral bluish-grey pigmentation over the face along the ophthalmic and maxillary division of the trigeminal nerve consistent with Nevus of Ota []. The sclera, nasal mucosa and palate also showed patchy bluish-grey pigmentation bilaterally [Figure and ]. Soft tissue hypertrophy of the left lower limb was seen in association with nevus flammeus and varicose veins over the left leg. A difference of 3 cm was noted in the circumference of both lower legs at the mid-calf region. The patient also had right-sided scoliosis. Neurological and ophthalmic examinations did not reveal any abnormality. Routine hematological investigations were normal. Radiological examination of the left lower limb showed soft tissue swelling without evidence of bony changes. Color Doppler of the affected limb showed varicosities of short saphenous vein with incompetence of the perforators. There was no history of seizures. Also, there was no history of similar pigmentary or vascular lesions in any of his family members.
|
[[30.0, 'year']]
|
M
|
{'30920161': 1, '3994413': 1, '1997390': 1, '12588390': 1, '12773803': 1, '15781681': 1, '23984239': 2}
|
{}
|
162,822 |
3752482-1
| 23,984,240 |
noncomm/PMC003xxxxxx/PMC3752482.xml
|
A case of zosteriform Darier's disease with seasonal recurrence
|
A 35-year-old woman presented with mildly pruritic, unilateral, hyperpigmented, keratotic papules localized to the right infra mammary region []. For the past 3 years, these lesions occurred strictly in summers, from March to June, and regressed spontaneously afterwards. There was no history of similar skin lesions in any of the family members. No oral, nail or hair abnormalities were detected. General physical examination was normal. Routine hematological and biochemical investigations were normal. Histopathological examination of the skin biopsy showed hyperkeratosis, elongation of rete ridges, suprabasal acantholysis and marked dyskeratosis in the form of corps ronds and grains [Figures and ] along with a mild lymphohistiocytic inflammatory infiltrate in the dermis consistent with DD.
|
[[35.0, 'year']]
|
F
|
{'7702264': 1, '15505549': 1, '7284250': 1, '1390140': 1, '17337395': 1, '10441323': 1, '26500868': 2, '9301591': 1, '21393978': 1, '10491500': 1, '12403314': 1, '26312676': 2, '1619075': 1, '23984240': 2}
|
{'4540510-1': 1, '4594397-1': 1}
|
162,823 |
3752483-1
| 23,984,241 |
noncomm/PMC003xxxxxx/PMC3752483.xml
|
A rare case of woolly hair with unusual associations
|
A 4-year-old boy, product of third degree consanguineous marriage, presented with history of light colored curly hair on the scalp and skin-colored pinhead type of raised lesions over the body since birth. The skin lesions began on the scalp and later spread to the whole body. He also gave a history of recurrent pus-filled lesions over the body since the age of 3 months. There was no delay in developmental milestones.\nExamination revealed curled hypopigmented scalp hair []. The scalp hairs were short and thinner in diameter. The body hair was also sparse, shorter and lighter in color. Multiple skin colored, spiny follicular papules were present over his scalp, back and arms [Figures and ]. The eyebrows had sparse hair. Multiple bullae were present over his extremities, some of which were filled with yellow fluid with a positive hypopyon sign []. There was canaliform dystrophy of the bilateral great toe nails []. Dental examination revealed increased interdental spaces and dental caries []. Eye examination was normal. There were no cardiac manifestations or any other systemic involvement.\nInvestigations revealed normal hematological and biochemical parameters. Skin biopsy of the keratotic papules revealed features consistent with keratosis pilaris []. Gram stain of pus from the bullous lesion revealed gram positive cocci, and the culture grew Staphylococcus aureus. Microscopy of hair revealed an elliptical cross-section, axis rotation and calibre variation. There was no evidence of trichorrhexis nodosa. X-ray chest, electrocardiogram and echocardiography were normal.
|
[[4.0, 'year']]
|
M
|
{'29267480': 2, '31332722': 1, '2347106': 1, '30719357': 2, '17651168': 1, '19052410': 1, '26538742': 2, '11063735': 1, '2945574': 1, '11453928': 1, '10902626': 1, '4467886': 1, '668970': 1, '23984241': 2}
|
{'4601463-1': 1, '5726711-1': 1, '6335686-1': 1}
|
162,824 |
3752485-1
| 23,984,243 |
noncomm/PMC003xxxxxx/PMC3752485.xml
|
Symmetrical peripheral gangrene associated with peripartum cardiomyopathy
|
Thirty-year-old, para 4, seven days post-partum with unbooked pregnancy, home conducted delivery with alive infant was admitted with chief complaints of progressive dyspnoea for 4 days, orthopnea for 1 day, cough with pink frothy sputum, decreased urine output, and swelling feet for 1 day. There was no history of chest pain, palpitation, and fever. There were no neurological complaints. Lochia, urinary, and bowel habits were normal. At admission, patient was afebrile, had blood pressure of 96/60 mm of Hg, pulse rate of 102/min, and respiratory rate was 28/min. Jugular venous pressure was raised up to 6 cm above angle of Louis. Pedal edema was present. There was bluish discoloration of fingers of both hands. Beside this dorsal aspect of bilateral feet showed edema, lividity, and cyanotic hue on plantar aspect. Bilateral toes showed symmetrical gangrenous changes with eschar formation [Figures -]. All peripheral pulses were palpable, regular, and of normal volume. On systemic examination, there were bilateral basal crepitations in chest, tender hepatomegaly, and S3 gallop. Investigations revealed hemoglobin 9.8 g% and total leukocyte count 15,600/cumm. Peripheral blood smear revealed normocytic hypochromic picture with neutrophilia and shift to left. Biochemistry revealed following parameters: Random blood glucose-110 mg%, total bilirubin-1 mg%, SGOT-110 IU/L, SGPT-102 IU/L, alkaline phosphatase-90 IU/L, albumin-3.0 g%, urea-120 mg%, creatinine-1.5mg%, uric acid-3.6 mg%, calcium-9 mg%, and phosphorous-4.6 mg%. Electrolytes, lipid profile, and coagulogram were normal. Urine showed albumin 1+ on dipstick and was negative for pus cells, red blood cells cast, active sediment. Urine and blood cultures were sterile. HBsAg, anti-HCVIgG, VDRL, ELISA for HIV, and antinuclear antibody were negative. Chest X-ray revealed bat wing appearance with cardiomegaly. Electrocardiogram showed sinus tachycardia. 2D echocardiogram revealed global hypokinesia with left ventricular ejection fraction (LVEF) of 40%. Doppler study for upper and lower limb arteries was normal. After examination and investigation, clinical possibility of PPCM with SPG was kept. Patient was treated with back rest, oxygen inhalation, enoxaparin (low molecular weight heparin), aspirin, diuretics, and low dose angiotensin-converting enzyme (ACE) inhibitors. After 5 days of in hospital treatment, patient's blood pressure normalized to 110/80 mm of Hg. Pedal edema and raised jugular venous pressure resolved. Over next few days, patient's renal function test and liver function test were normalized, gangrenous changes in fingers improved, and dry gangrene became confined to bilateral toes. Patient was ambulatory at discharge, normotensive, and advised follow up in general surgery for management of dry gangrene of toes. On follow up at 4 weeks, 2D echo showed LVEF of 52% and bilateral toes were dry, shriveled with features of auto amputation.
|
[[30.0, 'year']]
|
F
|
{'7683845': 1, '28300932': 2, '4197291': 1, '15645963': 1, '33083179': 2, '3896158': 1, '28948150': 1, '11372011': 1, '5424498': 1, '23984243': 2}
|
{'7567307-1': 1, '5325031-1': 1}
|
162,825 |
3752486-1
| 23,984,244 |
noncomm/PMC003xxxxxx/PMC3752486.xml
|
Acute generalized exanthematous pustulosis: A rare side effect of a common over-the-counter drug, Acetylsalicylic acid
|
A 48-year-old male patient, with no known comorbidities, presented with complains of mildly itchy rash with fever of two-day duration. The rash started from neck and progressed over two days to involve entire trunk and proximal extremities []. He gave history of taking a tablet of ASA for headache, few hours before development of the rash and fever. He had taken the same drug earlier innumerable times in last 15 years, without any side effects; however, it was a 325 mg tablet this time. There was no history of any other drug intake, previous drug allergy, or insect bite. There was no family or personal history of Psoriasis.\nExamination revealed numerous pinhead-sized pustules extensively distributed over upper arms, neck, trunk, and upper thighs over an erythematous background []. The mucous membranes, scalp, palms, and soles were spared. Nails and hair were normal.\nHis Hb was 14.4 g%; TLC, 10 200/mm3; DLC - N 78, L 18, M 02, E 02; Platelet count, 244 000/mm3; and ESR, 30 mm/hr. Liver function tests and urinalysis were within normal limits. No organisms were seen on Gram's stain or isolated on culture of the pustules. Histopathological examination showed subcorneal pustules, a mixed neutrophil-rich interstitial and mid-dermal infiltrate. Tortuous and dilated blood vessels were absent []. The Naranjo Score was 5, which suggested a probable causal association for ASA in this case. The clinicopathological correlation ruled out Pustular Psoriasis, the most common differential diagnosis, in favor of AGEP. He was managed with tapering doses of oral steroids. He responded well and all lesions resolved within 10 days [].
|
[[48.0, 'year']]
|
M
|
{'19681339': 1, '32695700': 1, '15840114': 1, '7829242': 1, '12847757': 1, '12773073': 1, '8475362': 1, '11390425': 1, '11226910': 1, '17622365': 1, '6989310': 1, '10856665': 1, '12130947': 1, '23984244': 2}
|
{}
|
162,826 |
3752487-1
| 23,984,245 |
noncomm/PMC003xxxxxx/PMC3752487.xml
|
Speckled lentiginous nevus syndrome with median nerve paresis: A rare syndrome with a new association
|
A 23-year-old Indian girl presented with a large pigmented lesion on her left arm and hand since birth. She reported darkening of the hyperpigmented patch over the years with the development of darkly pigmented spots over it. She also complained of weakness of the grip of left hand for the past 3 years. There was no history of trauma. Her medical history was otherwise unremarkable.\nCutaneous examination revealed a large café au lait macule running along the antero-medial aspect of left arm extending down to involve the palmar and the dorsal surface of the hand []. This macule was superimposed by multiple dark brown macules of size 0.2-1 cm. There was mild atrophy of the thenar eminence of the left hand []. Motor examination revealed deficient opposition and thumb flexion with positive pen test. Sensory examination revealed sensory loss to touch, temperature, and pain over medial nerve distribution of hand. A complete neurological checkup did not reveal any additional findings.\nNerve conduction studies showed involvement of the left median nerve (both motor and sensory) as non-recordable with normal left ulnar nerve and right median (both motor and sensory) nerve conduction. There was weakness in the left abductor pollicis brevis muscle on electromyography documentation. Magnetic resonance imaging (MRI) of the cervical spine was normal. Histopathological examination from one of the darker macule showed features consistent with nevus spilus [].
|
[[23.0, 'year']]
|
F
|
{'8548990': 1, '8340503': 1, '15459538': 1, '9703145': 1, '9115921': 1, '3579111': 1, '11872407': 1, '8148284': 1, '8923953': 1, '15781681': 1, '23984245': 2}
|
{}
|
162,827 |
3752488-1
| 23,984,246 |
noncomm/PMC003xxxxxx/PMC3752488.xml
|
A rare case of malignant chondroid syringoma of scalp
|
A 61-year-old female presented with a large, fungating, and ulcerated growth over the occipital region of scalp []. The history was that of a painless, slow growing mass over a 9-month time period. Clinically the patient was suspected to have a squamous cell malignancy of scalp (which was the most confusing differential diagnosis). Initial biopsy of the lesion favored a benign mixed eccrine tumor of the scalp, that is, a benign CS. The patient was then referred for contrast enhanced computerized tomography (CECT) scan of head. The scout image was suggestive of a soft tissue lesion in the occipital region with erosion of the adjacent occipital bone []. CECT revealed a moderately and heterogeneously enhancing soft tissue density mass lesion of size approx. 8.0 1.4 cm, arising from the occipital scalp, causing lytic destruction of the adjacent occipital bone. Also, the underlying dura appeared focally thin, with white matter edema in the occipital region, suggesting dural invasion []. Wide local excision with primary closure was done. Histopathology revealed small groups as well as scattered pleomorphic epithelial cells having hyperchromatic nuclei and scanty cytoplasm with one to two mitotic figures per high power field, surrounded by abundant basophilic chondromyxoid stroma, diagnostic of malignant CS []. The patient developed high-grade fever and altered sensorium, and died on the 2nd postoperative day, possibly due to meningitis. This infection could have spread to the meninges from operative site, as there was certain evidence of meningeal invasion on CECT.
|
[[61.0, 'year']]
|
F
|
{'26430319': 2, '8721597': 1, '29384887': 1, '30200138': 1, '28892909': 1, '6274261': 1, '33304693': 2, '31723522': 2, '6283274': 1, '25478357': 1, '13652101': 1, '12562350': 1, '13907712': 1, '22421860': 1, '27203613': 1, '2848409': 1, '26171105': 1, '16087034': 1, '23984246': 2}
|
{'7720919-1': 1, '4579620-1': 1, '6825454-1': 1}
|
162,828 |
3752489-1
| 23,984,247 |
noncomm/PMC003xxxxxx/PMC3752489.xml
|
Erosive adenomatosis of the nipple masquerading as Paget's disease
|
A 23-year-old unmarried woman presented with history of oozing of serous and very rarely sanguineous discharge from right nipple for more than a year. There was no definite history of exacerbation in relation with menstrual cycles, which were normal. There was no family history of similar illness or carcinoma of breast. On examination, the skin over the nipple was rough and thickened with erosion and superficial fissuring []. The examination of the breasts and regional nodes were normal. The ultrasonogram done after a course of antibiotics was normal. She was diagnosed with EAN and treated with antibiotics and short-term mild topical steroids with remission but was not sustained. When she saw discharge of frank blood, the alarmed patient sought opinion from various specialists and was advised mastectomy by some of them. A biopsy of the nipple was performed, which showed features of EAN [Figures and ]. Being an unmarried girl, radiofrequency is being planned rather than excising the nipple. She will be followed up regularly for recurrence if any.
|
[[23.0, 'year']]
|
F
|
{'9486687': 1, '2985661': 1, '27206635': 2, '33363915': 2, '4335982': 1, '10321629': 1, '23984247': 2}
|
{'4873987-1': 1, '7752568-1': 1}
|
162,829 |
3752490-1
| 23,984,248 |
noncomm/PMC003xxxxxx/PMC3752490.xml
|
A case report of focal dermal hypoplasia-Goltz syndrome
|
A five-year-old female born out of non-consanguineous marriage presented to the outpatient department for right-sided facial deformity with multiple generalized skin lesions since birth. She was delivered normally with no untoward perinatal event. She was second in birth order and her two sisters were normal. She did not have developmental delay and was going to school. She was weighing 10.2 kilograms and her height was 96 centimeters as against expected weight and height of 18 kilograms and 105 centimeters, respectively. She had right-sided facial hypoplasia [] with unilateral notching of right ala nasi, deformed pinna with low set ears. She had concomitant squint with coloboma iris in right eye along with patchy alopecia. Dental check up showed maloccluded, hypoplastic irregular dentition. Cutaneous examination revealed multiple linear atrophied hypo- and hyperpigmented macules along the lines of Blaschko []. She had limb deformities in the form of syndactyly in both feet, polydactyly in left foot [] and clinodactyly of right fifth finger. She also had multiple papillomas on lips, fat herniation over the lower limbs and umbilical hernia. Onychodystrophy was also present. Her right-sided chest was flattened and lordosis was observed on standing.\nSystemic examination was normal. Ultrasound of abdomen, echocardiography was normal. However, the patient did not consent for a skin biopsy. Radiographs of the long bones showed the features of osteopathia striata in the form of symmetrical striations in metaphyses. Goltz syndrome was considered and the patient was counseled accordingly. Patient was referred first to plastic surgeon for polysyndactyly and to dental surgeon for malocclusion teeth and counseled to visit next to orthopedician & ophthalmologist.
|
[[5.0, 'year']]
|
F
|
{'10602117': 1, '34720501': 2, '13948891': 1, '34434364': 2, '7346416': 1, '27721997': 2, '9220199': 1, '16394441': 1, '6630607': 1, '23984248': 2}
|
{'8543741-1': 1, '5046003-1': 1, '8383521-1': 1}
|
162,830 |
3752856-1
| 23,984,262 |
noncomm/PMC003xxxxxx/PMC3752856.xml
|
Testicular adrenal rest “tumor” or Leydig cell tumor? A report of a challenging case with literature review
|
A 15-year-old male known to have the CAH salt-wasting type diagnosed earlier in childhood. He presented with synchronous and progressive enlargement of bilateral testicular masses during substitutive medical therapy.\nOn examination, he had normal stature (body mass index: 21.2 kg/m2). Genital examination demonstrated firm painless 8 cm mass involving the right testis and 10 cm mass involving the left testis.\nSemen analyses revealed azoospermia. Serum hormonal screening showed high 17-OH progesterone; 24.1 nmol/L (1.5-6.4 nmol/L).\nSerum tumor markers were low; α-fetoprotein was 1 ng/mL (0-44 ng/mL); β-human chorionic gonadotrophin was <12 IU/L (<5 IU/L).\nTesticular ultrasound examination confirmed the presence of bilateral hyperechogenic hypervascularized lesion; right: 8.6 cm × 3.5 cm; left: 8.4 cm × 5.5 cm []. These features although non-specific, raised the possibility of a testicular neoplasm.\nConsidering the possibility of malignant testicular neoplasms, a surgical intervention was scheduled.\nAt surgery, bilateral large firm, lobulated masses were replacing the testicular tissue. The patient underwent bilateral testicular incisional biopsies and the specimens were sent to our department for intra-operative consultation.\nMacroscopically, both specimens (2.5 cm from the right testis and 1.8 cm from the left testis) appeared light brown with lobular rubbery cut surface. Frozen sections from each were examined. Microscopic examination showed a complete replacement of the normal testicular tissue by sheets and nests of large round and polygonal cells with defined cell borders, abundant eosinophilic cytoplasm and round central nuclei. Nests of cells were separated by dense fibrous tissue []. The morphological features were of “LCT-like” lesion! Nevertheless, Reinke crystals were not seen. At this point, the differential diagnosis was either LCT or mass-forming TART.\nThe clinical picture of CAH and the bilaterality of the lesions were more compatible with the TART. However, rapid enlargement and the destruction of the testicular parenchyma implying irreversible damage together with worrisome atypical ultrasound features were in keeping with LCT. Two known TART characteristic features if present could strengthen its probability: Hilar location and evidence of response to suppressive therapy. In our case, the lesions occupied the entire testis without definitive hilar location. In addition, no suppressive therapy was tried; the patient was on substitutive therapy when operated.\nBeing indistinguishable from TART on H and E sections, LCT was difficult to exclude. The pathologic frozen section diagnosis was of benign neoplasm.\nA decision of bilateral orchiectomy was made and the specimen was sent to our department for permanent examination.\nMacroscopically, the lesions were bilateral involving almost the entire testes separated into lobules with prominent fibrous bands [].\nMicroscopically, no normal testicular tissue was identified. The lesions were composed of sheets, nests and cords of polygonal cells with abundant eosinophilic cytoplasm. Few of these cells contained lipochrome pigments, but Reinke's crystals were absent. There was mild nuclear pleomorphism without mitotic activity. Some lymphoid aggregates were seen []. Immunohistochemical analyses were performed []. The polygonal cells showed positivity to four markers known to be shared between LCT and TART namely inhibin alpha, melan A, vimentin, and calretinin. However, the cells showed a distinguishing immuno-profile of TART: Intense and widespread staining for CD56, patchy yet strong staining for synaptophysin and non-reactivity to CD10.\nThese immunohistochemical features with the absence of Reinke crystals leaded to the final diagnosis of TART and implied a better prognosis.
|
[[15.0, 'year']]
|
M
|
{'21686875': 1, '19500764': 1, '26351608': 2, '20704142': 1, '12835972': 1, '29531157': 1, '22248786': 1, '11157817': 1, '21259051': 1, '29430117': 2, '22606635': 2, '21456481': 1, '27696245': 1, '12930931': 1, '17543962': 1, '16949566': 1, '21378545': 1, '21707702': 1, '31917682': 1, '18528248': 1, '18660859': 1, '17595257': 1, '17307866': 1, '29038332': 1, '16124976': 1, '17222630': 1, '23984262': 2}
|
{'4553183-1': 1, '5798100-1': 1, '3350130-1': 1}
|
162,831 |
3752857-1
| 23,984,263 |
noncomm/PMC003xxxxxx/PMC3752857.xml
|
Red discoloration of urine caused by Serratia rubidae: A rare case
|
A 40-year-old female patient presented with fever, urgency, frequency, and burning micturition since 6 days. The patient also gave a history of passage of pale reddish urine since the last 2 days. She was a known type 2 Diabetes mellitus patient, on oral hypoglycemic drugs for the last 10 years. The blood investigations were as follows: Fasting blood glucose-330 mg/dl, urea 24 mg/dl, creatinine-0.98 mg/dl. The patient did not give any history suggestive of previous episodes of UTI.\nThe mid-stream urine sample collected aseptically was cloudy, with a reddish tinge. The urine routine microscopy interestingly showed 5-7 pus cells/high power field and bacilli but no red blood cells. The dipstick test performed for detecting microscopic hematuria was also negative. The gram stain showed pus cells and gram-negative cocco-bacilli. Urine sample was inoculated onto blood agar and MacConkey agar, incubated overnight at 37°C aerobically. Semi-quantitative technique was followed for colony count. After overnight incubation, pure growth of red pigmented colonies with a significant colony count of >105 CFU/ml was observed. Red pigment was also produced on Nutrient agar. On further testing, it was found to be a motile gram negative cocco-bacillus. Biochemical reactions showed catalase-positive, oxidase-negative, showed K/A (alkaline slant/acid butt) with gas production on triple sugar iron agar, ortho-Nitrophenyl-β-galactoside (ONPG)-positive fermented acid with adonitol, arabinose, lactose, raffinose, sucrose, and xylose. It did not ferment sorbitol and rhamnose. Indole was not produced but utilized citrate. It was confirmed as Serratia rubidae by standard biochemical techniques.[] Strain was found to be susceptible to ciprofloxacin, piperacillin, cotrimoxazole ceftazidime, amikacin, meropenem and was resistant to nitrofurantoin and polymixin B by the Kirby–Bauer disc diffusion technique as per Clinical Laboratory Standards Institute (CLSI) guidelines []. The minimum inhibitory concentration of ciprofloxacin was 0.02 μg/ml. The patient was treated with ciprofloxacin to which the patient responded well with the relief of the symptoms. Repeat mid-stream urine sample after 3 weeks did not yield any growth on the culture medium and the urine microscopy was normal.
|
[[40.0, 'year']]
|
F
|
{'8748310': 1, '12654765': 1, '23267624': 1, '17321092': 1, '23984263': 2}
|
{}
|
162,832 |
3752858-1
| 23,984,264 |
noncomm/PMC003xxxxxx/PMC3752858.xml
|
Renal artery embolization for managing uncontrolled hypertension in a kidney transplant candidate
|
A 34-year-old anuric male with end-stage renal failure (glomerular filtration rate (GFR) <5 mL/min/1.73 m2) secondary to focal segmental glomerulosclerosis presented to the Emergency Department complaining of confusion and restlessness. The patient has a poorly-followed hypertension treated with metoprolol 100 mg bid, amlodipin 5 mg bid, fosinopril 20 mg qd and calcium carbonate 500 tid for 8 years. The patient was on hemodialysis for 7 months prior to admission and he developed malignant hypertension and tonic-clonic seizures after one of the dialysis sessions about 2 month before admission. Consequently, the patient was admitted to the intensive care unit and received intravenous nitroglycerine for 1 week with modifying his medications to: Valsartan 160 mg daily doxazosin 4 mg, fosinopril 10 mg bid. The decision for kidney transplantation was made, but was not possible because of his drug-resistant hypertension.\nAfter a few days, he developed two tonic-clonic seizures, which were treated with diazepam and IV phenytoin. His BP was 230/140 mmHg after these seizures. He received hemodialysis sessions twice a week for 2 months (weight before dialysis: 56 kg, dry weight: 52 kg) until the decision was made to perform RAE. Abdominal multi-slice computed tomography scan prior to performing RAE showed 60% stenosis in the left renal artery and 90% stenosis in the right renal artery [] and renal sizes were 7.3 cm on the right and 8.2 cm on the left.\nRAE was carried out through a right common femoral artery access using the n-butyl-2-cyanoacrylate (Histoacryl; B. Braun, Melsungen, Germany) and lipidol delivered via a 5 Fr Cobra catheter [] with no major periprocedural complications. The patient developed the post-embolization syndrome following the procedure manifested by severe flank pain treated with analgesics.\nAfter performing RAE, the patient's blood pressure declined to 170/100 mmHg, and he was discharged home on amlodipine 5 mg bid, clonidine 150 mcg bid, and nebivolol 5 mg bid. Renal transplantation was performed successfully without complications and he was discharged on amlodipine 5 mg and nabivolol 5 mg qd. 6 month following transplantation, the patient's creatinine was 1 mg/dl and the blood pressure normalized to 120/80 mmHg.
|
[[34.0, 'year']]
|
M
|
{'18391085': 1, '904036': 1, '356390': 1, '23204638': 1, '12207195': 1, '19221759': 1, '2021844': 1, '16191179': 1, '21411466': 1, '33041489': 1, '9603165': 1, '12736004': 1, '12695724': 1, '10037359': 1, '25536394': 1, '23984264': 2}
|
{}
|
162,833 |
3752861-1
| 23,983,417 |
noncomm/PMC003xxxxxx/PMC3752861.xml
|
Hyperammonemic coma in a post-partum patient with undiagnosed urea cycle defect
|
A 33-year-old primigravida, four days post-cesarean section, was referred to us with 2 days history of altered sensorium progressing to coma. A pre-admission MRI brain with cerebral venography was unremarkable. The peripartum period was uneventful. She had past history of self-limiting episodes (3 in the last 5 years) of altered behavior and confusional state. In the intensive care unit (ICU), she was found to be in grade IV encephalopathy (Glagow Coma Scale (E1V1M2), pupils were bilateral mid dilated and reactive to light. Bilateral plantars were extensor, and deep tendon reflexes were absent. Neck rigidity was absent, and there was generalized hypotonia. She was hemodynamically stable. The trachea was intubated for airway protection. Her blood investigations showed a serum ammonia 286 mmol/L and serum urea of 13 mg/dL. Arterial blood gases showed well compensated respiratory alkalosis. Rest of the investigations including liver function tests and blood glucose levels were normal.\nPlasma amino acid levels and urine orotic acid levels were sent. A protein-free nasogastric feed was started. Anti-ammonia measures were instituted in the form of lactulose (30 ml q4h) and tablet rifaximine (300 mg twice-daily) through nasogastric tube.\nThe next day, ammonia levels rose to 300 mmol/L, despite passage of good amount of loose stools. Decision of instituting hemodialysis was taken. On day 3, we received the report of amino acid levels with citrulline levels of 933 (normal <70) micromol/L, glycine 970 (normal <505) micromol/L and phenyalanine 181 (normal <120) micromol/L. Urinary orotic acid – result value 31.20, reference range in % 0.30, elevation factor 104.00. Ammonia levels after a second cycle of hemodialysis was 160 mmol/L.Serum ammonia level showed a progressive decline [] over the next 3 days through 3 cycles of hemodialysis. She was extubated on day 5. Ammonia levels stayed below 50 mmol/L with no further dialysis required. She could be transferred out of ICU on day 7 and discharged on day 9 of hospitalization in a stable condition.
|
[[33.0, 'year']]
|
F
|
{'9213187': 1, '1782729': 1, '7774516': 1, '15050979': 1, '6510017': 1, '3748082': 1, '20471629': 1, '17538087': 1, '12450653': 1, '7941540': 1, '1720458': 1, '11688701': 1, '11007104': 1, '23983417': 2}
|
{}
|
162,834 |
3752862-1
| 23,983,418 |
noncomm/PMC003xxxxxx/PMC3752862.xml
|
Hypertensive encephalopathy following snake bite in a child: A diagnostic dilemma
|
An 8 year old male was brought to the hospital with the history of difficulty in breathing since morning and an episode of convulsions followed by unconsciousness while on his way to the hospital. On examination he had increased surface temperature (37.8°C), tachypnoea with paradoxical respiration, tachycardia (124/min), hypertension (210/140 mmHg), Glasgow Coma Scale (GCS) of 3/15 and arterial oxygen saturation (SpO2) of 93% on 4 liters of oxygen. He was immediately intubated with a provisional diagnosis of hypertensive encephalopathy. All investigations being inconclusive to establish a diagnosis, the history was reviewed. It was revealed that at night the child was sleeping on the floor in open air. He suddenly woke up at 3.30 a.m. and complained of severe abdominal pain before going to sleep again. Two hours later he again woke up and complained of difficulty in breathing, swallowing and speaking. He also developed double vision. On his way to the hospital he had an episode of convulsions followed by unconsciousness. Considering the clinical history, physical findings (bulbar and motor paralysis) and inconclusive investigations, an Elapid snake bite was suspected. However, the absence of fang marks or localized swelling and the unusual presentation (hypertension, convulsions and unconsciousness) led to a mistaken diagnosis that stopped us from administering anti snake venom (ASV). Meanwhile the child was managed with ventilator support, Nitroglycerine infusion, intravenous Phenytoin and broad spectrum antibiotics. However, persistent motor paralysis with no improvement in GCS for more than 20 h with no identifiable cause led us to consider an ASV trial. Accordingly, 10 vials of polyvalent anti-venom were administered following which there was a dramatic improvement in both GCS and motor power. However, as he still had abdominal respiration another 10 vials of ASV were administered. Despite the full course of ASV the respiratory muscles appeared weak as tidal volumes generated were low requiring high pressure support mechanical ventilation. A single dose of neostigmine 0.8 mg and atropine 0.1 mg intravenously was given without much improvement. Thereafter the patient was gradually weaned and extubated after 8 days of mechanical ventilation and was discharged from the ICU on the ninth day without any residual morbidity.
|
[[8.0, 'year']]
|
M
|
{'9856873': 1, '11384723': 1, '24701075': 1, '20701896': 1, '16677986': 1, '23983418': 2}
|
{}
|
162,835 |
3752865-1
| 23,983,421 |
noncomm/PMC003xxxxxx/PMC3752865.xml
|
Status epilepticus: An association with pyrethroid poisoning
|
A 35-year-old male was admitted to our emergency department with giddiness as the major complaint following ingestion of an unknown quantity of an unknown poison. Patient was conscious, oriented with stable cardio-respiratory parameters at the time of arrival. After sometime, despite being well oxygenated via face mask, patient started having generalized tonic-clonic seizures. Initial attention to airway, breathing and circulation (ABC) was given, followed by a bolus dose of diazepam. Seizures subsided for a brief period only to recur repeatedly.\nOn repeated enquiry, the patient's relative brought empty bottles of “ALL OUT,” a commercial composition of pyrethroid used as insecticides providing a circumstantial evidence of the nature of the poisoning.\nPatient was given a bolus dose of thiopentone sodium, and soon his trachea was intubated. This was followed by a loading dose of the anti-convulsant phenytoin to control seizures.\nPatient was shifted to the intensive care unit for further management. On examination, he was deeply comatose. There was profuse sweating. His pulse rate was 136 per minute, and the blood pressure was 90/60mmHg. His pupils were dilated bilaterally and sluggishly reacting to light. Examination of the other systems was unremarkable. Hemogram, liver and kidney function tests, X-ray chest, ECG, and arterial blood gases were normal. Patient was put on a ventilator on the SIMV mode.\nAgain the patient started showing tonic–clonic seizures, which were continuous and unresponsive to anti-convulsant therapy. Thereafter, thiopentone sodium and midazolam infusions were administered and titrated clinically as no bedside EEG monitoring was available. Gradually, thiopentone sodium and midazolam infusions were tapered off, and patient was weaned off the ventilator to be extubated after 72 hours. The patient was discharged from the hospital on the 7th day after a psychiatry consultation.
|
[[35.0, 'year']]
|
M
|
{'15081275': 1, '33031856': 1, '24872662': 1, '32021002': 1, '15591679': 1, '10778904': 1, '31998671': 1, '9282587': 1, '16180930': 1, '8841090': 1, '19881195': 2, '31753823': 1, '16180929': 1, '23983421': 2}
|
{'2772251-1': 1}
|
162,836 |
3752875-1
| 23,983,415 |
noncomm/PMC003xxxxxx/PMC3752875.xml
|
Management of post-intubation tracheal membrane ruptures: A practical approach
|
In the emergency department, a 76-year-old woman, intubated out of hospital, following a prolonged seizure, developed acute airway obstruction, which resolved on endotracheal suctioning of mucosal tissue debris. Cardiac arrest with pulseless electrical activity ensued. Bilateral tension pneumothoraces, apparently related to jugular central venous catheterization, were relieved by thoracocentesis and tube thoracostomy. Spontaneous cardiac output and oxygenation were restored. However, progressive abdominal distension developed. A plain chest radiograph (CXR) [] demonstrated subphrenic and subcutaneous air. Computed tomography [Figures and ] confirmed extensive subcutaneous air, residual pneumothoraces, pneumomediastinum and tension pneumoperitoneum. Gastrograffin contrast imaging excluded oesophageal perforation.\nIn the intensive care unit (ICU), she was stable. The abdomen was distended, but soft. There was no acidosis, normal lactate, and negative diagnostic peritoneal lavage. Diagnostic laparotomy was deferred and fiberoptic bronchoscopy was performed.\nBronchoscopy demonstrated a 4 cm long full thickness defect in the posterior membranous trachea, 1 cm proximal to the carina []. Following consultation, thoracic surgical repair of the tracheal tear or complex stenting were ruled out due to the high operative risk. A conservative approach was necessary. Bridging the defect by double lumen endotracheal tube (ETT) beyond the distal end of the tear was not possible due to the proximity of the main carina, and risk of the herniation of the ETT cuff into the posterior wall defect, Therefore, a cuffed ETT was placed proximal to the defect, and a low volume lung ventilation strategy was adopted, to allow the defect to recover without over-distension and exacerbating pneumomediastinum. Mechanical ventilation was as follows: Volume (5-6 ml/kg), frequency (25/min), pressure limited (mean airway pressure <25 cm H2O) ventilation with permissive Hypercapnia. Tazobactam-piperacillin was commenced empirically for suspected mediastinitis and pneumonia. As part of a cluster care strategy, blind tracheal suctioning, and patient rotation were avoided to prevent ETT migration. Post-pyloric feeding was established after confirming an intact esophagus and twice-daily bronchoscopy for airway clearance, and correct ETT position above the proximal defect.\nThe patient was weaned with percutaneous tracheostomy and discharged from ICU after 27 days. Follow-up bronchoscopy [] revealed complete linear mucosal healing.
|
[[76.0, 'year']]
|
F
|
{'14759406': 1, '8633963': 1, '21524499': 1, '12169951': 1, '21987439': 1, '15919275': 1, '16899839': 1, '11932162': 1, '19369087': 1, '14749562': 1, '10654516': 1, '34306717': 2, '8993280': 1, '17462432': 1, '25861593': 2, '29962621': 1, '28203437': 1, '17684721': 1, '23983415': 2}
|
{'3752875-2': 2, '8297638-1': 1, '4381825-1': 1}
|
162,837 |
3752875-2
| 23,983,415 |
noncomm/PMC003xxxxxx/PMC3752875.xml
|
Management of post-intubation tracheal membrane ruptures: A practical approach
|
A 69-year-old female was admitted with coma following a mixed overdose of benzodiazepines and narcotics. She was intubated, using an ETT with stylet.\nPersistent leak around her ETT, despite cuff inflation and tube changes initiated bronchoscopy. A 7 cm posterior tracheal tear extending to 2 rings above the carina contained large thrombus and mucopus. The ETT was withdrawn to above the proximal extent of the defect and meropenem for suspected mediastinitis (penicillin allergy).\nThoracic surgical consultation was sought due to the size and length of the defect, the potential for failure of bridging, and the chance of mediastinitis. Conservative management was advised, unless active endobronchial bleeding or progressive ventilatory failure ensued. A protective ventilation strategy, avoidance of blind tracheal suctioning and cluster care to avoid excessive ETT movement on patient repositioning were adopted. Bronchoscopy allowed airway clearance and monitoring of the defect. Spontaneous healing occurred, allowing tracheostomy, weaning, and discharge at 1 month.
|
[[69.0, 'year']]
|
F
|
{'14759406': 1, '8633963': 1, '21524499': 1, '12169951': 1, '21987439': 1, '15919275': 1, '16899839': 1, '11932162': 1, '19369087': 1, '14749562': 1, '10654516': 1, '34306717': 2, '8993280': 1, '17462432': 1, '25861593': 2, '29962621': 1, '28203437': 1, '17684721': 1, '23983415': 2}
|
{'3752875-1': 2, '8297638-1': 1, '4381825-1': 1}
|
162,838 |
3752881-1
| 23,983,913 |
noncomm/PMC003xxxxxx/PMC3752881.xml
|
The Place of Carotico-Subclavian Bypass Surgery in Angina Treatment
|
A 54-year-old male was admitted to our hospital with complaints of severe dyspnea, inability to lie in supine position, decrease in effort capacity, and pain in the left arm. Physical examination revealed tachycardia and 3/6 apical systolic murmur; bilateral rales in lower lung zones. Brachial, axillary, and radial pulses of the left arm were not palpable but were clearly palpated over the right arm. Lower extremity pulses were palpable. Past medical history revealed that he underwent coronary bypass graft operation five years prior to presentation.\nHe was assessed to have New York Heart Association Functional Classification Class III-IV, with a clinical diagnosis of ischemic cardiomyopathy (CMP), decompensated heart failure. An echoacradiogram was performed which showed increased left ventricular diameter and left ventricular ejection fraction of 18% by the modified Simpson method. He was started on diuretic and vasodilator treatment with regression of failure symptoms. However, he continued to have symptoms of angina and left arm pain responsive to isosorbide dinitrate. A differential diagnosis of CSSS was considered and patient underwent coronary angiography. It was observed on coronary angiography that point of origin of the left subclavian artery in the aorta was totally congested beginning from approximately 1 cm proximal []. A vertebral artery angiography was showed subclavian in bridge collaterals and flow to LIMA were observed in late period.\nUsing a ringed polytetrafluoroethylene (PTFE) graft (Vascutek, Germany) with a diameter of 6 mm, a left carotid-subclavian bypass was performed on the patient in elective conditions. Carotid shunt was not used while systemic heparin (5000 units) was administered during the operation. Postoperatively, a good graft pulse was felt in addition to easily palpable left upper extremity pulses. There were no complications. Following the operation and in the postoperative period, the complaints of the patient related to chest pain, dyspnea, and left arm pain progressively decreased. The patient was discharged on the postoperative day 5. Control coronary-subclavian angiogram 1 month later revealed an intact PTFE graft between carotid and subclavian artery [].
|
[[54.0, 'year']]
|
M
|
{'16516713': 1, '17245504': 1, '2934559': 1, '16368420': 1, '17712215': 1, '1993774': 1, '10691251': 1, '17670115': 1, '23983913': 2}
|
{}
|
162,839 |
3752882-1
| 23,983,914 |
noncomm/PMC003xxxxxx/PMC3752882.xml
|
Massive Lipomatous Hypertrophy of the Right Atria
|
A 70-year-old female with a history of hypertension, atrial fibrillation, pacer implantation for symptomatic bradycardia, and a prior cerebrovascular accident was transferred to our institution for further evaluation and management of a recently identified persistent methicillin-sensitive Staphylococcus aureus bacteremia.\nDuring workup of her bacteremia, a transesophageal echocardiogram was requested to rule out the presence of endocarditis. Although no vegetations were seen on either pacer wires or cardiac valves, a massive homogeneous thickening of the superior portion of the interatrial septum was noted [ and ]. This mass effect extended to the posterior and roof portions of the right atrial wall as well as to the superior vena cava, causing proximal compression of this vessel [Figure and ]. In view of these findings, a chest computed tomographic examination was requested for better definition of this mass density. Following contrast administration, the mass effect noted by transesophageal echocardiography was identified as intrapericardial fat density that extended toward the interatrial septum without evidence of infiltration of the interatrial septum directly []. Additionally, a nodular opacity was also found in the lateral left upper lobe with a greatest diameter of 1 cm that was thought to be a potential septic embolus given the recent history of bacteremia (not shown).\nThe initial continuous infusion of Nafcillin was later changed to Oxacillin, as surveillance blood cultures were all negative. The plan was to remove her transvenous pacer and replace it once she had completed her antibiotic therapy and follow-up blood cultures off antibiotics remained negative.
|
[[70.0, 'year']]
|
F
|
{'17060107': 1, '17629452': 1, '30055568': 2, '20471803': 1, '29633754': 1, '9124119': 1, '17064791': 1, '8509546': 1, '23983914': 2}
|
{'6064128-1': 1}
|
162,840 |
3752883-1
| 23,983,915 |
noncomm/PMC003xxxxxx/PMC3752883.xml
|
Giant Interatrial Septal Aneurysm Mimicking a Left Atrial Mass
|
A 41-year old male patient was referred to our institution by his primary care physician for transthoracic echocardiography to evaluate his hypertensive heart disease. The transthoracic echocardiography (TTE) showed a large mass measuring 1.4 × 1.4 cm in the left atrium that could represent a thrombus or myxoma []. The patient was asymptomatic and his past medical history was unremarkable except for hypertension. Clinical and laboratory examinations demonstrated no abnormality. Computed tomographic (CT) scan of the chest and heart with intravenous contrast did not show any cardiac tumor. TEE was then done and it showed a giant IASA bulging into the left atrium and mimicking a left atrial mass []. The patient had not had stroke or other cardio embolic phenomenon; therefore no further interventions were undertaken other than starting aspirin.
|
[[41.0, 'year']]
|
M
|
{'9813752': 1, '17041713': 1, '15078999': 1, '4067118': 1, '15743569': 1, '1629640': 1, '7758185': 1, '9555164': 1, '17515346': 1, '21859651': 1, '8910184': 1, '23983915': 2}
|
{}
|
162,841 |
3754372-1
| 23,793,189 |
noncomm/PMC003xxxxxx/PMC3754372.xml
|
Cartilaginous melanoma: case report and review of the literature
|
A 47-year-old woman presented with a painful subungual lesion on the right big toe which appeared one year before as a hyperkeratotic lesion and treated with oral terbinafine, with no improvement. Twelve years ago she underwent laser therapy for a lesion at the same location. A histopathological examination was not performed.\nPhysical examination revealed a painful subungual nodule on her right big toe. There was no regional lymphadenopathy.\nAn excisional biopsy of the nodule was performed. Histopathological examination showed an ulcerated tumor extending in a diffuse pattern from the epidermis to the inferior limit of the specimen. Rounded cells with vesicular nucleus, scant cytoplasm, numerous mitotic figures, dyskeratotic and apoptotic cells were observed ().\nThe presence of nests of large, bizarre chondrocytes embedded in a chondroid matrix was observed in around one third of the lesion, strongly suggesting positivity for Alcian Blue ().\nOn the periphery of the specimen hyperplasia and acanthosis of epidermis were observed as well as intracytoplasmic melanin pigment in small aggregates (). Nests of atypical melanocytes were observed at the dermoepidermal junction without evidence of pagetoid spread, and isolated atypical melanocytes were present in the upper dermis ().\nImmunohistochemistry showed positivity of the junctional component and of melanocytes in the upper dermis for S-100 protein and positivity of the tumor cells for HMB-45 (, and ). The cartilaginous component showed positivity for S-100 protein and for neuron specific enolase (). We diagnosed melanoma with cartilaginous differentiation. The tumor had a Breslow depth higher than 5 mm (Clark level V).\nThe patient subsequently underwent amputation of the distal phalanx of the big right toe. Histopathological examination of the lesion confirmed the biopsy findings of malignant melanoma with cartilaginous differentiation, with a Breslow thickness of 9,9 mm and a Clark level of V. Sentinel lymph node biopsy was also performed, which proved negative for tumor. According to the TNM staging this malignant melanoma was T4b N0 M0, stage II B.\nTwo years after surgery an ulcerated lesion at the same location appeared. This was excised and proved by histopathological examination to be a local recurrence. The big and second toes were amputated. This subsequent wider excision showed no residual melanoma.\nNeither local recurrence nor metastasis were observed during the following three years of followup.
|
[[47.0, 'year']]
|
F
|
{'30374898': 1, '11553315': 1, '17448201': 1, '19384075': 1, '4007220': 1, '33936664': 2, '20546349': 1, '20164055': 1, '18973120': 1, '9777392': 1, '10218678': 1, '16176296': 1, '18926730': 1, '23793189': 2}
|
{'8077358-1': 1}
|
162,842 |
3754374-1
| 23,793,191 |
noncomm/PMC003xxxxxx/PMC3754374.xml
|
Argyria - Case report
|
A 70-year-old male rural worker, with a part history of chronic sinusitis and diagnosed with colon adenocarcinoma around one month prior to our observation, was referred to us with widespread grey pigmentation of the skin and nails ( and ). The condition had been asymptomatic for its entire duration (5 years). The patient denied the use of drugs, namely fenotiazines, antimalarials, amiodarone and mynocicline.\nHowever he reported past intranasal application of 10% Silver Vitellinate as a nasal decongestant and antiseptic. He could provide no details of the posology or length of application of this drug, allegedly prescribed by his otolaryngologist. He denied any other forms of contact with silver in his job or elsewhere. We observed diffuse grey pigmentation of the skin (more evident on sun-exposed areas), and also of the oral and labial mucosae and nail plates.\nBlood tests failed to reveal any apparent alterations, namely in electrolytes, or in the metabolism of iron or copper. Histological examination of a biopsy of photoexposed truncal skin revealed an unaltered dermal and epidermal architecture, deposition of extracellular brownish-grey granules at the dermis, sparing the epidermis, arranged in clusters or individually, in a greater amounts at the basal membrane of the eccrine glands ( and ).\nBearing in mind the diagnosis of Argyria, the recent identification of a locally advanced rectum adenocarcinoma, the patient's age and overall clinical status, only measures associated with the aggravating factors were addressed i.e. to limit the amount of unprotected sun exposure. The patient declined further suggested follow up, having decided that his main priority was to care for his cancer.
|
[[70.0, 'year']]
|
M
|
{'20523812': 1, '16021155': 1, '27392933': 1, '34068024': 1, '15111684': 1, '21686727': 1, '31117201': 1, '11705252': 1, '21188244': 1, '21883362': 1, '21595676': 1, '14512929': 1, '8063942': 1, '23793191': 2}
|
{}
|
162,843 |
3754375-1
| 23,793,190 |
noncomm/PMC003xxxxxx/PMC3754375.xml
|
Shiitake dermatitis: the first case reported in Brazil
|
Male patient, 30 years old, white, born and living in Rio de Janeiro, RJ, Brazil,\ncomplained of intense pruritus followed by disseminated erythematous lesions with onset\nless than 24 hours before. He had no history of associated diseases, use of any\nmedications or any other associated factors. On the first inspection we noted small\nerythematous papules and some petechiae that assumed a linear pattern located on the\ntrunk, lower and upper limbs. There were no mucosal abnormalities, fever or any other\nsystemic symptoms ( and ). Based on the peculiar rash, the patient was\nquestioned about the ingestion of shiitake and confirmed he had eaten a\nlarge amount of raw mushrooms five hours before the cutaneous lesions appeared, leading\nus to the diagnosis of flagellate erythema due to shiitake\ningestion.
|
[[30.0, 'year']]
|
M
|
{'28082791': 1, '31543768': 2, '12534625': 1, '16536844': 1, '25831007': 1, '1395630': 1, '22714764': 1, '21798479': 1, '16700810': 1, '25207196': 1, '27483228': 1, '26506993': 2, '34408892': 2, '23793190': 2}
|
{'8366069-1': 1, '4674452-1': 1, '6738184-1': 1}
|
162,844 |
3754376-1
| 23,793,220 |
noncomm/PMC003xxxxxx/PMC3754376.xml
|
Cutaneous histoplasmosis disclosing an HIV-infection
|
An urban 57-year-old male patient reported a cutaneous lesion on his nose. The lesion\nhad been initially noticed three months before. General complaints included a 3-kg\nweight loss, sporadic fever and malaise. Dermatologic examination showed a crusted\nulcerated lesion surrounded by an erythematous halo on the nose and few erythematous\npapular nodules on his mentum ( and ). Oral examination revealed a sublingual atypical\nulcerated lesion suggesting a traumatic etiology. Clinical examination was unremarkable.\nMicroscopic examination of representative cutaneous lesions and of the oral lesion\nshowed chronic lymphohistiocytic inflammation with granuloma formation on the dermis.\nMultiple intracellular structures were observed in the cytoplasm of histiocytes and\ngiant cells, which were better observed and demonstrated on especial staining, such as\nGrocott-Gomori ( and ). Culture from biopsy material in Sabouraud dextrose-agar and\nMycosel® was positive for Histoplasma capsulatum ().\nAdditional investigation revealed interstitial infiltration and nodules on both lungs\nwhich were suggestive of pulmonary histoplasmosis. Serology tests were positive for HIV\ninfection, at that point unknown to the patient and negative for HBV and HCV. Blood\nCD4+ cell count was 7/mm3; CD8+ cell count was\n236/mm3 and HIV RNA measurement performed on plasma revealed a viral load\nof 241,265 copies and a log of 5.383.\nThe patient was treated with amphotericin B deoxycholate, 2065 mg of total dose,\nfollowed by itraconazole 200mg/daily as a maintenance treatment, with clinical\nresolution of all lesions and improvement of general conditions. Anti-retroviral therapy\nand nutritional support were added to treatment as well.
|
[[57.0, 'year']]
|
M
|
{'9504056': 1, '19112605': 1, '3039334': 1, '27438207': 1, '17223625': 1, '22147050': 1, '18672088': 1, '17806045': 1, '21738984': 1, '20597943': 1, '29568629': 2, '17397349': 1, '23793220': 2}
|
{'5842979-1': 1}
|
162,845 |
3754377-1
| 23,793,212 |
noncomm/PMC003xxxxxx/PMC3754377.xml
|
Vibrio vulnificus infection in Southern Brazil - Case report
|
A 39-year-old male patient, diagnosed with ulcerative colitis and sclerosing cholangitis\n10 years ago, was admitted to the hospital for elective liver transplantation. The\npatient was taking azathioprine 100mg/d, ursacol 1.2 g/d, prednisone 10mg/d, simvastatin\n20 mg/d, spironolactone 100mg/d, folic acid and calcium carbonate. On admission his\ngeneral condition was good, and he had a healthy skin tone, was well hydrated,\nfeverless, jaundiced +++/IV, with stable vital signs. On physical examination, he had\ntarget painless hepatomegaly, spider veins and lower limb edema. Twelve hours after\nadmission, the patient had high fever, tachycardia, myalgia in the calves and\nanuria.\nCeftriaxone was empirically started. Within hours, lesions resembling purplish\nerythematous plaques occurred on the lower limbs, with rapid growth and proximal\nprogression.\nThe patient reported a recent trip to the coastal area of the State of Paraná, one day\nbefore the admission. Samples for leptospirosis, dengue, yellow fever, spotted fever and\nmeningococcemia were collected and were found to be negative.\nThe patient became unresponsive to volume, had dyspnea and respiratory distress. He was\ntransferred to the ICU and needed vasoactive drugs and mechanical ventilation. His\nclinical condition progressively worsened associated with increased need for vasoactive\ndrugs. The skin lesions became confluent, forming blisters, and there was discharge of\nsero-sanguineous fluids (). Therapy with\nceftriaxone was changed to meropenem and oxacillin. Blood cultures revealed growth of a\ngram-negative bacillus, which was later identified as Vibrio\nvulnificus. Approximately 32 hours after the onset of infection, the patient\ndied.
|
[[39.0, 'year']]
|
M
|
{'12856219': 1, '19255188': 1, '17853628': 1, '31844623': 1, '10843244': 1, '8627070': 1, '26599487': 1, '9841854': 1, '15842598': 1, '14982266': 1, '9585771': 1, '23793212': 2}
|
{}
|
162,846 |
3754378-1
| 23,793,203 |
noncomm/PMC003xxxxxx/PMC3754378.xml
|
Cutaneous neonatal lupus with cutis marmorata\ntelangiectatica congenita-like lesions
|
A 3-month-old female infant born at term showed erythematous and scaly lesions on the\nface after photoexposure at 4 weeks of life. At 2 months, she showed marble-like,\nslightly infiltrative erythematous, purpuric lesions, which resembled CMTC lesions, on\nthe limbs ( and ). Histopathological analysis of the lesions on the limbs showed\nchronic lichenoid interface dermatitis, acantholysis, spongiosis, and vacuolization of\nthe basal layer, which was highly suggestive of cutaneous lupus (). The results of anti-Ro autoantibody analysis were\npositive for both the patient and her mother, confirming the diagnosis of neonatal\nlupus. The results of haematologic screening involving blood cell count and erythrocyte\nsedimentation rate (ESR), hepatic screening involving liver function and liver enzyme\nanalysis, and cardiological testing involving electrocardiography and echocardiography\nwere normal.\nThe treatment of lesions was only preventive, avoiding sun exposure, which caused\nregression of lesions at 7 months without scarring. The patient's mother was\nasymptomatic at the time of pregnancy, with an ESR of 116 mm/h, a fine speckled\nanti-nuclear antibody pattern, and an ANA titre of 1:640. Therefore, she was instructed\nto ensure outpatient follow-up because of the possibility of developing connective\ntissue diseases.
|
[[3.0, 'month']]
|
F
|
{'18067477': 1, '17542891': 1, '12765470': 1, '8806125': 1, '32851278': 1, '10321592': 1, '19515045': 1, '19196300': 1, '20064177': 1, '18797891': 1, '23793203': 2}
|
{}
|
162,847 |
3754379-1
| 23,793,204 |
noncomm/PMC003xxxxxx/PMC3754379.xml
|
Cutaneous malakoplakia: case report and review
|
A 51-year-old white man from Brazil, suffering from idiopathic chronic renal failure, presented with a immunosuppressive agentes. 2-year history of asymptomatic cutaneous lesion on the left groin, noticed by his nephrologist during hospitalization due to sepsis caused by catheter infection.\nThe patient was frequently catheterized at this site since an unsuccessful kidney transplantation 2 years before.\nThe lesion was a yellow-erythematous-purple plaque measuring around 1 cm in diameter, on the left groin, near a femoral vein catheter ().\nThe lesion was sampled for histopathologic and culture studies. The culture results revealed the growth of Providentia spp and Candida albicans. Histopathologic analysis revealed a chronic inflammatory process characterized by sheets of closely packed macrophages containing PAS-positive inclusions (von Hansemann cells) and calcospherites known as Michaelis-Gutmann bodies, as demonstrated by Von Kossa stain, which shows the homogeneous bodies in black ( e ). Prussian blue staining demonstrated the presence of hemosiderin inside macrophages, which may explain the purple color of the lesion ().\nThe patient was treated with surgical excision in association with sulfametoxazol-trimetoprin antibiotic therapy. No evidence of recurrence was detected on 3-year follow-up, as shown in .
|
[[51.0, 'year']]
|
M
|
{'4356990': 1, '33665278': 1, '9036125': 1, '216276': 1, '4130030': 1, '7960344': 1, '21244383': 1, '16097160': 1, '8210124': 1, '4260751': 1, '3531960': 1, '6275731': 1, '18181662': 1, '5013466': 1, '3885752': 1, '9252757': 1, '2254487': 1, '15030043': 1, '20137752': 1, '17609043': 1, '7770942': 1, '6253612': 1, '4352678': 1, '223519': 1, '30406173': 1, '25812742': 2, '8655720': 1, '18025372': 1, '8210125': 1, '10901721': 1, '6308195': 1, '7025762': 1, '2165078': 1, '9557790': 1, '27154024': 1, '6275732': 1, '884891': 1, '7009885': 1, '7513327': 1, '17403486': 1, '3336949': 1, '21899721': 1, '2657104': 1, '9688025': 1, '20398824': 1, '19626641': 1, '7915685': 1, '1556497': 1, '15462510': 1, '27524799': 1, '20123657': 1, '12853832': 1, '16572658': 1, '200843': 1, '8604965': 1, '7020170': 1, '3570595': 1, '8733761': 1, '2418936': 1, '4240085': 1, '12611142': 1, '2830572': 1, '31015237': 1, '14661439': 1, '9487224': 1, '2679816': 1, '23793204': 2}
|
{'4367118-1': 1}
|
162,848 |
3754380-1
| 23,793,197 |
noncomm/PMC003xxxxxx/PMC3754380.xml
|
Genitogluteal porokeratosis - Case report
|
Male patient, 37 years old, complained of the onset of skin lesions on the groin and buttocks for approximately two years accompanied by intense local itching. The dermatological examination showed erythematous papules and plaques with elevated and well-defined borders on the scrotum; brownish macules and papules on the groin and thighs; well-defined brownish erythematous keratotic papules and annular plaques on the buttocks and gluteal cleft (, and ). The lesions started located on the scrotum and groin, with progression to the buttocks region (gluteal cleft). Currently stable. The patient received previous treatment with systemic and topical antifungal drugs, isolated or combined topical corticosteroids, without clinical improvement. No significant personal or familiar pathological history. The previous topical therapy was discontinued, and an incisional biopsy of a papule of the left scrotum was performed. The histopathological examination showed superficial perivascular dermatitis with columns of parakeratosis, consistent with the diagnosis of porokeratosis ().
|
[[37.0, 'year']]
|
M
|
{'18358198': 1, '29750048': 1, '34675580': 2, '16882170': 1, '21929548': 1, '19891931': 1, '21899589': 1, '27579746': 1, '19590410': 1, '18193505': 1, '31507344': 1, '18702625': 1, '23793197': 2}
|
{'8504708-1': 1}
|
162,849 |
3754381-1
| 23,793,192 |
noncomm/PMC003xxxxxx/PMC3754381.xml
|
Unilateral punctate porokeratosis - Case report
|
Our case involved a 20-year-old basically healthy adult male with multiple keratotic papules, central keratin plug, 2-3 mm in diameter, located on the left palmar surface of the third finger, hypothenar eminence and fifth finger. Some papules had a central depression ( and ). These lesions, all asymptomatic, occurred when he was a teenager. No similar lesions were found elsewhere, (e.g. soles of the feet). He was unaware of ever having been exposed to arsenic, and as far as he knew none of his relatives had been affected with the same lesions.\nA punch biopsy specimen of one of the palmar papules revealed the presence of compact columns of parakeratotic hyperkeratosis - cornoid lamella - sharply demarcated by a surrounding prominent orthokeratotic hyperkeratosis (). Below the cornoid lamella, the granular layer was thinner, and dyskeratotic cells and vacuolation of some keratinocytes were present (). The underlying papillary dermis presented an inflammatory infiltrate of mononuclear cells. Given the typical clinical manifestations and histopathological findings, the diagnosis of punctate porokeratosis was established. The patient had no complaints or signs of discomfort - the reason why no treatment regime had been hitherto established.
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[[20.0, 'year']]
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M
|
{'753851': 1, '6696485': 1, '18068266': 1, '4273370': 1, '21393947': 1, '21050621': 1, '1535351': 1, '5131713': 1, '32675969': 1, '10189241': 1, '17555681': 1, '23793192': 2}
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{}
|
162,850 |
3754382-1
| 23,793,215 |
noncomm/PMC003xxxxxx/PMC3754382.xml
|
Proximal-type epithelioid sarcoma - Case report
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In 2009, a 25-year-old man was referred to the dermatology department with a 3-month history of a rapidly growing painful mass on his right buttock which subsequently ulcerated. Skin examination revealed an erythematous infiltrated plaque and an ulcerated lesion with fibrinous exudate in the gluteal region (). There were no lymphadenopathies or other abnormalities on physical examination. A skin biopsy of the ulcerated lesion revealed proliferation of pleomorphic epithelioid cells with eosinophilic cytoplasm and vesicular nuclei with prominent nucleoli. Scattered rhabdoid cells characterized by abundant glassy cytoplasm, eccentric nuclei and prominent nucleoli were observed throughout the lesion (). Immunohistochemistry showed positivity for vimentin, cytokeratin, EMA, CAM 5.2, MIB and CD34 for the latter marker positivity was focal confirming the diagnosis of proximal-type epithelioid sarcoma (). Blood count and serum biochemistry were unremarkable, and culture for mycobacteria, fungi and aerobic bacteria were negative. At the time of diagnosis, the tests to define clinical staging, which included a computed tomography scan, revealed numerous metastatic lesions in the brain and lungs (). The patient received chemotherapy at a reference oncology institute but died in the ninth month of follow-up.
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[[25.0, 'year']]
|
M
|
{'33889459': 2, '11454997': 1, '15078349': 1, '33796273': 1, '18976402': 1, '14675288': 1, '29076075': 1, '12641789': 1, '9042279': 1, '5476785': 1, '23793215': 2}
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{'8057122-1': 1}
|
162,851 |
3754383-1
| 23,793,200 |
noncomm/PMC003xxxxxx/PMC3754383.xml
|
Behçet disease in association with Budd-Chiari syndrome and multiple thrombosis - Case report
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A 25 year-old man was hospitalized in a public hospital with the following complaints: ascites, prominent venous collaterals on the abdominal wall, swelling in the legs and cutaneous lesions. Two years earlier, he had developed asymmetric recurrent migratory arthritis, aseptic meningitis, moderate and intermittent fever, recurrent lesions in the oral cavity and unilateral blindness. He denied smoking and alcoholism. Physical examination showed jaundice, acneiform eruptions on the abdomen, oral ulcers, reduced vesicular murmur at right lung base, ascites with varicose veins in the abdomen near the skin surface, an enlarged and tender liver and edema of legs (++/4) ( and ). Laboratory tests detected hypochromic and microcytic anemia; nonreactive viral hepatitis serology, HIV and syphilis infection serology; negative autoantibodies; normal rheumatoid factor and serum complement; low levels of protein C and S, and normal levels of antithrombin III; high hemosedimentation velocity and C reactive protein; serum ascites albumin gradient greater than 1.1; and a negative skin pathergy test. Histopathology of papulopustular lesion showed show perifollicular and perivascular mononuclear and neutrophilic infiltration (). Endoscopy showed oesophageal varices. Doppler ultrasound examination and computed tomography showed ascites and absence of flow in the suprahepatic and cava veins ( and ). Doppler ultrasound of lower limbs showed thrombosis. The correlation of dermatological, pathological and imaging studies confirmed the diagnosis of BD in association with BCS. Symptomatic treatment was established with diuretics, oral corticosteroids, azathioprine, colchicine and anticoagulants. After such treatment was begun the patient had significant improvement, but died five months later due to haemorrhage complications.
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[[25.0, 'year']]
|
M
|
{'18473410': 1, '12165284': 1, '7846925': 1, '25934795': 1, '10555901': 1, '18400436': 1, '29166496': 1, '20360979': 1, '6696522': 1, '1970380': 1, '21437518': 1, '21869912': 1, '23793200': 2}
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{}
|
162,852 |
3754384-1
| 23,793,194 |
noncomm/PMC003xxxxxx/PMC3754384.xml
|
Argyria mimicking a blue nevis: dermoscopy features
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A 30-year-old female patient was referred with asymptomatic induration of the right ear lobule. The posterior region of this area of skin presented a 10-mm oval-shaped macule with an intense steel-blue coloration, under which a small nodule was palpable (). The patient remembered experiencing a previous local inflammatory episode generated by a silver earring 25 years ago. Dermoscopy examination of the macule revealed an area comprising blue-grey structures uniformly distributed across a yellow background (). The lesion was composed of the following three structural types: annular structures, short linear structures observed between the former structures, and multiple dots. The distribution of the lesions was homogeneous and of a parallel aspect (Figure 2B). A white area with a radiated aspect was clearly visible in the center of the lesion (). We performed a cutaneous biopsy of the more indurated area and extracted a metallic piece belonging to a silver earring (). The histopathological study revealed the presence of brown-pigmented granules that had accumulated inside the dermic papillae and densely populated the interpapillary dermis over the elastic fibers and vessel walls surrounding the eccrine glands ().
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[[30.0, 'year']]
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F
|
{'18565180': 1, '22068765': 1, '11254422': 1, '34068024': 1, '21839327': 1, '34214264': 1, '2206978': 1, '1619110': 1, '23793194': 2}
|
{}
|
162,853 |
3754388-1
| 23,793,206 |
noncomm/PMC003xxxxxx/PMC3754388.xml
|
Case for diagnosis
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A 30 year-old Brazilian woman of skin phototype IV and pregnant for 35 weeks sought medical care for presenting hyperchromic lines on both legs for 5 weeks. Hyperchromia in the axillae and groin, which had appeared earlier in the pregnancy, were concurrent complaints. There were no associated symptoms. She had a history of gestational diabetes, which was been treated with NPH insulin since the 26th week of pregnancy and was under control. It was her second pregnancy, and she denied similar alterations in the previous one. Hormonal disorders had been previously discarded by an endocrinologist. Physical examination revealed demarcation lines from the perineum to the posteromedial portion of the thighs extending to the ankles through the popliteal fossae, bilaterally and symmetrically, in the interface between a hyperchromic lateral portion and a lighter medial portion ( and ). Hyperchromic axillae and prominent linea alba were also seen.
|
[[30.0, 'year']]
|
F
|
{'11790186': 1, '3819100': 1, '21699524': 1, '26955166': 2, '26622156': 2, '17134418': 1, '21700539': 1, '18412872': 1, '23793206': 2}
|
{'4639956-1': 1, '4763684-1': 1}
|
162,854 |
3754389-1
| 23,793,211 |
noncomm/PMC003xxxxxx/PMC3754389.xml
|
Case for diagnosis
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A 23-year-old female patient with no comorbidity reports a lesion in the cubital fossa of the superior left arm which has been present for two years. Initially, the lesion appeared as a purulent hyperchromic papule that evolved into a nodular lesion with posterior ulceration and elimination of a liquid substance ( and ).\nShe reported previous use of topical neomicin with no healing. On dermatological examination, a 1.5 x 1.0 cm ulcerated tumor with fibrous consistency, a hyperchromic halo and clean background could be observed in the left cubital fossa. No lymphadenomegaly was found.\nThe following diagnostic hypotheses were posed: leishmaniasis, squamous cell carcinoma, lymphoma, sporotrichosis and dermatofibrosarcoma. An excisional biopsy was performed. Histopathological sections revealed a dermal lesion, formed by big cells, with an abundant granular cytoplasm and a small hyperchromatic nucleus without abnormalities. Malignant signs were absent and the borders were clear of tumor ().
|
[[23.0, 'year']]
|
F
|
{'19445877': 1, '20096083': 1, '29127127': 1, '20661017': 1, '10410172': 1, '23793211': 2}
|
{}
|
162,855 |
3754390-1
| 23,793,217 |
noncomm/PMC003xxxxxx/PMC3754390.xml
|
Do you know this syndrome?
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The case described here refers to a female patient, black, 2-years-old, accompanied by her mother who reported the increase of hair in the external ear and face of her baby since birth. At 5 months, the thin, light blond lanugo hair covered the entire face, armpits, groin and lower limbs. The parent denied the presence of lanugo hair on the mucous membranes, palms and plants. The patient was born by cesarean delivery at term and had had normal psychomotor development, but with delayed dentition. The dental units available were deformed. The child's parents were second cousins. The mother denied the use of drugs or alcohol during pregnancy, as well as any family members with similar signs or symptoms. On examination, the patient had long thin and light-colored hair on the face, especially on the upper lip and mandibular regions, axillae, external genitalia, back and lower limbs ( and ). The presence of five abnormal dental units was observed. The patient, showing no other associated anomalies, was diagnosed with Congenital Hypertrichosis Lanuginosa, and referred for evaluation to the dentistry, genetics and ophthalmology clinics.
|
[[2.0, 'year']]
|
F
|
{'18789097': 1, '9256919': 1, '21690547': 1, '5424483': 1, '21079317': 1, '23793217': 2}
|
{}
|
162,856 |
3754489-1
| 23,986,632 |
noncomm/PMC003xxxxxx/PMC3754489.xml
|
Rifampicin-resistant Mycobacterium leprae in an elderly leprosy patient in the people’s Republic of China
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A 66-year-old male Chinese leprosy patient was referred to the authors’ hospital for investigation as a suspected case of drug-resistant M. leprae caused by inadequate treatment, poor compliance, and clinical relapse. The patient was diagnosed with lepromatous leprosy at the age of 46 years and treated with DDS 50 mg/day. He stopped taking pills half a year later when the skin lesions had cleared. However, the patient continued experiencing progressive and worsening numbness of the limbs for the next 18 years, during which he was out of medical record and took alternative medicine instead. In April 2009, the patient sought medical help from a private practitioner for itchy rashes on his abdomen, buttocks, and groin. He was prescribed isoniazid, RFP, and DDS, but the patient only took RFP irregularly. An initial response to treatment was observed, but new nodules and ulcers soon developed all over the patient’s body. On July 4, 2011, the patient was finally admitted and smears showing a bacillary index of 5.0 were taken. He was diagnosed with relapsed lepromatous leprosy with possible RFP resistance.\nAcid-fast bacilli were isolated from a skin biopsy specimen (). Identification of the isolate by polymerase chain reaction and gene sequencing of M. leprae-specific repetitive element and 16S rDNA genes was carried out., The sequence analysis of M. leprae-specific repetitive element and 16S rDNA genes showed 100% similarity with M. leprae. Amplification and DNA sequencing of folP1, rpoB, and gyrA genes – involved in resistance to DDS, RFP, and quinolones, respectively – were also performed (). Sequence analysis of these genes revealed a mutation within codon 441 of the rpoB gene (GAT→AAC), which indicates that it is the third reported strain harboring this mutation but a new two-base substitution (). No mutation of folP1 or gyrA gene was found in this strain. The sequences were analyzed with the BLAST® version 2.0 software (National Library of Medicine, Bethesda, MD, USA), available at .\nA regimen including 500 mg clarithromycin twice daily, 400 mg moxifloxacin once daily, 100 mg DDS once daily, and 50 mg clofazimine once daily was prescribed. The patient attended regularly for 3 months and then was lost. On his last visit, observations showed that the skin lesions of the patient had gradually subsided and that his bacillary index had dropped to 3.2.
|
[[66.0, 'year']]
|
M
|
{'33322356': 1, '7325636': 1, '63780': 1, '8460911': 1, '11709358': 1, '20509341': 1, '11731943': 1, '4625182': 1, '18982056': 1, '9921490': 1, '32322091': 1, '8996430': 1, '15603834': 1, '23986632': 2}
|
{}
|
162,857 |
3755571-1
| 23,986,860 |
noncomm/PMC003xxxxxx/PMC3755571.xml
|
Reuse of a previously transplanted kidney: does success come with a price?
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A 42-year-old African American male, whose reported cause of end-stage renal disease (ESRD) was hypertension, received a one-antigen-matched deceased donor kidney transplant in June 2005.\nA 38-year Caucasian female (donor B), who developed ESRD due to type 1 diabetes mellitus, received a living donor kidney transplant in 1997, and a pancreas transplant in 2002. Both organs failed and she subsequently received a simultaneous kidney-pancreas (SPK) transplant in April 2005. She was at intermediate risk for cytomegalovirus (CMV) infection at the time of the SPK transplant (D−/R+) and her maintenance immunosuppression consisted of tacrolimus, mycophenolate mofetil (MMF) and prednisone. Her records indicated that she was treated for CMV infection based on symptomatology (fever and diarrhea) with intravenous ganciclovir about a month after SPK transplant for an undetermined period of time followed by prophylaxis with oral valganciclovir at 450 mg/day. Her cause of death was a spontaneous intracranial bleed, and at the time of recovery of her transplanted kidney, CMV IgM was not detected in serum. A frozen section of donor B's kidney revealed normal renal parenchyma with only one obsolescent glomerulus of 100 in the sample. However, the final interpretation, communicated 2 days after the transplant, revealed focal and segmental glomerulosclerosis (FSGS), with collapsing features, diffuse C4d staining in the peritubular capillaries (D) and acute tubular necrosis suggestive of acute humoral rejection. Electron microscopy (EM) revealed diffuse podocyte foot process effacement.\nThe original donor (donor A) was an 18-year-old African American male who had died due to blunt force trauma to the head causing an intracranial bleed.\nWe proceeded with the transplant based on the frozen section findings, terminal creatinine value (1.2 mg/dL) and the total cold ischemia time (27 h and 22 min). Our patient received induction therapy with anti-rabbit thymocyte globulin (ATG) and methylprednisolone; intravenous ganciclovir was used as prophylaxis against the CMV since he had delayed graft function and was receiving ATG. Since the renal allograft had lesions of FSGS, the urine protein-to-creatinine ratio (U P/Cr) was monitored, and the initial ratio was 2.8. ATG was continued for 2 weeks and ganciclovir for 3 weeks (0.625 mg/kg three times a week for 2 weeks followed by 0.625 mg/kg/day for 1 week) after which he received oral valganciclovir 450 mg/day (adjusted to glomerular filtration rate, GFR). Serum creatinine decreased from 13.9 to 3.5 mg/dL on day 13 post transplant, at which point dialysis treatments were stopped and immunosuppression was maintained with tacrolimus, MMF and prednisone.\nOn day 24 post transplant, his white blood cell count decreased to 2400 cells/mm3, which led to the lowering of the MMF (from 2000 mg to 1000 mg/day). The leukopenia persisted for another week and his blood tested positive for CMV DNA by PCR (307 000 copies/mL) at which point MMF was discontinued and intravenous ganciclovir at 2.5 mg/kg/day was substituted for oral valganciclovir. He then became symptomatic with fever and malaise and the CMV levels in the blood rose to 1 199 000 copies/mL over a 2-week period despite adequate doses of ganciclovir. The possibility of mutant CMV strain resistant to ganciclovir was considered and intravenous foscarnet 3 g every 12 h (50 mg/kg every 12 h for estimated GFR of 58 mL/min) was started. His symptoms improved quickly and as depicted in , CMV decreased dramatically over the next 2 weeks to 3000 copies/mL. A mutation for ganciclovir resistance tested positive at the UL-97 location. On day 75 post transplant, CMV was no longer detectable in his blood. Foscarnet was continued for a total of 3 months, his tacrolimus level during this episode was 5–8 ng/mL and the U P/Cr ranged between 1.25 and 2.5. His maintenance immunosuppression was changed to tacrolimus, leflunomide and prednisone.\nA biopsy performed on day 110 post transplant revealed persistent lesions of FSGS (EM revealed only focal foot process effacement) and diffuse C4d staining in the peritubular capillaries (A and E). Since the donor-specific antibodies (DSA) tested negative, no treatment was initiated. A second allograft biopsy at 5.5 months post transplant still revealed FSGS and only focal C4d staining.\nOver the next year, CMV DNA was monitored monthly and was not detected. Another biopsy performed 13 months post transplant still revealed FSGS lesions (C), but C4d staining was negative. However, tubular atrophy increased to ∼40%. The U P/Cr was 0.6–0.8 and the serum creatinine level was 1.6–2.0 mg/dL. At last follow-up, 5 years after transplant, his serum creatinine level was 2.1 mg/dL, with a U P/Cr (obtained several months earlier) of 0.12. The clinical course of our patient is depicted in .
|
[[42.0, 'year']]
|
M
|
{'26000278': 2, '18336698': 1, '30223782': 2, '31537615': 1, '15575906': 1, '10968438': 1, '1851583': 1, '12694055': 1, '10620213': 1, '3296361': 1, '19422344': 1, '19729438': 1, '30119629': 2, '21199348': 1, '11181808': 1, '28659683': 1, '12694046': 1, '22533598': 1, '20028494': 1, '23986860': 2}
|
{'6098651-1': 1, '6142365-1': 1, '4427155-1': 1, '4427155-2': 1, '4427155-3': 1, '4427155-4': 1, '4427155-5': 1}
|
162,858 |
3755705-1
| 24,003,304 |
noncomm/PMC003xxxxxx/PMC3755705.xml
|
Small-aperture corneal inlay in presbyopic patients with prior phakic intraocular lens implantation surgery: 3-month results
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A 55-year-old woman had presbyopia correction with inlay implantation in her left eye. Her preoperative visual acuity was evaluated using a Snellen chart for distance and Log-MAR for near vision (which was converted to a Jaeger chart thereafter). Preoperative spherical equivalent (SE) was −0.25 diopter (D); uncorrected distance visual acuity (UDVA) and corrected distance visual acuity (CDVA) were 20/20 and 20/16, respectively; and uncorrected near visual acuity (UNVA) and corrected near visual acuity (CNVA) were J4 and J1, respectively. Corneal thickness was 603 μm. The patient underwent a comprehensive preoperative examination. During surgery, the corneal pocket creation was done for the KAMRA inlay implantation with a Crystal Line Femto LDV (Ziemer Ophthalmic Systems AG, Port, Switzerland). The KAMRA inlay implantation was done with a 230 μm pocket depth, not 200 μm as is usual, due to the presence of 603 μm central corneal thickness. The inlay was carefully placed in the pocket over the estimated line of sight based on the midpoint of the first Purkinje image and the pupil center with coaxial patient fixation. Three-month results showed an improvement in UNVA to J2, with even better outcomes for UDVA, which improved to 20/16 (). SE was −1.0 D. CDVA and CNVA remained stable during the follow-up period. The patient did not report needing reading glasses in any light conditions.
|
[[55.0, 'year']]
|
F
|
{'22018596': 1, '12470747': 1, '19006739': 1, '27051527': 1, '25609913': 1, '27274194': 1, '22520302': 1, '28390052': 1, '22340607': 1, '11280854': 1, '10328383': 1, '21262559': 1, '27981057': 1, '22105801': 1, '28553423': 1, '22045576': 1, '7287567': 1, '24003304': 2}
|
{'3755705-2': 2, '3755705-3': 2}
|
162,859 |
3755705-2
| 24,003,304 |
noncomm/PMC003xxxxxx/PMC3755705.xml
|
Small-aperture corneal inlay in presbyopic patients with prior phakic intraocular lens implantation surgery: 3-month results
|
A 54-year-old woman with a history of a LASIK procedure that was done soon after her prior phakic IOL implantation surgery complained about her near vision. The patient underwent a rigorous ophthalmic examination. UDVA and CDVA were both 20/16; UNVA and CNVA were J6 and J1, respectively. SE was −0.5 D and pachymetry was 487 μm. During surgery, the corneal pocket formation was done for her KAMRA inlay implantation with a Crystal Line Femto LDV (Ziemer Ophthalmic Systems AG). The KAMRA inlay was implanted using a pocket depth of 200 μm. The inlay was placed in the pocket the same way as has already been described. Three-month results showed an improvement in UNVA to J4 with minimal change in UDVA, which was 20/20. SE was −0.38 D. CDVA and CNVA remained stable during the follow-up period. Regarding patient satisfaction, the patient complained of a slight worsening of her near vision at night.
|
[[54.0, 'year']]
|
F
|
{'22018596': 1, '12470747': 1, '19006739': 1, '27051527': 1, '25609913': 1, '27274194': 1, '22520302': 1, '28390052': 1, '22340607': 1, '11280854': 1, '10328383': 1, '21262559': 1, '27981057': 1, '22105801': 1, '28553423': 1, '22045576': 1, '7287567': 1, '24003304': 2}
|
{'3755705-1': 2, '3755705-3': 2}
|
162,860 |
3755705-3
| 24,003,304 |
noncomm/PMC003xxxxxx/PMC3755705.xml
|
Small-aperture corneal inlay in presbyopic patients with prior phakic intraocular lens implantation surgery: 3-month results
|
A 51-year-old woman was a candidate for presbyopia treatment by KAMRA inlay implantation surgery. One month before inlay surgery, the patient underwent a LASIK procedure in order to correct the refractive error after her first phakic IOL implantation procedure. The patient underwent a comprehensive preoperative examination the same as the other patients. SE just before inlay implantation surgery was 0.00 D. UDVA and CDVA were both 20/16. UNVA and CNVA were J10 and J1, respectively. Corneal thickness was 494 μm. The KAMRA inlay was implanted the same way as with the case 2 patient at a depth of 200 μm. There was an improvement in UNVA at the 3-month follow up, from J10 to J5. A minimal change in UDVA was observed, but it was still 20/20 postoperatively. SE was −0.5 D. CDVA and CNVA remained stable. At the 3-month follow-up the patient mentioned needing reading glasses only occasionally.
|
[[51.0, 'year']]
|
F
|
{'22018596': 1, '12470747': 1, '19006739': 1, '27051527': 1, '25609913': 1, '27274194': 1, '22520302': 1, '28390052': 1, '22340607': 1, '11280854': 1, '10328383': 1, '21262559': 1, '27981057': 1, '22105801': 1, '28553423': 1, '22045576': 1, '7287567': 1, '24003304': 2}
|
{'3755705-1': 2, '3755705-2': 2}
|
162,861 |
3756129-1
| 24,003,371 |
noncomm/PMC003xxxxxx/PMC3756129.xml
|
Inadvertent Self-Detachment of Solitaire AB Stent during the Mechanical Thrombectomy for Recanalization of Acute Ischemic Stroke: Lessons Learned from the Removal of Stent via Surgical Embolectomy
|
A 78-year-old female presented with left hemiparesis (2/5) at four hours from onset of symptoms. She was taking oral anticoagulation medication (Warfarin 2 mg daily) due to atrial fibrillation. The baseline National Institute of Health Stroke Scale score was 18. The computed tomography (CT) brain scan was normal, magnetic resonance imaging (MRI) showed acute infarction in diffusion weighted MRI and diffusion and perfusion mismatch (). Right ICA occlusion from the petrous segment was confirmed by cerebral angiography (). In our practice, forced suction thrombectomy with the Penumbra reperfusion catheter (Penumbra, Alameda, CA, USA) is usually first undertaken to recanalize large vessel occlusion, and if failure occurs, Solitaire stent assisted thrombectomy is then performed.\nUnder local anesthesia, forced suction thrombectomy with the 041 F Penumbra Reperfusion catheter was performed. Following two attempts of forced suction thrombectomy, a 10 mm sized visible clot was retrieved, and the ICA was fully recanalized. However, a distal M1 segment occlusion remained (). We switched to Solitaire AB stent assisted thrombectomy after failure of the remained occlusion with previous technique. After confirming the location of the occlusion via distal angiography with a Prowler Selector Plus microcatheter (Cordis Neurovascular, Miami Lakes, FL, USA), a Solitaire stent 4×20 was deployed into the M1 and M2 segments through the occlusion site for the purpose of temporary opening and thrombus removal. The occluded M1 segment was opened with stent-deployment. We waited several minutes, then, the stent was carefully retrieved after partial withdrawal into the Prowler microcatheter under applying negative pressure through the guiding catheter. During the passage of the distal ICA and siphon, some resistance was encountered. So, the endovascular neurosurgeon reinforced to retrieve the stent, meanwhile, the stent was detached unexpectedly. Following angiography revealed that the detached stent was located from cavernous segment to communicating segment of the ICA, and partial radiolucent area was contained within the distal part of the stent, which suggested the thrombus was captured at the area (). Then, we tried to remove the detached stent using micro-snare and to open the occlusion with another attempt of forced suction thrombectomy, but failed to achieve recanalization with endovascular means. After declaration of endovascular failure, we first verified no significant increase in infarction size using repeated diffusion weighted image MRI. Then, we decided to perform surgical removal of the stent. The patient was operated on immediately under informed consent. The time spent on the endovascular procedure was 1 hour, and the time from the declaration of endovascular failure to the induction of general anesthesia in an operating room was 50 minutes.\nThe patient underwent an extended superciliary approach as canvassed in a previous report by the present authors. We first created a supraorbital craniotomy, and dissection of the proximal sylvian fissure revealed an intracranial ICA that was diffusely atherosclerotic and occluded with the Solitaire stent harboring the embolus (). A part of superior wall of the ICA that was not atherosclerotic and contained the distal part of the stent was chosen for arteriotomy. A 5-mm longitudinal incision was required to remove the stent and associated embolus. The neurovascular surgeon first pulled the stent carefully but failed to remove, which was probably caused by some strut of the stent engaging a part of calcified lumen, then reinforced the pulling force resulted in successful removal of the stent finally. The stent grabbed the main thrombi at distal part of the stent and both proximal and distal markers of the stent were preserved (). The arteriotomy site was repaired by a clip assisted micro-suture technique. Persistent arterial blood flow below the clip was ascertained with a microvascular Doppler. Postoperative angiography demonstrated complete recanalization of the ICA (). The patient's neurological deficits improved, and the modified Rankin scale score was 2 at three months after surgery.\nBased on the operative findings, the stent grabbed the main thrombi but was likely to fail to pass the acutely angled and circumferentially calcified ICA segment, and it finally detached inadvertently at the tortuous segment. Notably, bone window images of the baseline CT scan corresponded to the operative findings and showed severe and circumferential calcification at the supraclinoid ICA (arrow, ).
|
[[78.0, 'year']]
|
F
|
{'34357030': 1, '22569939': 1, '30693345': 1, '21088087': 1, '25628804': 1, '21087940': 1, '20538693': 1, '32424667': 1, '22932715': 1, '27051402': 1, '22500197': 1, '19934937': 1, '29719552': 1, '24003371': 2}
|
{}
|
162,862 |
3756130-1
| 24,003,372 |
noncomm/PMC003xxxxxx/PMC3756130.xml
|
Delayed Unilateral Soft Palate Palsy without Vocal Cord Involvement after Microvascular Decompression for Hemifacial Spasm
|
A 33-year-old female was presented to our out-patient clinic with a history of left hemifacial spasm for 5 years. Her past medical history was unremarkable. The patient underwent microvascular decompression in 2010 at our medical center ().\nIntra-operatively, bilateral facial electromyography and brain stem auditory evoked potential was monitored. After the dura incision, gentle retraction of the cerebellum was applied using Greenburg retractor and we have exposed the lower cranial nerves. Dissection of the arachnoid was done from the rostral border of the lower cranial nerves. The arachnoid band was very tough and difficult to dissect, but no obvious injury occurred to the lower cranial nerve during the dissection. The left anterior inferior cerebellar artery was the offending vessel compressing the facial nerve from the caudal side and decompression was successfully completed without any adverse events and with no change in the intraoperative monitoring of brainstem auditory evoked potential. Patient recovered well from anesthesia with reduced facial spasm, compared to the pre-operative state. Postoperatively, neurologic exam revealed no abnormalities and also patient's swallowing and vocalization function was intact. Immediate postoperative brain CT scan performed on postoperative day showed no sign of hemorrhage.\nOn postoperative 5th day, the patient started to exhibit hoarsness with swallowing difficulty. Barium swallowing test was done to evaluate dysphagia, and minimal nasal regurgitation was demonstrated due to unilateral soft palate palsy. On endoscopic exam, performed by an otolaryngologist, the vocal cord was intact in both sides with unilateral left soft palate palsy, which suggested tensor and/or levator veli palatini muscle weakness (). Under the impression of possible lower cranial nerve palsy caused by postoperative edema of the nerve, steroid (prednisolone) was prescribed and we decided to observe the symptoms. Symptoms persisted with slight improvement with steroid therapy but repeatedly aggravated with steroid tapering. She received speech rehabilitation therapy for persistent difficulty of phonation and swallowing.\nOn postoperative 19th day, patient complained of difficulty breathing during sleep. Polysomnography was done to evaluate sleep apnea. Mild obstructive sleep apnea syndrome was observed secondary due to soft palate palsy. We encouraged her to sleep on her side; then her symptom improved.\nDespite persistent speech rehabilitation, symptoms still persisted. We performed cranial nerve MRI to evaluate for the possibility of any structural abnormalities, such as delayed hematoma or possible infection. However, MRI showed no abnormal structural lesions or abnormal enhancement, which may suggest infection (). The patient continued to receive speech rehabilitation with subjective improvement of swallowing and speech.\nOn postoperative 25th day, the patient developed grade II facial palsy by House-Brackmann grade on the left side. Patient's facial palsy improved with administration of acyclovir for 5 days, but hoarseness with swallowing difficulty showed little improvement.\nThe patient received prolonged speech and swallowing rehabilitation therapy, and follow up examination was done before discharge showed improvement of nasalization, but persistent hypernasality. Patient was discharged with recommendation for prolonged rehabilitation.\nPatient visited our out-patient for a follow up in postoperative 2 years. Endoscopic examination revealed normalized soft palate palsy and no abnormality in the vocal cord mobility (). However, patient's subjective difficulty of speech still persisted and we decided to observe her symptoms for any changes in the future.
|
[[33.0, 'year']]
|
F
|
{'24570824': 1, '9874534': 1, '21395388': 1, '7310438': 1, '21739100': 1, '20617090': 1, '20532157': 1, '21752534': 1, '7209243': 1, '10067935': 1, '19214937': 1, '21898419': 1, '11551239': 1, '21271569': 1, '16804640': 1, '31534894': 1, '26382646': 1, '24003372': 2}
|
{}
|
162,863 |
3756132-1
| 24,003,374 |
noncomm/PMC003xxxxxx/PMC3756132.xml
|
Middle Cerebral Artery Aneurysm in a Premature Neonate
|
A 26-day-old female patient had normal delivery in prematurity at the gestation of 34th week. During delivery, any medical assistances were not required and the patient was normal on the physical examinations. Routine sonography of the brain did not show any significant findings. And then, the patient has been treated with antibiotics under the impression of sepsis for approximately 2 weeks. On the 26th day after birth, reduced spontaneous activity, bulging of the anterior fontanel and right hemiparesis were observed. Computed tomography (CT) showed a large subcortical hemorrhage with intraventricular hemorrhage and subarachnoid hemorrhage in the left cerebral hemisphere. A 1 cm sized, round enhancing lesion suspected of the cerebral aneurysm was found together (). Light reflex of both pupils was prompt with no dilatations. It was thought that subarachnoid hemorrhage of Hunt-Hess grade IV was caused by rupture of infectious aneurysm. At first, frameless stereotactic aspiration of the intracerebral hematoma and extraventricular drainage were performed. Gram stain and culture for cerebrospinal fluid and hematoma were done together. After that, the patient kept stable without further neurological deteriorations. The follow-up CT angiograms showed a large intracerebral hemorrhage due to rebleeding and a 3×7 mm sized saccular aneurysm on the middle cerebral artery bifurcation (). Analysis of cerebrospinal fluid and echocardiogram showed no significant results. The patient underwent hematoma evacuation and aneurysmal neck clipping with craniotomy. Any findings suggested of the infectious origin were not found intraoperatively although resection of aneurysm sac could not be accomplished due to adherent perforators (). The neurological deficits have been improved gradually during follow-up period. 3 months after craniotomy, ventriculoperitoneal shunt was performed for hydrocephalus ().
|
[[26.0, 'day']]
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F
|
{'11354404': 1, '19381651': 1, '16807726': 1, '3779680': 1, '28251324': 1, '19005375': 1, '22693125': 1, '15029447': 1, '15883063': 1, '1815731': 1, '2644400': 1, '24003374': 2}
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{}
|
162,864 |
3756133-1
| 24,003,375 |
noncomm/PMC003xxxxxx/PMC3756133.xml
|
Cystic Abducens Schwannoma without Abducens Paresis : Possible Role of Cisternal Structures in Clinical Manifestation
|
A 76-year-old male patient, without significant medical illnesses, presented with right facial numbness and hearing impairment for a month. The patient showed no neurological symptoms or signs except hypoestheia/hypoalgesia of the trigeminal nerve and mild hearing impairment on the right side. Magnetic resonance imaging revealed a multi-septated cystic mass on the right cerebellopontine angle (). The epidermoid cyst was excluded as a possible preoperative diagnosis based on diffusion-weighted image (). There was no enlargement of the internal auditory canal on computed tomography scans with bone window (). Pure tone audiometry and speech discrimination score showed almost normal hearing status. There were no limitations observed with the extraocculomotor movement (EOM). The preoperative diagnosis was a trigeminal schwannoma which was mainly cystic nature. Surgical resection was performed with the standard right lateral suboccipital approach. A thin-walled cystic mass displaced the lower CNs inferolaterally, the vestibulo-facial CN complex laterally, and the trigeminal nerve superiorly. After being fenestrated through its cyst wall, the mass was found to be originating from the abducens nerve. The abducens nerve seemed normal in contour and diameter, although it compressed other surrounding CNs. The tumor and its origin CN were medially located anterior to the pontine membrane and coursed within the cerebellopontine cistern (). Following a meticulous dissection, the cystic tumor was totally removed without any injury of the origin CN. Pathological examination revealed a schwannoma (). Postoperatively, the patient complained of transient diplopia without definitive EOM limitation. His symptom disappeared by 3 months after operation.
|
[[76.0, 'year']]
|
M
|
{'19418078': 1, '3173665': 1, '12009546': 1, '19357806': 1, '1082498': 1, '1440207': 1, '19200646': 1, '24003375': 2}
|
{}
|
162,865 |
3756134-1
| 24,003,376 |
noncomm/PMC003xxxxxx/PMC3756134.xml
|
Large Perforation of Hypopharynx Secondary to Anterior Cervical Approach : A Complicated Case
|
A 58-year-old male transferred to our emergency room (ER) complaining of painful swelling in the anterior cervical region. The patient underwent C3-4 discectomy and total disc replacement 3 days ago with the diagnosis of C3-4 disc herniation in local spine clinic. A physical examination identified painful edema in the surgical site of the anterior cervical region and necrotic skin tissue. Other findings included subcutaneous emphysema with crepitus in the area of the surgical site. His body temperature was 37.2℃ when he was transferred to ER. A hematological analysis demonstrated that his leukocyte count was 9670/mL, with an erythrocyte sedimentation tare of 70 mm/hr and a C-reactive protein of 19.9 mg/dL. Subcutaneous and mediastinal emphysema were identified by cervical computed tomography scans (). An esophagogram with gastrografin showed that a large amount of contrast medium had leaked into the right lateral cervical region (). Based on these findings, the patient was diagnosed with a perforation in the hypopharynx following the anterior cervical discectomy. As a result, an emergency surgery was performed to repair the perforation under general anesthesia. The operative findings included extensive soft tissue necrosis and abscess formation, both of which were removed and cultured. The perforated site was approximately 2 cm long and was found outside the pyriform sinus in the right hypopharynx (). The mucous membrane was sutured with Vicryl 3-0 in two layers from the outside. There was an attempt to reinforce the perforated part with the surrounding muscle, but severe inflammation prevented its use. Consequently, Tissel® was spread on the surgical site before the tube was inserted for drainage. On the 10th day after the operation, the drainage tube was removed. An esophagogram conducted on the 13th day after the operation showed no contrast leakage (). A liquid diet was permitted 15 days after the operation. Thereafter, the patient was transferred to the plastic surgery department of our institute to receive skin graft. A full-thickness skin graft was performed before the patient was discharged from the hospital. The patient was monitored for six months after the operation and showed no sign of complications.
|
[[58.0, 'year']]
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M
|
{'12897507': 1, '3724326': 1, '19096688': 1, '12753990': 1, '8204237': 1, '2926551': 1, '4021688': 1, '9051016': 1, '16010770': 1, '2222052': 1, '17906571': 1, '24003376': 2}
|
{}
|
162,866 |
3756135-1
| 24,003,377 |
noncomm/PMC003xxxxxx/PMC3756135.xml
|
Precedence of Parenchymal Enhancement on CT Angiography to a Fatal Duret Hemorrhage
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A 66-year-old man was admitted to the emergency department with a 3-day history of progressive headache, nausea and vomiting. He had been in a bed-ridden state with a bilateral posterior cerebral arterial infarction due to cardioembolism. He had taken aspirin (100 mg/day) and warfarin (4-5 mg/day) as well as hypertension medications. Physical examination revealed no definite neurologic deficits except for cognitive defects and bilateral medial hemianopsia. Both of his legs were slightly weak due to disuse atrophy. His vital signs were stable. Laboratory investigations revealed a coagulation abnormality with a prolongation of prothrombine time (33.3 sec), prothrombine time international normalized ratio (3.14), and activated partial thromboplastin time (37 sec). Brain CT on admission revealed left-side tentorial acute SDH and bilateral hemispheric chronic SDH, as well as a transtentorial downward herniation of the uncus with signs of increased intracranial pressure, such as sulcal obliteration and sylvian fissure obliteration (). The brain stem was unremarkable (). CTA was acquired with precontrast and arterial phase 2 hours after the initial CT for the evaluation of stroke risk. CTA revealed a prominent, wedge-shaped, enhancing lesion in the ventral pontomesencephalic area arterial phase (). During the first hospital day, his mental state rapidly decreased to stupor with pupil dilation and impaired light reflex. Subsequent brain CT revealed a small, acute hemorrhage in the tegmentum of the pontomesencephalic junction area and an increase in the amount of tentorial SDH (). After the coagulation abnormality was corrected to normal with the administration of fresh frozen plasma, the chronic SDH was operated with trephination as usual. After the operation, the patient was still in a stupor with pupil dilation and impaired light reflex. A postoperative brain CT revealed a large pontine and midbrain hemorrhage with an intraventricular hemorrhage (). He remained in a vegetative state for approximately 2 years and died due to respiratory distress.
|
[[66.0, 'year']]
|
M
|
{'19012479': 1, '13361934': 1, '5951398': 1, '5837730': 1, '18258832': 1, '15891158': 1, '24003377': 2}
|
{}
|
162,867 |
3756136-1
| 24,003,378 |
noncomm/PMC003xxxxxx/PMC3756136.xml
|
Upward Migration of a Peritoneal Catheter Following Ventriculoperitoneal Shunt
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An 8-month-old boy was admitted to our clinic with scalp swelling that developed 21 days after a VP shunt operation. He had no other neurological symptoms except scalp swelling. He was a preterm baby born at 24 weeks of gestational age and was only 520 g at birth. The patient had developed a massive intraventricular hemorrhage associated with hydrocephalus on brain ultrasonography. Furthermore, the QUAD test for preterm screening was positive for Down's syndrome. He had many severe preterm complications, including hematological problems such as anemia and thrombocytopenia that required transfusion; pulmonary problems such as respiratory distress syndrome treated with surfactant and a chest tube was inserted to manage pneumothorax. He also had retinopathy and many cardiac problems such as patent ductusarteriosus (PDA), ventricular septal defect, right ventricular hypertrophy, and a patent foramen ovale. We intended to wait for natural closure for most problems but PDA required ligation surgery. Endocrinological problems such as hyperglycemia, hypothyroidism, and osteopenia were managed with hormones and mineral replacement. Urological complications such as a dilated bladder and ureter and hydronephrosis developed but were mild; thus, we decided to follow-up closely without surgical intervention. He also had a small bowel perforation and bilateral inguinal hernia, which had gone through repair surgery.\nFor only 25 weeks after birth, he had 3 surgeries, brain ultrasonography was conducted and progression of the hydrocephalus and encephalomalacic changes in the right frontal lobe was found (). Spinal tapping for intracranial pressure control was held every day until shunt surgery was capable. At 30 weeks of his gestational age (14 weeks of corrected age) his body weight was 4500 g (<10 percentile) a VP shunt has been inserted using an ultra small, low pressure valve system (Strata®; PS Medical, Gola, CA, USA) and a distal catheter of about 30 cm in length was placed in the peritoneal cavity. No complications occurred except mild redness of the left clavicle area where the catheter passed. The patient was discharged without any complications 12 days after surgery.\nHe visited our outpatient office with prominent swelling of the surgical site 21 days after surgery, and a round coil like mass was palpable under the scalp, but no neurological changes were noticed. Simple chest, abdomen, and skull X-ray images were taken, and no shunt catheter on the trunk was found, but the distal catheter had migrated upward into the subgaleal space (). Brain computed tomography scans indicated decreased ventricle size compared to those taken before surgery (). Shunted cerebrospinal fluid (CSF) was thought to be absorbed in the subgaleal space and shunt function seemed to be maintained.\nThe distal catheter inserted previously for the VP shunt was found coiled freely in the subgaleal space under the primary incision during revision surgery. The shunt was otherwise functioning, but the reservoir was filled with an old hematoma, and the CSF was bloody and turbid (). We placed an extraventricular drainage (EVD) tube rather than a shunt system to wait for the CSF to clear out to prevent shunt system blockage. The VP shunt was reinserted 1 week after the EVD, and the patient was discharged. No further problems were noted during regular follow-ups at the outpatient office.
|
[[8.0, 'month']]
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M
|
{'7444744': 1, '22424557': 2, '19350205': 1, '12235495': 1, '28491419': 1, '21842723': 1, '14368347': 1, '3042135': 1, '19096671': 1, '16935511': 1, '17999030': 1, '16815025': 1, '975690': 1, '8748857': 1, '11007499': 1, '22222434': 1, '7842429': 1, '22392753': 1, '25553524': 1, '28194301': 2, '34667670': 1, '24003378': 2}
|
{'5299149-1': 1, '3338073-1': 1}
|
162,868 |
3756160-1
| 24,003,410 |
noncomm/PMC003xxxxxx/PMC3756160.xml
|
Recurrent Prosthetic Mitral Valve Dehiscence due to Infective Endocarditis: Discussion of Possible Causes
|
A 30-year-old male patient had undergone mitral valve replacement with a No. 27 St. Jude metallic valve six years previously. He also underwent mitral valve replacement with a bioprosthetic valve one year previously due to dehiscence of the metallic valve and cardiogenic shock caused by PVE (, ). Six weeks after this second operation, the patient again was evaluated for cardiogenic shock and prosthetic valve dehiscence was noted. He underwent a third operation, and the mitral valve was replaced with a No. 27 St. Jude metallic valve. Vancomycin (2 g/day), rifampicin (600 mg/day), and gentamicin (80 mg/day) were started immediately. After the third operation, the patient received six weeks of antibiotic therapy and was discharged without sequelae. Several blood cultures were drawn, and all were negative for a causative agent. He was scheduled for outpatient follow-up monthly to adjust the warfarin dose. Fourteen months after the last operation, he was admitted to our clinic with fever for nearly two weeks. Transthoracic echocardiography showed a mobile mass on the mitral valve prosthesis. Transesophageal echocardiography (TEE) was performed, and a partially mobile mass on the prosthetic valve was revealed. The mass was on the atrial side of the medial valve within the suture line and sized 8×5 mm (). Laboratory evaluation showed an increased white blood count (13,500 mm/L), erythrocyte sedimentation rate (80 mm/hr) and C-reactive protein (161 mg/L). The international normalized ratio (INR) was 2.4. The patient was then hospitalized for PVE, and three sets of blood cultures were drawn. Vancomycin (2 g/day) and rifampicin (600 mg/day) were started immediately. Blood cultures were negative for a causative agent. On follow-up, clinical and laboratory values were improved. After six weeks of treatment, the mass was shown to regress on TEE (). By adjusting the dose of warfarin, a steady INR level between 3 and 3.5 was achieved and the patient was discharged. There was no relapse during the first six months of close follow-up.
|
[[30.0, 'year']]
|
M
|
{'15956145': 1, '32603469': 1, '11250980': 1, '11136490': 1, '22347645': 1, '15958370': 1, '20713537': 1, '16007540': 1, '24003410': 2}
|
{}
|
162,869 |
3756161-1
| 24,003,411 |
noncomm/PMC003xxxxxx/PMC3756161.xml
|
Cardiac Resynchronization Therapy Using a Dual Chamber Pacemaker in Patients with Severe Left Ventricular Dysfunction and a Left Bundle Branch Block
|
A 51-year-old female with mild dyspnea of New York Heart Association (NYHA) functional class II heart failure and dysarthria due to a transient ischemic attack was diagnosed with dilated cardiomyopathy (ejection fraction 23%) through echocardiography and three-vessel disease through coronary angiography (proximal left anterior descending artery 60% stenosis, middle left anterior descending artery 60% to 70% stenosis, and distal left circumflex artery complete occlusion). The patient was transferred to our hospital for coronary artery bypass graft (CABG) surgery.\nShe had a diagnosis of hypertension and a history of an intraventricular block eight years earlier that was treated with digoxin, diuretics, beta-blockers, and an angiotensin-receptor blocker. Cardiomegaly was found on a posteroanterior chest radiograph, and a left bundle branch block (LBBB) pattern and prolonged QRS interval were identified on an electrocardiogram (ECG). Echocardiography also demonstrated left ventricle (LV) distension, severe LV dysfunction with a left ventricular ejection fraction (LVEF) of 28%, and mild mitral regurgitation. Pro-B-type natriuretic peptide was 2,070 pg/mL, and cardiac markers were normal. On-pump CABG was performed on day two of hospitalization. The left anterior descending coronary artery and diagonal branch were connected to the left internal mammary artery in situ, and a saphenous vein graft was used to connect the posterior descending artery and posterolateral artery. The patient had LV incompetence. Cardiac resynchronization therapy was attempted. Two temporary, unipolar, atrial pacing wires were inserted in the right atrium wall, and two temporary, bipolar, ventricular pacing wires were inserted into the right ventricular anterior wall and the left ventricular inferior wall. Temporary pacemakers (Medtronic 5388 Dual Chamber Temporary Pacemaker; Medtronic Inc., Minneapolis, MN, USA) were used since cardiac resynchronization therapy equipment was unavailable (). The rate was set to 66 ppm, and the sensitivities were set to 0.4 mV for the atria and 2.0 mV for the ventricles. The output was set to 10 mA for the atria and 20 mA for the ventricles. Wires inserted in the right atrium and left ventricular inferior wall were used, and a 196-millisecond PR interval verified from a preoperative ECG was used as a standard. QRS intervals were observed via ECG, and the PR interval was manipulated. The narrowest QRS was found using the PR interval standard, and the setting was changed (). Before cardiac resynchronization therapy (CRT) was initiated, intraoperative transesophageal echocardiography showed that the LVEF measured below 25%. On initiation of CRT, the LVEF increased visibly to about 40%. The cardiac output was measured immediately, and one hour and twelve hours after arrival in the intensive care unit. The cardiac output changed from 2.8, 2.4, and 3.6 L/min without pacing to 3.5, 3.4, and 3.5 L/min on initiation of pacing ().\nThe patient's postoperative vital status was stable on intravenous dopamine and nitroglycerin. CRT was used for 18 hours. A cardiac output of 3.8 L/min was maintained after turning the CRT off, and the cardiac output was 3.9 L/min when the patient was transferred to the general ward.
|
[[51.0, 'year']]
|
F
|
{'2924415': 1, '11259720': 1, '11084115': 1, '20447832': 1, '12379588': 1, '15753115': 1, '24003411': 2}
|
{}
|
162,870 |
3756162-1
| 24,003,412 |
noncomm/PMC003xxxxxx/PMC3756162.xml
|
Gastropleural Fistula: A Rare Complication of Ewing Sarcoma
|
A 30-year-old man was admitted to our clinic with complaints of abdominal pain and fever. He had a history of Ewing's sarcoma diagnosed 18 months earlier on his chest wall and he had undergone pneumectomy with negative excision margins, followed by chemotherapy. On physical examination, the patient had decreased breath sounds on his left hemithorax and tympanic percussion. His saturation was 91% despite oxygen treatment given at a 10-1/min rate through an oxygen mask. After oral administration of methylene blue, leakage of the substance from the thoracic tube was detected. A contrast-enhanced computed tomography and barium study showed a gastropleural fistula between the stomach and the thorax. Gastroscopy confirmed the diagnosis of a fistula, with a massive amount of pus coming from the thorax. Treatment with ampicillin/sulbactam and fasting relieved his abdominal pain and fever. After oral feeding was started, his symptoms worsened; therefore, the patient was administered parenteral nutrition. Since the conservative treatment failed, the patient underwent laparoscopic surgery. The gastropleural fistula was in the greater curvature of the stomach in the fundic area. Wedge resection of the fistula was performed by three trocars and a 60 GIA stapler (Ethicon Endo-Surgery, Cincinnati, OH, USA), and the diaphragm was repaired with a prolene graft. The thoracic tube was extracted on the second postoperative day, and the patient was discharged on the fifth postoperative day. Pathologic evaluation of the specimen demonstrated the recurrence of Ewing's sarcoma, which may have played a role in the formation of the gastropleural fistula.
|
[[30.0, 'year']]
|
M
|
{'4037204': 1, '14421290': 1, '21245693': 1, '1984967': 1, '19727349': 2, '31058019': 2, '17670447': 1, '24876505': 1, '28458144': 1, '33274086': 2, '31296637': 1, '28299235': 2, '31267717': 1, '8303639': 1, '21916185': 1, '24003412': 2}
|
{'7683165-1': 1, '5341304-1': 1, '2732079-1': 1, '6485830-1': 1}
|
162,871 |
3756163-1
| 24,003,413 |
noncomm/PMC003xxxxxx/PMC3756163.xml
|
Intrapulmonary Solitary Fibrous Tumor Masquerade Sigmoid Adenocarcinoma Metastasis
|
A 51-year-old Caucasian female was referred to our institution because of an abnormal nodule detected in her right lung. This had at first been detected four months earlier when she underwent an urgent Hartmann procedure due to refractory adenocarcinoma of the sigmoid colon (pT4N1 stage). Due to the urgency of the surgery, the patient was not staged prior to the surgery but was initially staged after the operation. The only pathologic finding in the computed tomography (CT) of the lung was a nodule in the lower right lobe of 2.5 cm at its longest dimension (), and the patient was staged as cT4N1M1. She received 4 cycles of chemotherapy for the sigmoid adenocarcinoma before she was referred to us for excision of what was believed to be a single metastatic nodule. Although the radiologic findings supported a benign tumor, neither positron emission tomography-CT nor any other procedure to attempt to diagnose the nodule was performed due to the patient's willingness to undergo complete removal of the mass even if it were benign. The patient underwent video-assisted thoracoscopic (VATS) wedge excision of the tumor. She had an uneventful postoperative course and was discharged on the 4th postoperative day.\nThe specimen of the resected lung contained a firm intrapulmonary white-colored well-defined mass with dimensions of 2.5×2.3×2.2 cm. Microscopically, the tumor had a "patternless pattern," with proliferation of bland spindle cells in alternating hypocellular and hypercellular areas, accompanied by a collagenous stroma () with branching hemangiopericytoma-like vessels (). The tumor had no evidence of increased mitotic activity (0 to 1 mitoses per 10 high power fields using an Olympus BH-2 microscope, with a 40× field, 0.5 mm diameter, and area of 0.196 mm2), any significant atypia, or necrosis. Immunohistocemically, the tumor cells were positive for vimentin, CD34 (), and Bcl-2. A few cells were also focally and weakly positive for estrogen and progesterone receptors. The index of cellular proliferation with the antibody Ki-67 is low and estimated at <1% of the cellular population. Immunohistochemistry staining of the tumor cells was negative for alfa-smooth muscle actin (SMA), muscle specific actin (HHF-35), h-caldesmon, CD117 (c-kit), S-100 protein, epithelial antigens (wide spectrum cytokeratins [AE1/AE3] and epithelial membrane antigen), and thyroid transcription factor-1. The resection margins were free of disease. One year after the operation, the patient is well, with no evidence of recurrent disease.
|
[[51.0, 'year']]
|
F
|
{'17351947': 1, '20667378': 1, '18805198': 1, '18470694': 1, '19308764': 1, '20105613': 1, '21225405': 1, '17468826': 1, '24003413': 2}
|
{}
|
162,872 |
3756165-1
| 24,003,415 |
noncomm/PMC003xxxxxx/PMC3756165.xml
|
Intra-thoracic Parathyroid Adenomatosis: A Case Report
|
A 37-year-old female who had undergone a total parathyroidectomy 4 months previously for a parathyroid adenoma presented in our clinic with high serum calcium (10.3 mg/dL) and high intact parathyroid hormone levels (iPTH; 1,378 pg/mL). A technetium-99m sestamibi scan was performed to determine whether there was any remnant parathyroid tissue or whether there was a satellite adenoma. A focal nodule with increased uptake of technetium was detected in the left lower paratracheal area and suspected to be an ectopic parathyroid adenoma (). The mass was located on the left side of the pulmonary trunk, and we decided to perform a surgical biopsy. Preoperatively, we performed a chest computed tomography (CT) scan to localize the mass more accurately without enhancement because of her impaired renal function. She had been diagnosed with chronic rejection following transplantation of both kidneys, and was on hemodialysis. The mass was located between the aortic arch and the pulmonary trunk, apparently adhering to the inferior side of the aortic arch in the CT scan ().\nBecause the nodule was located deep inside the lower paratracheal area and was thought to adhere to the aortic arch, and a recurrent laryngeal nerve was nearby, excision through a posterolateral thoracotomy was planned. After opening the left 5th intercostal space with one lung ventilation, the mediastinal pleura was opened in the aorto-pulmonary window. A firm and brownish mass about 2 cm in diameter was seen to be in contact with the lesser curvature of the aortic arch. During the operation, the recurrent laryngeal nerve was saved by snaring. The mass was carefully dissected free from the aorta, and it was sent for pathological examination. A frozen biopsy revealed a parathyromatosis. A 24 Fr chest tube was inserted and the wound was closed layer by layer. She was then transferred to a general ward with tolerable vital signs.\nThe immediately postoperative serum iPTH level was 32.9 pg/mL, and it had decreased to 5.1 pg/mL by the time of discharge. The postoperative course was uneventful and the patient was discharged on postoperative day 6 without any problems. The last follow-up took place 4 months after the excision, and the patient had been doing well, without any complications.
|
[[37.0, 'year']]
|
F
|
{'3812520': 1, '19193908': 1, '98860': 1, '10654517': 1, '20494022': 1, '15862504': 1, '16490559': 1, '21871292': 1, '24003415': 2}
|
{}
|
162,873 |
3756166-1
| 24,003,416 |
noncomm/PMC003xxxxxx/PMC3756166.xml
|
Naturally Occurring Mediastinal Teratoma with Malignant Transformation in an Adult Male
|
A 47-year-old male presented with a mass in the anterior mediastinum. The mass was incidentally detected on a chest X-ray during the evaluation of a minor trauma that he had sustained two months prior to his presentation to Asan Medical Center (). As such, he was referred to our hospital for further evaluation. On his admission, a chest computed tomography (CT) scan was taken, which revealed an 8.9 cm×7.1 cm×8.0 cm heterogeneous mass in the anterior mediastinum. The mass was located anterior to the ascending aorta and the main pulmonary artery in the left hemithorax (). The mass was well demarcated without the overt signs of invasion to the adjacent structures. Also, there was neither pleural effusion nor lymph node enlargement. The differential diagnosis for this tumor based on the radiologic findings indicated a thymoma, a germ cell tumor, or a mediastinal sarcoma. Due to the proximity to the aorta and pulmonary artery, a pre-operative tissue biopsy was not considered. Instead, it was decided that the patient undergo an excision. The procedure was performed via median sternotomy. Intraoperatively, a well-encapsulated mass was identified and noted to arise from the thymus. There was neither adhesion nor invasion to the adjacent structures such as the aorta, pulmonary arteries, or lung parenchyma. The tumor was excised completely with negative margins for a residual tumor. The intraoperative frozen biopsy revealed a rhabdomyosarcoma. The postoperative course did not show any particular issue; the patient was discharged on postoperative day four. The final pathology report identified a mature teratoma with embryonal rhabdomyosarcoma (). Postoperatively, the patient underwent five cycles of chemotherapy and subsequent radiotherapy. However, six months after the primary surgery, the patient was found to have a nodule, which was highly suspected to be a tumor recurrence, in the upper lobe of the left lung. On the serial follow-up CT scans, we learned that the nodule had grown in size up to 17 mm in the 8 months after primary surgery. After discussions with the medical oncology team, we decided to treat him with another cycle of chemotherapy, which shrunk the size of the nodule down to 15 mm (). Eleven months after the primary surgery, the patient underwent wedge resection of the nodule, which turned out to be a metastatic rhabdomyosarcoma from the primary mediastinal mass. As of the writing of this paper, the patient has finished the seventh cycle of chemotherapy and has not shown another tumor recurrence.
|
[[47.0, 'year']]
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M
|
{'9474169': 1, '24448436': 1, '18573447': 1, '11752948': 2, '11886012': 1, '18603085': 1, '8160647': 1, '21881357': 1, '24003416': 2}
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{'2718186-1': 1}
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162,874 |
3756167-1
| 24,003,417 |
noncomm/PMC003xxxxxx/PMC3756167.xml
|
Fixation of Traumatic Sternal Fractures Using SternaLock Plating System
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A 43-year-old man, impacted in his chest by a car accident, complained of severe chest pain in his anterior chest wall with palpable sternal instability. Computed tomography (CT) of the chest showed a displaced compound mid-body sternal fracture (). Troubled with fracture of several cervical bones accompanied by sternal fracture, he was scheduled for open sternal fixation 3 days after the trauma because of combined operation with spine surgery. Open reduction and internal fixation of the sternum was performed using the SternaLock system (Biomet Microfixation Inc., Jacksonville, FL, USA).\nAfter a midline longitudinal incision over the sternum, the fracture site was carefully debrided of any fibrous union and old hematoma to expose healthy bone. Before plate fixation, manual reduction of the sternal fracture was assisted by the use of bone reduction forceps placed within the surrounding intercostal spaces. Three 4-holed straight plates were used vertically and horizontally due to compound sternal fracture (), manually contoured to the underlying sternum, and secured using self-drilling, self-tapping screws. The screw length was 10 mm, which was chosen by the thickness of the sternum (as measured on chest CT) at each point of screw placement. The wound was irrigated and closed. The patient was not discharged because he was receiving rehabilitation treatment for his leg, which had been paralyzed due to the cervical spine trauma. The 3-month follow-up demonstrated normal wound healing with no complaints of symptoms associated with instability. The repair was palpably stable and non-tender.
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[[43.0, 'year']]
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M
|
{'8694615': 1, '21256325': 1, '10209593': 1, '9774924': 1, '15613884': 1, '24003417': 2}
|
{}
|
162,875 |
3756168-1
| 24,003,418 |
noncomm/PMC003xxxxxx/PMC3756168.xml
|
Porcine Dermal Collagen (Permacol) for Sternal Reconstruction
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A 63-year-old male visited the hospital for chest pain. A simple chest radiologic examination suggested an anterior mediastinum tumor. Other than the chest pain, the patient did not show myasthenia gravis or any other notable symptoms on physical examination. A chest computed tomography (CT) showed a 6.8 cm tumor at the anterior mediastinum (). The tumor seemed to cover the left innominate vein and invade the thoracic wall. This tumor had invaded the sternum, left side of the parasternal area, ribs, and intercostal muscles. Based on the positron emission tomography--CT results, hypermetabolic uptake lesions were noted at the main mass and lymph nodes of the 3rd and 4th left costal bones and paratracheal area. Accordingly, preoperative percutaneous needle biopsy was executed for the main mass, and the result came out as thymic carcinoma with the possibility of squamous cell carcinoma.\nFive cycles of neoadjuvant chemotherapy (paclitaxel+cisplatin) were followed. After chemotherapy for three months, the tumor size seemed to have increased, but did not show any other metastasis according to the other test results. Considering the patient and disease status, surgical treatment was planned.\nAfter general anesthesia, a single-lumen endotracheal tube was inserted and the operation proceeded in the supine position. After a median skin incision, the mass invading the chest wall was observed. Thus, undermining of both subcutaneous layers and muscle layers was performed in order to determine the invasion range. In addition, extensive resection procuring the tumor margin was performed at the sternal body and 2nd through 5th intercostal rib cartilages using an oscillating saw and rib cutter (). The tumor not only had invaded the sternum and both chest walls, but had also invaded the left jugular vein and the brachiocephalic vein, which were shrunken due to the tumor and had adhered to the left upper lobe. Hence, after saving and detachment of the left phrenic nerve, division at the superior vena cava-innominate vein junction and left jugular vein proximal area was performed by vascular endo-GIA. Despite the obstruction of the innominate vein and left jugular vein, symptoms such as left arm and facial swelling did not appear preoperatively. Therefore, only vascular resection without reconstruction was done, and no such symptoms were noted postoperatively. Tumor invasion to both lungs was also found. Therefore, both pleurae were opened, and wedge resections of the right and left upper lobes were performed using GIA staplers. Since the tumor was also abutting the aortic arch, the parietal pericardium was opened and the tumor was cautiously detached and removed from the aortic wall ().\nThe sternum and chest wall defect was wide and chest wall reconstruction using a Permacol patch (20×15 cm) was planned. The margin of the defect was calculated as stated in , and was tailored based on the shape of the defect. Using steel wire for the upper margin, suture of the manubrium and a tailored patch were performed. The tailored patch was anchored at the lateral margins of the bilateral ribs and the lower margin with multiple intermittent sutures using 1/0 polypropylene. Finally, the chest wall reconstruction was completed ().\nPostoperative pathological examination confirmed that the tumor was thymic carcinoma (large-cell neuroendocrine carcinoma). Despite a normal appearance on intraoperative gross examination, the resection margins of the superior, medial, and lateral areas showed tumor involvement. In addition, metastasis to one lymph node (LN11) was confirmed.\nThe patient was transferred to the intensive care unit after the surgery, was extubated after 20 hours, and was transferred to the general ward on day 2 postoperatively. The mediastinal chest tube was removed on postoperative day 5, the pericardial Hemovac drain was removed on day 10 postoperatively, and the patient was discharged on postoperative day 19 without showing any other complications.\nConsidering R1 resection at the surgical margins, postoperative chemoradiation (chemotherapy, low-dose cisplatin: 7 cycles, radiotherapy, total 6,300 cGy/34F) was applied beginning from day 29 after surgery. Based on chest CT results taken 6 months after surgery, no signs of tumor relapse were observed and the patient did not show any abnormal signs or symptoms ().
|
[[63.0, 'year']]
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M
|
{'15111216': 1, '33234766': 2, '17674112': 1, '31384233': 1, '12963221': 1, '19820953': 1, '12078759': 1, '24003418': 2}
|
{'8548202-1': 1}
|
162,876 |
3756182-1
| 24,003,392 |
noncomm/PMC003xxxxxx/PMC3756182.xml
|
A Case of Fixed Drug Eruption Due to Doxycycline and Erythromycin Present in Food
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A 57-year-old female patient visited our clinic with a 12-year history of repeated outbreaks of well-demarcated erythematous patches with hyperpigmentation over the entire body. She had no history of allergic disease or chronic medical illness. She denied taking any medication before the lesion first developed or before the recurrences. The lesions developed every 2 or 3 months, at the same sites, when she ate pork or fish. She had therefore followed a nearly vegetarian diet for more than 10 years.\nPatch tests were performed using acetaminophen, the nonsteroidal anti-inflammatory drug ibuprofen, and antibiotics, including cephalosporins, amoxicillin, sultamicillin, trimethoprim-sulfamethoxazole, gentamicin, neomycin, rifampin, doxycycline, and erythromycin. There were no definite reactions to these patch tests. Oral provocation tests with the same medications were then performed. When the patient ingested 10 mg of doxycycline as a single dose, she experienced an erythematous change on an existing pigmented lesion, accompanied by an itching sensation (). One month after recovery from this lesion, the oral provocation testing was continued with the remaining drugs. After an erythromycin dose of 25 mg, she again experienced more intense pruritus and erythema at the site of a previous lesion ().\nInterestingly, the patient had no history of taking medication, including doxycycline or erythromycin. According to the Korea Food and Drug Administration, doxycycline and erythromycin are commonly used in livestock farming and sea farming in Korea. We did not know whether antibiotics in food cooked at high temperatures could induce an FDE, so we conducted a simple experiment to assess the heat stability of doxycycline and erythromycin. Using the disk-diffusion method, we found that doxycycline and erythromycin are stable at 100℃ and even at autoclave temperatures reaching 121℃ ().
|
[[57.0, 'year']]
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F
|
{'15280825': 1, '8718742': 1, '19474709': 1, '9039180': 1, '18373348': 1, '20171434': 1, '34007755': 2, '19456785': 1, '17101493': 1, '22950038': 2, '8864622': 1, '32414023': 1, '1894215': 1, '11702319': 1, '18566551': 1, '10435334': 1, '24003392': 2}
|
{'3423606-1': 1, '8121196-1': 1}
|
162,877 |
3756201-1
| 24,003,279 |
noncomm/PMC003xxxxxx/PMC3756201.xml
|
A Case of Eccrine Porocarcinoma: Usefulness of Immunostain for S-100 Protein in the Diagnoses of Recurrent and Metastatic Dedifferentiated Lesions
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A 78-year-old Japanese woman visited our hospital, complaining about the left inguinal skin tumor, increasing in size (). Since biopsy revealed the lesion is malignant, the dermal tumor was excised, and local lymphadenectomy was also performed. Neoplastic cells proliferated in lobular downwards growth, and connected to the epidermis (). The neoplastic cells have atypical oval nucleus, and mitotic figures were found. A small number of lumens were observed in the nests. Melanin granules were not found. Immunostain for carcinoembryonic antigen (CEA) and epithelial membrane antigen (EMA) is positive at the rims of the lumens (). Majority of the lesion was immunoreactive for AE1/AE3. On immunohistochemistry for S-100 protein, scattered stained dendritic cells were found (). On that for HMB-45 and Melan-A, scattered positive cells were found partially. Some tumor cells appeared to be periodic acid schiff (PAS) stain positive, and PAS-positive substance was digested by diastase. There was no nodal metastasis. According to these facts, the diagnosis of EPC was confirmed. After fourteen months, a tumor occurred in the same location. Epithelioid cells diffusely proliferated in the subcutaneous tissues (). The histology looked like epithelioid melanoma. Immunostain for CEA and EMA was negative, but immunoreactivity for AE1/AE3 was diffusely observed. Scattered S-100 protein positive cells were found (). But, immunoreactivity for Melan-A and HMB-45 disappeared. The cells contain no PAS-positive glycogen. Since the tumor location is same with that of the primary lesion, and the stainings for S-100 protein and AE1/AE3 between the two are similar, the lesion was diagnosed as recurrent EPC with dedifferentiation. Three months later, metastasis to the lungs was found. Biopsied specimens showed similar histologic findings of the secondary inguinal lesion, and the diagnosis of dedifferentiated metastatic EPC was made. Immunoreactivity for AE1/AE3 was diffusely observed, and scattered immunoreactive cells for S-100 protein were also maintained. Nevertheless, immunostains for EMA, HMB-45, and Melan-A were all negative. Two months later, the patient died for aggravation of general condition.
|
[[78.0, 'year']]
|
F
|
{'27085107': 1, '7541147': 1, '17683381': 1, '28721214': 1, '9580812': 1, '9001989': 1, '9463588': 1, '7557914': 1, '20679885': 1, '11395548': 1, '11757866': 1, '24003279': 2}
|
{}
|
162,878 |
3756202-1
| 24,003,280 |
noncomm/PMC003xxxxxx/PMC3756202.xml
|
Touraine-Soulente-Golé Syndrome: A Rare Case Report and Review of the Literature
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A 27-year-old male came with complaints of repetitive wrinkling and thickening of skin on face and scalp along with broadening of hands since 8 years ago. He also complained of increased oiliness on the face. This healthy Indian male with normal physique and intelligence level was the 1st son of non-consanguineous parents, his elder brother was 31. He has a 3 years old son and a 5 years old daughter. Family history was unremarkable. History of joint pains, oral and genital ulceration, hoarseness of voice, epistaxis and sensory loss was denied. No similar history was found in the family. Physical examinations revealed scalp skin was folded, giving appearance of peculiarity cutis verticis gyrata (), whereas the hair growth appeared normal. Eyebrows appeared dense. Skin over face was thickened, non-pinchable, greasy to touch and folded, giving appearance of leonine faces (). Follicular openings were prominent and so were the video-dermoscopy. In addition, clubbing of fingers and toes was presented along with broadening of hands and fingers (). Cutaneous examination over the rest of his body including mucosae was normal. Laboratory investigations included growth hormone assay, thyroid profile, and Venereal Diseases Research Laboratory Assay and were found to be within normal limits. Erythrocyte sedimentation rate was elevated (45 mm in 1st hour). Serum calcium, alkaline phosphatase and other biochemical tests were also within normal limits. Smears for lepra bacilli were negative. Radiological investigations included radio-graphs' of skull, which were normal including sella turcica. Long bones of legs showed minimal periosteal reaction along the shaft () and his feet showed evidence of cortical erosions and tufting ends of terminal phalanges. Histopathological examination from skin behind ear lobule showed a hyperplastic epidermis and dermis (). On the basis of history, clinical features, radiological and lab findings, the diagnosis of TSG syndrome was formulated.
|
[[27.0, 'year']]
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M
|
{'7756124': 1, '16416623': 1, '1623671': 1, '28116207': 2, '33505684': 2, '7962775': 1, '1575598': 1, '7396613': 1, '16059578': 1, '17497611': 1, '16283874': 1, '14740519': 1, '10728444': 1, '18273728': 1, '11343811': 1, '18500342': 1, '28112140': 2, '24003280': 2}
|
{'5322714-1': 1, '5237730-1': 1, '7813118-1': 1}
|
162,879 |
3756203-1
| 24,003,281 |
noncomm/PMC003xxxxxx/PMC3756203.xml
|
Metallic Discoloration on the Right Shin Caused by Titanium Alloy Prostheses in a Patient with Right Total Knee Replacement
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A 75-year-old woman had a large blue patch on the right shin for 3 years. She underwent a left total knee replacement 18 years ago and a right total knee replacement 14 years ago due to severe osteoarthritis of both knees. Each of the operations was carried out successfully without any serious adverse events. Eleven years after the right total knee replacement, she noticed a discoloration of her right shin, and the lesion continued to enlarge slowly over time. She was referred to a dermatology clinic where a large, well-demarcated bluish-gray patch was noted on her right shin. The surface of the skin was smooth with no palpable infiltration. For 1 year, she experienced pain when walking on the right shin. She had a 10×15 cm well-demarcated bluish-gray patch on the extensor surface of her right shin (). Routine laboratory tests, including complete blood count, liver function tests and urine analysis, yielded normal findings. Histopathologic findings from the skin lesion showed perivascular, fine black particles in the dermis (). The black particles were stained positive with both melanin and demelanin stains. Polarizing microscopy of the skin specimen revealed refractile foreign materials in the perivascular area of the dermis (). Further, energy-dispersive X-ray spectrophotometry revealed the presence of titanium and aluminium (). Metallic discoloration was diagnosed on the basis of clinical, histopathological, polarizing microscopy and energy dispersive X-ray spectrophotometer findings. The radiographs revealed loosened and dislocated tibial components of the right knee prostheses. Preoperative and intraoperative cultures were negative for bacteria. During surgical revision, marked loosening of the tibial component and wearing of polyethylene were found. Additionally, an intense black staining of a substantial amount of wear debris adjacent to the tibial components and tibial bone defect was observed (). The patient was treated by debridement, and the right tibial component was replaced. After the revision procedure, metallic discoloration disappeared and has not reoccurred over the past 4 years.
|
[[75.0, 'year']]
|
F
|
{'12641795': 1, '8495576': 1, '30560172': 1, '10544883': 1, '32854483': 1, '2071635': 1, '1991768': 1, '14511005': 1, '16475494': 1, '27075137': 1, '17515554': 1, '2032695': 1, '3279037': 1, '17854377': 1, '18098055': 1, '24003281': 2}
|
{}
|
162,880 |
3756204-1
| 24,003,282 |
noncomm/PMC003xxxxxx/PMC3756204.xml
|
Generalized Dowling-Degos Disease: Case Reports
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The proband was an 82-year-old man who was presented with progressively generalized skin lesions since adolescence. He began to develop areas of hyperpigmentation, initially on the face, but then soon affecting the neck, axillae, groin, trunk and limbs (). The eruption has continued to become more extensive throughout adulthood leading to generalized pruritus. The patient was born of a non-consanguineous marriage. All of his offspring were affected with the same disease. His general physical examination was normal. Skin examination revealed a symmetrical reticulate hyperpigmentation predominantly affecting the lower face, skin folds, major flexures, back and legs. Symmetrically distributed reticulate hypopigmentation was also seen in the legs. Multiple pits varying in size from 1~3 mm and open comedone-like lesions were distributed over the cheeks, perioral area, neck and back. No breaks in the epidermal ridge pattern on the palms and soles were seen. The mucosa, nails, teeth and hair were normal. On investigation, complete blood count, blood chemistry, liver and renal function tests were all within normal limits.\nA biopsy was conducted from a hyperpigmented lesion over the shin, and histopathological examination revealed hyperkeratosis, acanthosis and irregular elongated thin branching rete ridges growing down into the dermis and increased melanin pigment in the lower part of the rete pegs (). Another skin biopsy from comedo-like lesions on the back shows keratin-filled cysts resembling comedones (). These features were entirely consistent with the clinical diagnosis of DDD,.
|
[[82.0, 'year']]
|
M
|
{'1720261': 1, '17637446': 1, '6838773': 1, '10071319': 1, '9621148': 1, '2713264': 1, '7889671': 1, '6232941': 1, '1377166': 1, '9036937': 1, '15482301': 1, '1911300': 1, '6860566': 1, '31544084': 2, '10233273': 1, '9529553': 1, '16465624': 1, '629578': 1, '12207773': 1, '16575392': 1, '24003282': 2}
|
{'3756204-2': 2, '3756204-3': 2, '6743403-1': 1}
|
162,881 |
3756204-2
| 24,003,282 |
noncomm/PMC003xxxxxx/PMC3756204.xml
|
Generalized Dowling-Degos Disease: Case Reports
|
A 58-year-old man (first son of the proband) was presented with reticulate hyperpigmented skin lesions over the face, chest, back, axillae and flexures since adolescence. Initially, the lesions, which first started over the face, were raised above the skin surface and were small. Gradually, these lesions progressed to form pits filled with blackish material. He developed similar lesions over the back and chest over the next year. There was no history of other skin diseases. His father, all his siblings and their offspring were affected with the same disease. His general physical examination was within normal limits. Skin examination revealed open comedone-like lesions and multiple pits of varying sizes distributed over the face, neck and limbs. The face and neck were more severely affected when compared to the trunk and limbs. There was diffuse reticulate pigmentation over the face, axillae, inguinal region and back. The rest of the skin examination was unremarkable.
|
[[58.0, 'year']]
|
M
|
{'1720261': 1, '17637446': 1, '6838773': 1, '10071319': 1, '9621148': 1, '2713264': 1, '7889671': 1, '6232941': 1, '1377166': 1, '9036937': 1, '15482301': 1, '1911300': 1, '6860566': 1, '31544084': 2, '10233273': 1, '9529553': 1, '16465624': 1, '629578': 1, '12207773': 1, '16575392': 1, '24003282': 2}
|
{'3756204-1': 2, '3756204-3': 2, '6743403-1': 1}
|
162,882 |
3756204-3
| 24,003,282 |
noncomm/PMC003xxxxxx/PMC3756204.xml
|
Generalized Dowling-Degos Disease: Case Reports
|
A 50-year-old woman, the younger sister of the patient in case 2, had progressively generalized skin lesions after puberty. Her skin lesions were very similar to his brother's lesions, with generalized reticulate hyperpigmentation, open comedo-like lesions and multiple pits of varying sizes on the face, perioral area, flexures and axillae. There was no history of inflammatory skin diseases prior to the onset of the lesion. There was no significant past medical, surgical and gynecological history. Skin examination revealed multiple pits of varying sizes distributed over the face, upper back, upper chest, arms, cubital fossa and over forearms. There was diffuse reticulate pigmentation over the cubital fossa, axillae, inguinal region and face. The rest of the skin examination was unremarkable. Her general physical examination and all relevant investigations were within the normal limit. We did not perform a genetic study in our patients due to their religious belief.
|
[[50.0, 'year']]
|
F
|
{'1720261': 1, '17637446': 1, '6838773': 1, '10071319': 1, '9621148': 1, '2713264': 1, '7889671': 1, '6232941': 1, '1377166': 1, '9036937': 1, '15482301': 1, '1911300': 1, '6860566': 1, '31544084': 2, '10233273': 1, '9529553': 1, '16465624': 1, '629578': 1, '12207773': 1, '16575392': 1, '24003282': 2}
|
{'3756204-1': 2, '3756204-2': 2, '6743403-1': 1}
|
162,883 |
3756205-1
| 24,003,283 |
noncomm/PMC003xxxxxx/PMC3756205.xml
|
Acquired Localized Hypertrichosis Induced by Internal Fixation and Plaster Cast Application
|
A 15-year-old boy was observed with some new excessive hairs on the right back of his hand for 3 weeks. Three months prior to this, he had been diagnosed with a closed fracture in the first metacarpus of right hand after a fall on the cement floor. He was operated with internal fixation by Kirschner wire on his right first metacarpus (). After the operation, a plaster of gypsum cast was applied from the wrist to his right elbow (). Six weeks later after the cast was removed, increased hair growth was localized on the right back hand where the cast was covered for internal fixation. Physical examination indicated a sheeted, coarse, dark hair area on his right back hand with a postsurgical scar which is approximate 5 cm in length (). There was no history of any systemic or topical medications known to cause hypertrichosis administered either before or after the surgery. The abnormal hair growth resolved spontaneously 4 months after the cast removal.
|
[[15.0, 'year']]
|
M
|
{'26403547': 1, '20590714': 1, '3960754': 1, '30607042': 2, '27601863': 2, '6821791': 1, '6074155': 1, '7278905': 1, '15492447': 1, '11207975': 1, '19954396': 1, '7212723': 1, '30034196': 1, '6939981': 1, '2724357': 1, '7811183': 1, '444781': 1, '12081714': 1, '8105263': 1, '24003283': 2}
|
{'4989394-1': 1, '6290290-1': 1}
|
162,884 |
3756241-1
| 24,003,427 |
noncomm/PMC003xxxxxx/PMC3756241.xml
|
First Case of Mycobacterium longobardum Infection
|
A 71-yr-old man presented with symptoms of pain, redness, and swelling in the left elbow on May 7, 2012. The patient had been previously diagnosed with left elbow bursitis and had undergone surgery to resect the infected tissue at a university hospital in January 2011. At that time, a pathology review of the excised tissue confirmed the diagnosis of tuberculous bursitis with chronic granulomatous inflammation, without isolation of Mycobacterium tuberculosis (MTB). The patient received the antituberculosis drugs of isoniazid, rifampicin, ethambutol, and pyrazinamide for seven months.\nThe patient had a history of being treated for hypertension and diabetes. Physical examination at presentation revealed surgical scarring and tenderness around the left elbow. The patient's electrolytes, liver function, and complete blood counts were normal. His blood pressure was 107/76 mmHg and his two-hour postprandial glucose level was 106 mg/dL. Magnetic resonance imaging (MRI) of the left elbow revealed localized bone marrow signal alterations at the left ulnar olecranon and substantial effusion with marked synovial hypertrophy in the radiocapitellar joint.\nThe patient was assessed as having tuberculous osteomyelitis according to the history and MRI results. The left elbow was incised and drained using sterilized devices on May 8, 2012. Histological examination of the resected tissue showed necrotizing granulomatous inflammation (). No organisms were detected on Gram or Ziehl-Neelsen staining, and the direct culture of the tissue sample for bacteria was sterile. In addition, there was no evidence of malignancy. The biopsied tissue was cultured for mycobacteria, and mycobacterial growth was observed on Löwenstein-Jensen medium 26 days later. The isolate was acid-fast bacillus and colonies grew rough and unpigmented both in the dark and after light exposure. The mycobacterium was identified as NTM using the Seeplex MTB/NTM ACE Detection Kit (Seegene Inc., Seoul, Korea).\nThe 16S rRNA gene was sequenced for the NTM identification. The primers and PCR setting used to amplify the target region, the first 500 bp of the 16S rRNA gene, were as previously described [, ]. Sequences were analyzed using an ABI PRISM 3730 series DNA Analyzer (Applied Biosystems, Foster City, CA, USA). For the first 500 bp of the 16S rRNA gene sequence, the isolate showed a 98.6% identity match with GenBank sequence JN571166.1 (M. longobardum), a 97.7% identity match with GenBank sequence FJ268583.1 (M. senuense), and a 97.5% identity match with GenBank sequences NR_043905.1 (M. senuense) and GQ184162.1 (M. terrae). However, the Clinical and Laboratory Standards Institute guidelines indicate that a Mycobacterium sp. that has a 95-99% nucleotide identity with 16S rRNA gene sequences of other species cannot be definitively identified by 16S rRNA gene sequencing [].\nTortoli et al. [] reported that 65-kDa heat shock protein (hsp65) and full 16S rRNA gene sequencing are useful for the identification of M. longobardum. For accurate identification, the hsp65 and additional 16S rRNA genes of the isolate were analyzed. Using primers amplifying 468-1,053 bp (F1 5'-TGC CAG CAG CCG CGG TAA-3', R1 5'-CGG GAC TTA ACC CAA CAT CT-3') and 1,010-1,500 bp (F2 5'-TGG CTG TCG TCA GCT CGT-3', R2 5'-AAG GAG GTG ATC CAA CCG CA-3') of the 16S rRNA gene, PCR was performed as described for sequencing of the first 500 bp of the 16S rRNA gene sequence. For the full 16S rRNA gene sequence, the isolate showed a 99.2% identity match with GenBank sequence JN571166.1 (M. longobardum), a 98.6% identity match with GenBank sequence HM770865.1 (M. terrae), and a 98.4% identity match with GenBank sequence GU084182.2 (M. heraklionense). The 16S rRNA gene phylogenetic tree of the mycobacterium isolated in this case was most closely related to JN571166.1 (M. longobardum) and was classified as M. longobardum (). The primers and PCR settings used to amplify the hsp65 gene were as described previously []. Moreover, hsp65 sequencing of the isolate showed a 99.4% match with sequences JN571166.1 (M. longobardum), EF601223.1 (M. terrae), and JX154097.1 (M. terrae). We concluded that the isolate was M. longobardum.\nAfter identifying M. longobardum, the patient was prescribed clarithromycin and ethambutol empirically. The antimicrobial susceptibility test (AST) using the broth microdilution method revealed that the isolate was susceptible to clarithromycin, ethambutol, moxifloxacin, and sulfamethoxazole, but resistant to amikacin, ciprofloxacin, and rifampicin. The therapy was maintained, and the patient was cured without further complications.
|
[[71.0, 'year']]
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M
|
{'22447702': 1, '18319471': 1, '17277290': 1, '25915177': 1, '25278573': 1, '2203812': 1, '12692101': 1, '19398805': 1, '26793457': 1, '24982839': 1, '27057825': 1, '27927928': 1, '7505291': 1, '10722426': 1, '16738122': 1, '7684243': 1, '18753344': 1, '17116985': 1, '26962085': 1, '24003427': 2}
|
{}
|
162,885 |
3756242-1
| 24,003,428 |
noncomm/PMC003xxxxxx/PMC3756242.xml
|
Novel c.300_301delinsT Mutation in PITX2 in a Korean Family with Axenfeld-Rieger Syndrome
|
A 4-yr-old girl was referred to our clinic because of uncontrolled intraocular pressure (IOP) under maximal tolerable medical therapy and corneal edema in both eyes. Her best-corrected visual acuity was 20/800 in both eyes. IOP as measured by Goldmann tonometry was 22 mm Hg (reference range: ≤21 mm Hg) in the right eye and 23 mm Hg (reference range: ≤21 mm Hg) in the left eye. The horizontal and vertical corneal diameter of both eyes was 9.5 mm and 10.0 mm, respectively. Posterior embryotoxon and a prominent Schwalbe's line were observed in both eyes. Iridocorneal adhesion and corectopia were also seen, and anterior insertion of the iris into the trabecular meshwork with prominent iris processes was observed by gonioscopic examination in both eyes. The optic disc was difficult to inspect because of corneal edema; the cup-to-disc (CD) ratio appeared to be 0.8 in both eyes. The patient had apparent microdontia.
|
[[4.0, 'year']]
|
F
|
{'20940740': 1, '16638982': 1, '14985297': 1, '29401568': 1, '11821690': 1, '19513095': 1, '8944018': 1, '16449236': 1, '20827438': 2, '19337485': 2, '10713890': 1, '27463523': 1, '28816964': 1, '23687430': 2, '8751862': 1, '416212': 1, '22199394': 1, '16936096': 1, '17197537': 1, '9326342': 1, '24003428': 2}
|
{'2934855-1': 1, '3654851-1': 1, '3654851-2': 1, '3654851-3': 1, '3654851-4': 1, '2655743-1': 1}
|
162,886 |
3757259-1
| 20,300,853 |
noncomm/PMC003xxxxxx/PMC3757259.xml
|
Fatal cerebral edema associated with serine deficiency in CSF
|
A 7-year old, normally developing girl was diagnosed with moderately severe asthma for which she used inhalation therapy with combination of salmeterol/fluticasone. The day before her death, she presented with a mild febrile condition, including malaise, headache, and nausea. Medical examination showed no abnormality, and domperidone was prescribed. The morning before her death, her mother found her unresponsive in bed, probably following a seizure. At that time, blood glucose, as measured by a bed-side apparatus, was 2.1 mmol/l. In the emergency room, the patient had convulsions, which responded to diazepam. Physical examination showed expiratory wheezing, normal blood pressure and capillary refill time, a relatively low heart rate (100/min), no hepatosplenomegaly, normal pupils, and no signs of trauma or bleeding. Hypoglycemia or electrolyte disturbances were excluded. Liver enzymes and bilirubin were slightly elevated, and blood ammonia was normal (15 µmol/l). She regained consciousness for 1.5 h but became progressively dyspneic and presented suddenly with apnea and desaturation, decortication rigidity, bilateral fixed mydriatic pupils, and deep coma. She was intubated and treated with dexamethasone and mannitol. A brain computed tomography (CT) scan showed bilateral central herniation and cerebral edema. There were indisputable signs of brain death, and she died 24 h after the first symptoms.\nAmino acid analysis of both plasma and CSF revealed strongly decreased serine concentrations (Tables , , ) comparable with levels observed in patients with 3-PGDH deficiency (de Koning et al. ). Enantiomer separation revealed D-serine to be 0.9 µmol/L (ref. 0.8–4.3 µmol/L) and L-serine 4.0 µmol/L (ref. 17.2–44.0 µmol/L), with slightly elevated D-serine/total serine ratio of 18% in CSF (Fuchs et al. ). Concentrations of the other amino acids were normal or decreased according to a nonspecific pattern (data not shown). A deficiency of 3-phosphoglycerate dehydrogenase was excluded in cultured fibroblasts (43 nmol/mg per min; normal 29.5 ± 2.7 nmol/mg per min). Further metabolic screening revealed increased ketone bodies and lactate in urine, plasma, and CSF (Table ). Plasma acylcarnitine profile showed an elevated concentration of OH-C4-carnitine. A fatty acid oxidation defect was excluded. Brain microscopy showed bilateral necrosis in the cerebral tonsils compatible with central herniation. No signs of encephalitis or meningitis were found, but diffuse interstitial edema was obviously present. Postmortem microbiology sampling yielded a parainfluenza type II virus in the lungs, probably explaining fever onset and asthmatic signs as her presenting condition. The clinical picture probably reflects a toxic encephalopathy.
|
[[7.0, 'year']]
|
F
|
{'23463425': 1, '12393813': 1, '17881883': 1, '9222972': 1, '17436247': 1, '7290229': 1, '2324546': 1, '11331719': 1, '15610810': 1, '28653176': 1, '8758134': 1, '15021249': 1, '12176074': 1, '11508546': 1, '15622525': 1, '9579653': 1, '12534373': 1, '11054547': 1, '12846552': 1, '15312798': 1, '7490620': 1, '14673469': 1, '6089514': 1, '17068790': 1, '20300853': 2}
|
{'3757259-2': 2}
|
162,887 |
3757259-2
| 20,300,853 |
noncomm/PMC003xxxxxx/PMC3757259.xml
|
Fatal cerebral edema associated with serine deficiency in CSF
|
A 4-year-old girl with normal mental development suffered from asthma for which she used Flixotide (a steroid, 2 dd 250 µg) and salmeterol (2 dd 25 µg). She had normal height but severe malnutrition [weight < 2 standard deviations (SD)] due to feeding difficulties related to behavioral problems. Because of sleep disturbances, the patient had been on treatment with Alimemazine (an antihistaminic sedative agent) for 4 months. Two days before her death (in the evening, day 1), she presented with fever (39–40°C) without other particularities. The next morning (day 2), she was found in bed with tonic clonic seizures. The seizures were resistant to multiple anticonvulsive drugs. There were no signs of respiratory or circulatory failure. On admission, serum glucose was 4.0 mmol/L, with CSF glucose 1.0 mmol/L; serum electrolytes were normal, as was blood ammonia (15 µmol/l). There were no signs of a bacterial central nervous system (CNS) infection in CSF, no pleocytosis, and bacterial and viral cultures remained negative; later nasal cultures, however, showed an adenovirus V. Blood C-reactive protein (CRP) was > 300 mg/ml.\nPhysical examination showed a very ill girl with coma scores E1, M4, V1. Intubation and cardiac support were effective for some hours, but a rapid deterioration was seen with an isoelectric electroencephalogram (EEG) pattern and absent stem reflexes. After a repeated isoelectric EEG, the next day, supportive treatment was discontinued. No postmortem examination was performed. Metabolic investigations in plasma and CSF taken at day 2 showed particularly low plasma and CSF serine concentrations. Concentrations of the other amino acids were normal or decreased according to a nonspecific pattern (data not shown). Unfortunately, no fibroblasts were available for analysis of 3-PGDH activity. Plasma lactate and 3-hydroxybutyrate were clearly increased, as was CSF lactate (Table ). Urine organic acid analysis showed a moderate ketonuria as well as a marginally elevated lactate excretion.
|
[[4.0, 'year']]
|
F
|
{'23463425': 1, '12393813': 1, '17881883': 1, '9222972': 1, '17436247': 1, '7290229': 1, '2324546': 1, '11331719': 1, '15610810': 1, '28653176': 1, '8758134': 1, '15021249': 1, '12176074': 1, '11508546': 1, '15622525': 1, '9579653': 1, '12534373': 1, '11054547': 1, '12846552': 1, '15312798': 1, '7490620': 1, '14673469': 1, '6089514': 1, '17068790': 1, '20300853': 2}
|
{'3757259-1': 2}
|
162,888 |
3757612-1
| 24,014,919 |
noncomm/PMC003xxxxxx/PMC3757612.xml
|
Unexpected death due to cefuroxime-induced disulfiram-like reaction
|
A 64-year-old Chinese male went into a rural out-patient with clinical history of chronic tracheitis and emphysema. The patient is a known smoker since 30 years. The patient was prescribed cefuroxime sodium 4.5 g infusion and 5% glucose in 250-ml saline. After the patient got one-third infusion of Cefuroxime sodium in general frequency, the doctor noticed that the patient presented with facial flushing, sweating, and weakness. The patient had a blood pressure of 95/60 mmHg and pulse of 110/min on examination. The patient had dyspnea and lost consciousness very soon, and died later despite of the resuscitation attempts. He already had received the same treatment for 2 days because of cough and expectoration. The investigation indicated that the patient had taken alcohol before he went to the clinic that day.\nAutopsy was carried out. There was mild to moderate eccentric atheroma detected in left anterior descending coronary artery and left circumflex, which caused <40% stenosis of vessel lumen. Low-grade emphysematous-like changes were seen in both the lungs. Microscopically, over-inflated alveoli and the lymphocytic infiltration in the submucous layer of the bronchial wall were also seen. A few eosinophilic granulocytes were present in the submucosal layer of the larynx, but not in other organ sections. Other organs were unremarkable on macro and microscopic examination.\nToxicological analysis of heart blood revealed elevated serum ethanol (2110 mg/L) and acetaldehyde (60 mg/L). Total IgE was 85.47 IU/ml (normal reference ranges: 1.31-165.30 IU/ml). Disulfiram-like reaction induced by cefuroxime sodium interacting with alcohol was identified as the cause of death, and coronary artery disease was likely to contribute to the patient's death.
|
[[64.0, 'year']]
|
M
|
{'8947362': 1, '20083883': 1, '25363464': 1, '22005600': 1, '19124444': 1, '29720921': 1, '31871085': 1, '1555782': 1, '24014919': 2}
|
{}
|
162,889 |
3757614-1
| 24,014,921 |
noncomm/PMC003xxxxxx/PMC3757614.xml
|
Terlipressin-induced hyponatremic seizure in a child
|
A 7-year-old male child presented with two episodes of hematemesis (around 100 ml of fresh blood). There was no history of abdominal pain, malena, fever, drug intake, and bladder/bowel complaints. There was no history of blood transfusion or jaundice in the past. His family history and birth history was normal. On admission, blood pressure was 78/58 mmHg, heart rate was 110 beats/min, and respiratory rate was 24 breaths/min. Pallor was present. There was no icterus, edema, cyanosis, or jaundice. Spleen was palpable 3 cm below left costal margin. Liver span was 8 cm with soft consistency and smooth margins. After initial fluid resuscitation, patient was given 15 cc/kg of packed cell transfusion. His hemoglobin was 5.7 g/dl; white blood cell count 7200/cumm; platelet count 1.6 lac/cumm. His liver function tests, serum electrolytes, renal function tests, prothrombin time, plasma thromboplastin time, and bleeding time were normal. A provisional diagnosis of extra-hepatic portal vein obstruction with variceal bleeding was made. An esophagogastroduodenoscopy (EGD) showed two large esophageal varices with active bleeding. Endoscopic variceal ligation was planned in the patient. However, as the patient was not hemodynamically stable, a bolus of 2 mg of terlipressin was initiated, followed by 1 mg every 6 hourly. Color Doppler sonography revealed multiple collateral channels replacing the portal vein (portal cavernoma) and splenomegaly. The patient was stable until the third hospital day when he had a generalized tonic seizure and became drowsy. His sodium level had dropped from 142 mEq/L on admission to 110 mEq/L and serum osmolality had decreased to 240 mOsm/kg. Intravenous correction for hyponatremia was started. Computed tomography scan of brain, cerebrospinal fluid examination, and electroencephalography were normal. After 2 days of starting sodium correction, the sensorium had slightly improved but hyponatremia was persistent. On the fifth hospital day, terlipressin was stopped and serum electrolytes measured the next day showed a dramatic increase in sodium level, although not to a normal level. After 4 days of stopping terlipressin, the serum sodium was normal. This can be considered as a ‘probable’ adverse drug reaction as per causality assessment with Naranjo's Scale.[] shows the serial serum sodium values during the hospital stay. The patient underwent endoscopic ligation of the esophageal varices and was discharged on the tenth day of admission.
|
[[7.0, 'year']]
|
M
|
{'28293079': 1, '8898643': 1, '20931555': 1, '12939586': 1, '19018483': 1, '10960437': 1, '30288282': 1, '8146855': 1, '21712934': 1, '20302535': 1, '25981229': 1, '17454890': 1, '24014921': 2}
|
{}
|
162,890 |
3757615-1
| 24,014,922 |
noncomm/PMC003xxxxxx/PMC3757615.xml
|
A case of thrombocytopenia caused by rifampicin and pyrazinamide
|
A 32-year-old male patient presented on 13/02/2012 in Department of General Medicine with complaints of fever since 1 month and history of antituberculosis treatment in 2002. On chest X-ray examination, the patient was found to have pleural effusion on the right side and was referred to Department of Pulmonary Medicine where 20 ml of straw-colored pleural fluid was aspirated. Pleural fluid was chiefly lymphocytic exudate with adenosine deaminase (ADA) 110 U/L, highly suggestive of tubercular pleural effusion. All routine investigations including complete hemogram, liver function tests (LFTs), renal function tests (RFTs), and complete urine examination were found within normal limits. On 17/02/2012, the patient underwent therapeutic tap with 1 L of straw-colored fluid removed from the pleural cavity and was put on three times a week Category II antituberculosis treatment under DOTS (streptomycin 750 g, isoniazid 600 mg, rifampicin 450 mg, ethambutol 1200 mg, and pyrazinamide 1500 mg) along with daily pyridoxine 10 mg at bed time. After about 20 days, on 10/03/2012, the patient presented in Department of Dermatology, Venereology & Leprosy (DVL) with complaints of ulceration in the mouth. Hemogram revealed hemoglobin (Hb) 8.3 gm%, total leukocyte count (TLC) 9800 cells/mm3, erythrocyte sedimentation rate (ESR) 45 mm/1 h, and platelet count 21,000/mm3. Peripheral smear revealed shift to left with thrombocytopenia, Prothrombin Time Index (PTI) 76.92% and International Normalized Ratio (INR) of 1.43. Enzyme-linked immunosorbant assay (ELISA) for human immunodeficiency virus (HIV) was negative, random blood sugar was within normal limits, and urine was also found normal.\nPatient was suspected of having thrombocytopenia due to rifampicin and was referred to the Department of Pulmonary Medicine where all drugs were stopped. On 21/03/2012, the ulcers healed, platelet count increased to 472,000/mm3, International Normalized Ratio (INR) was 1.82, and ESR was 30 mm/1 h. So, after taking informed consent, the patient was again started on the same regime, excluding rifampicin. Next day, the patient again had ulcers in the mouth and the platelet count decreased to 10,000/mm3. Treatment was again stopped and the patient recovered. One month later (on 19/04/2012), the patient returned for treatment. The platelet count (on 03/04/2012) was 505,000/mm3. It was decided that patient will be exposed to medicines one after the other. He was given only isoniazid 300 mg and the treatment was uneventful. On the third day, he was given 750 mg of pyrazinamide under observation. Within 24 h, the patient developed ecchymoses and ulcers in the mouth [] and the platelet count decreased to 23,000/mm3, forcing withdrawal of pyrazinamide; isoniazid (300 mg) was continued. Patient recovered, and so, believing that hypersensitivity was because of pyrazinamide and not because of rifampicin, after monitoring the platelet count, the patient was given rifampicin 150 mg along with isoniazid 300 mg on 26/04/2012. Within 6 h, the patient developed petechiae on legs and forearms [] and also fever with chills. Platelet count decreased to 25,000/mm3. Rifampicin was stopped and lesions subsided within 48 h. After 2 days, the patient was exposed to ethambutol and then to streptomycin uneventfully. Patient continued with isoniazid 300 mg, ethambutol 1000 mg, and streptomycin 750 mg without any further complaints.
|
[[32.0, 'year']]
|
M
|
{'5314737': 1, '7249508': 1, '30717702': 1, '5427483': 1, '3254638': 1, '25460494': 1, '19195976': 1, '1008352': 1, '24014922': 2}
|
{}
|
162,891 |
3757616-1
| 24,014,923 |
noncomm/PMC003xxxxxx/PMC3757616.xml
|
Severe photosensitivity reaction induced by topical diclofenac
|
A 65-year-old male farmer presented with severe rash on his lower back. One day earlier, he had complained of low backache and treated it with oral diclofenac, oral ranitidine, and topical diclofenac cream. The patient applied diclofenac cream on his lower back and went for his usual work in the field. Initially, the applied area became erythematous and then rapidly developed macular rash with blistering. The eruption was intensely itchy and spread from the lower to the upper back and anteriorly to abdomen []. Although the patient had noted some improvement in the backache, he stopped using the diclofenac cream because of the rash.\nUpon taking detailed history, he reported that he had used the same brand of topical diclofenac cream an year earlier for joint pain but had not developed any rash or erythema on his knee joints even after 1 week of application. As patient has used the same brand before, the reaction cannot be attributed to the excipients of the cream. He had no known allergies. The general examination of the patient revealed no abnormality with normal body temperature.\nLocal examination revealed an extensive, poorly demarcated, erythematous and scaly plaque on the lower back with vesicles and yellow crusting. The affected area extended from the lower back to anterior abdomen and corresponded to the area of application of the diclofenac cream. Only the part exposed to the sun was affected while the part covered with cloth and areas where cream was not applied was completely spared. The expiry date on label of diclofenac gel was checked and it was within its expiry period. Characteristic localization of the lesion to the area of exposure of topical diclofenac supported the diagnosis of diclofenac induced photosensitivity reaction. The causality assessment of the reaction was done by using WHO-UMC scale and Naranjos algorithm and the relation was categorized as probable.\nThe patient was managed by oral amoxicillin-clavulanic acid, antihistaminics, and prednisolone. Oral analgesics were deliberately avoided considering their tendency to exacerbate the reaction. He was advised to avoid sunlight. Patient did not require any intensive treatment or surgical intervention during the follow up and lesions healed without extensive scarring or other complications.
|
[[65.0, 'year']]
|
M
|
{'16787462': 1, '29547525': 1, '15500677': 1, '27882527': 2, '21342231': 1, '12762833': 1, '34451820': 1, '17101014': 1, '21231861': 1, '24014923': 2}
|
{'5120621-1': 1, '5120621-2': 1, '5120621-3': 1, '5120621-4': 1}
|
162,892 |
3757617-1
| 24,014,924 |
noncomm/PMC003xxxxxx/PMC3757617.xml
|
Inflamed psoriatic plaques: Drug toxicity or disease exacerbation?
|
A 50-year-old HIV negative male with plaque psoriasis involving 45% of the patient's total body surface area with a Psoriasis Area Severity Index (PASI) score of 17 was administered 7.5 mg methotrexate weekly orally after the recommended baseline investigations were carried out. A week later, there was increased activity of the lesions, with signs of increased inflammation. Dose of methotrexate was increased to 10 mg per week after repeating routine recommended investigations. Two weeks later patient came back with extremely painful superficial erosions of the pre-existing psoriatic plaques [Figures , ] along with history of headache, blurring of vision, and diarrhea.\nOn examination, the patient was conscious and normotensive. Cutaneous examination revealed intense erythema and erosions over the pre-existing psoriatic plaques [Figures , ], facial and palmar erythema [Figures , ], and mucositis. Systemic examination was otherwise normal. Laboratory studies revealed a hemoglobin of 11.2 g/dL, red blood cell count of 4.45 lakhs/μL, mean corpuscular volume of 96 fL, white blood cell count (WBC) of 5500/μL, and platelet count of 2,60,000/μL. Serum biochemistry showed a serum creatinine level of 0.8 mg/dL, blood urea nitrogen 35.0 mg/dL, total bilirubin 0.4 mg/dL, serum glutamate oxaloacetate transaminase (SGOT) 27 IU/L, serum glutamate pyruvate transaminase (SGPT) 25 IU/L, and alkaline phosphatase 113 IU/L. Prothrombin time and partial thromboplastin time were within normal limits. Urine and stool analysis, chest X-ray, and electrocardiogram were normal. Blood culture was sterile and there was no other evidence of systemic infection. Serum concentrations of methotrexate and metabolites were not measured due to limited resources.\nThough the baseline investigations at first and subsequent visits (7 and 14 days) were within normal limits, based on the clinical features, a possibility of methotrexate toxicity was considered. The patient was inappropriately self-administering 10 mg methotrexate daily orally. He was given injection leucovorin calcium 20 mg IV stat at the time of presentation. In view of normal hematological and biochemical parameters, further doses of leucovorin were not given. Further doses of methotrexate were withheld and simultaneously topical steroids (fluticasone propionate cream 0.05%) and oral antihistaminics (cetrizine) were administered, which resulted in dramatic improvement of the cutaneous lesions within 7 days and complete healing in 14 days [Figures -].
|
[[50.0, 'year']]
|
M
|
{'22136858': 1, '20579471': 1, '33804652': 1, '7249508': 1, '19052409': 1, '24014924': 2}
|
{}
|
162,893 |
3757638-1
| 24,014,992 |
noncomm/PMC003xxxxxx/PMC3757638.xml
|
Successful Use of Intravitreal Bevacizumab and Pascal Laser Photocoagulation in the Management of Adult Coats’ Disease
|
A 34 year-old male was referred to our department with rapidly reducing vision in the right eye over a 3-4 week period. He was otherwise medically healthy, with no relevant past ophthalmic history.\nAt presentation, his visual acuities were 6/18 and 6/5 in the right and left eyes, respectively. The intraocular pressures were 12 mmHg in each eye and slit-lamp examination of the anterior segment was unremarkable. Fundus examination revealed a subtotal temporal exudative retinal detachment of the right eye, with large intraretinal and subretinal exudates, encroaching the macula; with an associated large retinal vasoproliferative tumor affecting the temporal mid-periphery []. The left eye was clinically and angiographically normal.\nFluorescein angiography confirmed a profusely leaking temporal vasoproliferative tumor in the right eye with widespread telangiectatic vessels and aneurysmal dilatation of the capillary bed, in addition to diffuse areas of capillary non-perfusion of the right peripheral fundus []. Based on the features of the ophthalmic workup, the patient was diagnosed with vasoproliferative tumor of the retina (VPTR) with exudative retinal detachment secondary to Coats’ disease.\nThe patient was treated with two intravitreal Avastin (Genetech Inc., San Francisco, CA, USA) injections (1.25 mg), 4 weeks apart. Five days following the second injection, when he presented for laser treatment, the visual acuity of the right eye had improved to 6/5 unaided with no residual macular edema and complete regression of the VPTR. Panretinal photocoagulation was targeted towards areas of telangiectasia and peripheral ischemia, in addition to direct treatment of the VPTR using a 532 nm Pascal laser photocoagulator. A 3 × 3 square array pattern with pulse duration set at 20 ms and 200 micron spot size was used []. At the last follow-up, 12 months after initial intervention, visual acuity was maintained at 6/5, with no signs of recurrence.
|
[[34.0, 'year']]
|
M
|
{'21437759': 1, '21653215': 1, '33392305': 1, '17342503': 1, '32605612': 2, '21165239': 2, '20029156': 2, '24014992': 2}
|
{'2841384-1': 1, '7329434-1': 1, '7329434-2': 1, '2992568-1': 1}
|
162,894 |
3757639-1
| 24,014,993 |
noncomm/PMC003xxxxxx/PMC3757639.xml
|
Eyelid Angiosarcoma: A Case Report and Review of the Literature
|
A 77-year-old otherwise healthy woman noted a lesion on the left lower eyelid about 3 months prior to presentation. The lesion grew and developed a central ulcer over the 3 months. The patient had no history of skin cancer.\nExternal examination showed a tan-colored nodule with overlying crust-covered ulcer on the nasal aspect of the left lower eyelid, measuring 12 mm × 7 mm []. Complete surgical excision with a frozen section margin control was performed. Histopathologic examination showed vasoformative architecture with islands and sheets of spindle and epithelioid cells and little intervening stroma []. The cells showed copious amounts of either rounded or tapered eosinophilic cytoplasm with occasional intracytoplasmic lumina and contained large vesicular nuclei with prominent nucleoli []. The tumor cells showed intense positive immunoreactivity for CD34, CD31, Factor VIII, and Ki-67 [Figure -]. The mitotic count was 17/10 high-power fields. The tumor was diagnosed as eyelid angiosarcoma. The patient refused any further treatment including radiotherapy or chemotherapy. After 1 year follow-up, there has been no recurrence or development of metastasis.\nThe presentation of cutaneous angiosarcoma can vary widely, mimicking various benign and malignant pathologies. A review of 47 cutaneous angiosarcoma cases revealed that rapidly expanding erythematous-to-violaceous mass was the most common presentation in half of the patients, followed by solitary blue-to-violaceous nodules suggestive of lymphoma (20%), keratotic flesh-toned papule consistent with squamous or basal cell carcinoma (20%), multicentric grouped nodules reminiscent of metastases (10%), and well-circumscribed vascular lesion such as pyogenic granuloma (5%). Similarly, eyelid angiosarcoma most commonly presented with erythematous nodule (38%), followed by erythematous-to-violaceous maculopapular lesion (25%), red-to-violaceous plaque or infiltrative lesion (13%), yellow plaque or infiltrative lesion (13%), and yellow nodule (13%) []. Multifocal eyelid lesions or associated diffuse eyelid involvement in the form of eyelid swelling were seen in about half of the cases []. The differential diagnosis of angiosarcoma includes capillary hemangioma, epithelioid hemangioma, Kaposi's sarcoma, epithelioid hemangioblastoma, hemangiopericytoma. Clinical history and examination findings are helpful in differential diagnosis, but the diagnosis of angiosarcoma is based on the histopathological evaluation.\nHistopathologically, angiosarcomas show vasoformative architecture, and range from well-differentiated to poorly-differentiated lesions. Abnormal; pleomorphic malignant endothelial cells are the hallmark of angiosarcoma. Low-grade, well-differentiated lesions are composed of vascular channels that grew in an infiltrative fashion and had plump endothelial cells with hyperchromic nuclei and infrequent mitoses. High-grade, poorly-differentiated lesions are densely cellular tumors with focal vascular channels. The neoplastic cells in high-grade, poorly-differentiated lesions range from spindle to epithelioid cells with large irregular nuclei with coarse chromatin and eosinophilic cytoplasm. By immunohistochemistry, tumor cells on angiosarcoma stain positive for factor VIII-related antigen, and CD31, markers for endothelial lineage of neoplasms, and CD 34, marker for hematopoietic cells, endothelial progenitor cells, and endothelial cells of blood vessels.\nSurgical excision, followed by external beam radiotherapy (EBRT) has been the treatment of choice for angiosarcoma. Complete resection could be difficult because of invasive and often multifocal nature of angiosarcomas, tumor location, and its relation to other anatomical structures. Neoadjuvant chemotherapy and antiangiogenic molecules have been used in the treatment of cutaneous angiosarcoma. Lack of randomized trials and data based on few retrospective studies make it difficult to have specific management guidelines. In a review of 21 patients with cutaneous angiosarcoma of face with periorbital involvement, DeMartelaere et al., reported that 71% of cases were treated with neoadjuvant chemotherapy and 29% underwent surgery followed by adjuvant chemotherapy or radiotherapy. Following neoadjuvant chemotherapy, 93% of the patients showed complete clinical response and 60% of them did not require surgical resection. However, 60% of them had recurrences. In the patients who underwent surgical excision followed by adjuvant therapy, 83% showed a complete clinical response, and 40% had recurrences. A review of eyelid angiosarcoma cases in the literature showed that 31% of the patients were treated with chemotherapy alone in 23% of the patients, excisional biopsy followed by EBRT or plaque radiotherapy in 18%, excisional biopsy alone in 23%, excisional biopsy followed by EBRT and chemotherapy in 9%, excisional biopsy followed by chemotherapy in 9%, EBRT alone in 9% and observation in 5% []. Cutaneous angiosarcoma has a poor prognosis with 40% to 50% of the 5-year local regional control rate, and 20% to 40% of 5-year distant metastasis-free survival rate. On their review of the literature, Papalas et al. reported that patients with isolated, nodular eyelid involvement had a survival rate of 100% at a mean follow-up of 3 years although the patients with diffuse disease had a survival rate of 57% at a mean follow-up of 3 years. This is contrary to the poorly-differentiated histopathologic features and bad systemic prognosis in angiosarcomas of face and scalp with isolated, nodular tumors. A review of eyelid angiosarcoma cases in the literature showed 45% of cases were alive without recurrence after a mean follow-up of 45 months, 23% of cases died of systemic metastasis after a mean follow-up of 28 months, and 14% of cases died of natural causes []. The better prognosis of eyelid angiosarcomas could be related to the finding that more of the eyelid angiosarcomas being isolated, nodular tumors rather than facial angiosarcomas (51% in eyelid angiosarcomas vs. 30% in facial angiosarcomas). Careful long-term follow-up is necessary considering the high recurrence and low local control rates at 5-years follow-up.
|
[[77.0, 'year']]
|
F
|
{'18618615': 1, '17023791': 1, '15153886': 1, '30643767': 1, '26339448': 1, '20537949': 1, '20559124': 1, '18213722': 1, '9488271': 1, '24014993': 2}
|
{}
|
162,895 |
3757640-1
| 24,014,994 |
noncomm/PMC003xxxxxx/PMC3757640.xml
|
Bilateral Congenital Lacrimal Fistula in Down Syndrome
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A 3-year-old female presented with watering and mucoid discharge from both eyes and from small skin holes on both sides. She was a known case of Down's syndrome with mental retardation and delayed developmental milestones with no family history of similar complaints. On examination she had telecanthus and had typical mongoloid facies with upward slant of lateral canthus. Bilateral fistulous openings were seen inferonasal to medial canthus. Lacrimal sac regurgitation test was positive on both sides.\nEvaluation of the lacrimal system was performed under general anesthesia. The right eye had a direct fistulous tract 4.5 mm in length communicating with the lower canaliculus []. Two No. 1 Bowman's probes, one from the puncta and the other from the fistula were simultaneously guided till they touched each other. In the left eye the fistulous tract was communicating with the lower portion of lacrimal sac []. On bilateral probing, soft stops were encountered at the beginning of nasolacrimal ducts which were overcome with minimal force. Patency of the nasolacrimal duct was confirmed by syringing and retrieval of fluorescein dye from the nose on suction. Both the tracts were excised partially by performing a fusiform incision around the fistulous ostium along the skin tension lines. The tract was held with a tooth forceps and was separated from the surrounding tissue with Vannas scissors and 3/4 was excised. The base of the fistula was cauterized and no regurgitation of fluid was noted on syringing. Surrounding tissue and skin was sutured with 6-0 vicryl suture. Histopathology of the excised tracts showed duct lined by stratified squamous epithelium. At 4 months follow-up, the patient was symptom free and no fistulous openings were visible.
|
[[3.0, 'year']]
|
F
|
{'2310340': 1, '5384317': 1, '1624047': 1, '20497082': 1, '18307152': 1, '26090250': 2, '11897957': 1, '1532293': 1, '24014994': 2}
|
{'4450814-1': 1}
|
162,896 |
3757641-1
| 24,014,995 |
noncomm/PMC003xxxxxx/PMC3757641.xml
|
Acute Hydrops in the Donor Cornea Graft in Non-Keratoconus Patients
|
A 44-year-old human immunodeficiency virus positive Hispanic male with undetectable viral load presented to the clinic with a 5-week history of decreased vision, 1 year after undergoing PKP in the left eye. The patient had a history of herpes keratitis complicated by severe glaucoma in that eye. He had received a corneal transplant 2 years before for corneal decompensation. On the day of presentation, his best-corrected vision was 20/20 in the right eye and hand-motion at 6 feet in the left eye. His manifest refraction in the right eye was −3.00 + 0.50 × 148. The intraocular pressure was 15 mm Hg in the right eye. His corneal graft was very edematous, opaque, and protuberant making it impossible to measure the intraocular pressure in the left eye. The glaucoma drainage valve in the superotemporal quadrant was well-covered. There was no evidence of keratoconus in the fellow eye. Ocular coherence tomography (OCT) of the anterior segment showed a deep stromal cystic cavity consistent with hydrops in the left eye []. Ultrasound biomicroscopy (UBM) of the anterior segment revealed a Descemet's membrane detachment and severe corneal edema with stromal cystic cavities []. The patient received a repeat PKP of the left eye. During surgery, the glaucoma drainage tube was noted to be positioned close to the cornea and was trimmed under the host cornea rim. Pathology examination revealed a rupture and recoil of Descemet's membrane centrally and a near perforation with a substantial amount of corneal stromal edema, consistent with hydrops [].
|
[[44.0, 'year']]
|
M
|
{'28724824': 2, '17077671': 1, '17525669': 1, '7936572': 1, '33898858': 1, '24014995': 2}
|
{'3757641-2': 2, '5549419-1': 1}
|
162,897 |
3757641-2
| 24,014,995 |
noncomm/PMC003xxxxxx/PMC3757641.xml
|
Acute Hydrops in the Donor Cornea Graft in Non-Keratoconus Patients
|
A 91-year-old Caucasian male with a history of PKP in the right eye was referred to the clinic for descemetocele evaluation. He had a corneal transplant of the right eye originally for pseudophakic bullous keratopathy. The patient reported frequent eye rubbing. On examination, he had light perception with projection in the right eye and 20/25 best-corrected vision in the left eye. The manifest refraction in the left eye was −1.50 + 1.50 × 141. Intraocular pressure was not measurable in the right eye and was 14 mm Hg in the left eye. A very large pedunculated cyst was seen within the corneal graft in the right eye []. There was no evidence of keratoconus in the fellow eye. OCT of the anterior segment revealed a deep stromal cystic cavity consistent with the hydrops. UBM of the anterior segment showed the presence of an anterior chamber intraocular lens and a large cystic cavity with a suspected break in the superior region of Descemet's membrane. The patient subsequently received a PKP of the right eye. The anterior chamber intraocular lens was an open-loop Kelman-style and was left in place. The corneal graft was oversized by 0.5 mm. Pathology examination revealed marked central corneal edema consistent with the hydrops. Descemet's membrane was absent except for fragments on both sides of the button.
|
[[91.0, 'year']]
|
M
|
{'28724824': 2, '17077671': 1, '17525669': 1, '7936572': 1, '33898858': 1, '24014995': 2}
|
{'3757641-1': 2, '5549419-1': 1}
|
162,898 |
3757642-1
| 24,014,996 |
noncomm/PMC003xxxxxx/PMC3757642.xml
|
Oculocardiac Reflex in a Medial Orbital Wall Fracture without Clinically Evident Entrapment
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A 15-year-old male struck the left side of his head on the floor, resulting in a left medial orbital wall fracture. On computed tomography, obtained the day of injury, the adjacent medial rectus muscle was in a normal position, but was slightly rounded suggesting tethering by surrounding fibrous tissue []. Thereafter, he experienced daily 5-10 min episodes of dizziness, lightheadedness, chest pain, and nausea, typically occurring upon standing after prolonged sitting. During an emergency room visit 10 days after the injury, orthostatic blood pressures were: lying 117/54 mm Hg; standing 101/27 mm Hg, with associated nausea, lightheadedness, and visible pallor. No bradycardia was noted. The patient was diagnosed with a vasovagal reaction and anxiety. Twenty-one days after the injury he underwent a 24 h Holter monitor. Mean heart rate was 76 beats/min. One significant episode of bradycardia (heart rate 43) was documented, despite several recorded episodes of “dizziness and chest pain.” On oculoplastics examination 23 days after the injury, the patient had full extra ocular motility and was orthotropic in all fields of gaze and no diplopia. Because of the persistence of daily symptoms, the patient underwent fracture repair.\nPrior to incision, forced duction testing revealed no evidence of restriction and heart rate remained around 70 during the manipulation. Fat herniating through the bony defect was reposited into the orbit, and the defect was covered with a Medpor Titan Implant (Porex Surgical, Newnan, Georgia). The patient reported complete resolution of all symptoms immediately post-operatively and when interviewed 6 weeks later. The remainder of the examination including, motility remained normal.\nAlthough, seen with both, an oculocardiac reflex has been more commonly described with trapdoor than comminuted fractures. Trapdoor fractures most often involve the orbital floor and not surprisingly an oculocardiac reflex has most often been described in association with inferior trapdoor fractures. Medial trapdoor fractures with and without oculocardiac reflex have also been described. To our knowledge, this is the first case description of a patient with a comminuted medial wall fracture, with normal ocular motility manifesting an oculocardiac reflex.\nThe most similar previously published case that we are aware of was published by Joseph et al. in 2009. They described a patient with a large inferior orbital floor fracture with prolapsed orbital contents including the inferior rectus muscle. Despite normal extra ocular motility their patients had findings consistent with an oculocardiac reflex. Our patient differ in that the medial wall was involved and more notably the fracture was small without displacement of the adjacent rectus muscle.\nA noteworthy finding was the shape of the medial rectus muscle. On imaging the ipsilateral medial rectus muscle was slightly rounded on cross-section relative to the contralateral medial rectus muscle. This indicates that despite seemingly normal function, the muscle was under some tension. There is a very defined and extensive connective tissue network in the orbit (i.e., muscle sheaths, inter-muscular septae, Tenons’ capsule, fibrous septae within fat compartments), and it is likely that it is this connectivity resulted in tension being placed on the muscle despite not being displaced within the fracture. Subtle traction on connective tissue is presumably the source of the trigeminal stimulation responsible for the oculocardiac response.\nIn conclusion, in this report, we describe a patient with an orbital fracture presenting with vasovagal-type symptoms secondary to an oculocardiac reflex. Despite normal extra ocular motility repair led to immediate resolution of symptoms. This reinforces the guideline that even in the absence of overt muscular entrapment, non-resolving signs and symptoms of increased vagal tone in the setting of an orbital fracture are indications for surgical repair.
|
[[15.0, 'year']]
|
M
|
{'20651594': 1, '8496657': 1, '19935262': 1, '9842557': 1, '17711773': 1, '20145507': 1, '19386870': 1, '21959489': 1, '15309979': 1, '9682717': 1, '27928355': 1, '24014996': 2}
|
{}
|
162,899 |
3757776-1
| 24,014,946 |
noncomm/PMC003xxxxxx/PMC3757776.xml
|
Interesting case of G6PD deficiency anemia with severe hemolysis
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A 23 year old male patient presented with diffused pain abdomen and vomiting for two days, yellowish discoloration of urine, sclera and skin for one day, acute breathlessness for four hours, fever (100.4°F), pallor, moderate icterus, high pulse rate(124/minute), respiratory rate of 28/minute, cyanosis and reduced oxygen saturation, Hemoglobin 9.6 gm/dl, TLC 38,840/μl with neutrophilia, reticulocyte count 5%, serum bilirubin (T) 24.95 mg/dl, serum bilirubin (D) 3.43 mg/dl, serum bilirubin (I) 21.52 mg/dl , SGPT 61.39 IU/L, SGOT122.48 IU/L,GGT 39.37 IU/L, blood urea 68.62 mg/dl, S.Creatinine 0.62 mg/dl, G6PD (Qualitative)-discoloration in more than 60 minutes, urine – red/brown, negative screening for malarial parasite and dengue.\nIn Systemic Examination: Chest: Air entry diminished over bases, CVS: Normal, per Abdomen: mild distension (+) and liver was just palpable which was confirmed by ultrasonography.\nProvisional diagnosis: Sepsis with hemolytic jaundice (G6PD def)\nIntra venous Meropenam, Teicoplanin administered along with BIPAP support and O2 inhalation.\nOn day two patient’s condition deteriorated. Hemoglobin 5.4 mg/dl and total bilirubin 17.08 mg/dl, s.bilirubin (D) 4.10, s.bilirubin (I) 12.98 mg/dl. Treated with four units of leukocyte reduced packed RBCs. Hemoglobin increased to 8.0 gm/dl but patient started passing black color urine.\nRepeat blood grouping, auto control, direct and indirect coombs test were negative.\nFinal diagnosis: G6PD deficiency with hemolysis.
|
[[23.0, 'year']]
|
M
|
{'20568098': 1, '24014946': 2}
|
{}
|
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