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163,800 | 3806674-1 | 24,163,668 | noncomm/PMC003xxxxxx/PMC3806674.xml | Successful Salvage Chemotherapy with FOLFIRINOX for Recurrent Mixed Acinar Cell Carcinoma and Ductal Adenocarcinoma of the Pancreas in an Adolescent Patient | A 15-year-old boy presented in November 2009 with a 3.2-cm tumor of the head of the pancreas and multiple diffuse liver metastases (fig. ). Liver and kidney function tests were within normal limits, serum alpha-fetoprotein (AFP) was elevated (400 U/ml). Biopsy of the liver mass revealed a malignant tumor with acinar cell differentiation, bringing up the differential diagnosis of acinar cell carcinoma, or a mixed tumor with acinar cell differentiation including pancreatoblastoma.\nChemotherapy was initiated with two cycles of cisplatin and doxorubicin (PLADO regimen), resulting in a partial response of the primary tumor and the liver metastases. Based on the good response, a Whipple duodenopancreatectomy and simultaneous wedge resection of the metastases of the left liver with ligation of the right portal vein were performed in March 2010. Two additional cycles of the same chemotherapy were given postoperatively.\nThe metastases of the right liver lobe were resected by hemihepatectomy of the right liver, any other lesions in the remnant liver were removed by wedge resection. In addition, focally infiltrated parts of the diaphragm were also resected. Altogether, this accounted for a surgical tumor reduction of about 90%. A central liver lesion could not be resected due to its vessel proximity.\nSurgical pathology confirmed a mixed histology with differentiation of both, acinar cell carcinoma and ductal adenocarcinoma. Some morphologic features of the primary liver biopsy also resembled an embryonic tumor, but the pathognomonic squamoid differentiation of pancreatoblastoma was missing. One lymph node metastasis adjacent to the hepatic artery was found showing ductal differentiation. No neuroendocrine differentiation was detectable. Some tumor regression due to the preceding neoadjuvant chemotherapy was observed (fig. ). Immunostaining was focally positive for AFP in accordance with the initially elevated AFP serum levels. A diagnosis of a mixed acinar cell carcinoma/ductal adenocarcinoma was retained.\nTumor regrowth in the liver was observed on positron emission tomography/computed tomography (PET/CT) scan already 1 month after the second surgery. No tumor growth was seen in the remnant pancreas after Whipple resection. After subsequent second-line chemotherapy with two cycles of ifosphamide, carboplatin and etoposide (ICE regimen), a partial remission of the liver lesions was documented.\nA living donor liver transplantation (right hemiliver) from his brother was performed in November 2010. Due to a severe bile leak with abscess formation and finally hepatic artery thrombosis, the graft had to be replaced with a cadaveric liver graft after 10 days. Afterwards, the patient achieved complete recovery and was disease free. Immunosuppression with prednisone and tacrolimus was initially established. The former was subsequently tapered within 3 months, and tacrolimus was changed to everolimus.\nIn April 2011, multiple new lung metastases were detected while no tumor relapse was seen in the abdomen. Therefore, in May 2011 a new chemotherapy treatment with oxaliplatin, irinotecan, leucovorin and 5-fluorouracil (FOLFIRINOX regimen) was started. The new treatment was tolerated well apart from neutropenia and thrombocytopenia up to grade 4, resulting in dose reductions of the applied compounds. After six biweekly cycles, PET/CT showed a complete metabolic and partial morphologic remission of all lung lesions (fig. ).\nDue to the excellent response to FOLFIRINOX, we decided to consolidate with tandem high-dose chemotherapy using carboplatin, etoposide and paclitaxel as conditioning regimen with subsequent autologous stem cell transplantation (ASCT). Hematopoietic progenitor cells were successfully mobilized with filgrastim, and high-dose chemotherapy was performed in November 2011 and February 2012. Due to transiently elevated liver enzymes after the first high-dose treatment, etoposide was omitted in the second treatment to reduce the toxicity for the transplanted liver.\nIn August 2012, a progression of the pulmonary lesions was documented in a routine follow-up PET/CT. Treatment with FOLFIRINOX was once again initiated, resulting in a very good metabolic and morphologic remission after another six cycles until December 2012. Chemotherapy was continued for 3 additional months. While all lesions except one remained responsive to the treatment, the latter lesion was treated with stereotactic irradiation using 3 × 12 = 36 Gy.\nAs of today, the patient has a sustained metabolic remission of the known lung lesions and no new lesions developed with repeated use of FOLFIRINOX. He is currently in excellent general condition and has no limitations of his quality of life. | [[15.0, 'year']] | M | {'17575544': 1, '27857025': 1, '21561347': 1, '21696948': 1, '23217876': 1, '12488412': 1, '17331695': 1, '23741195': 2, '19159743': 1, '29052123': 1, '9673563': 1, '15960930': 1, '20632017': 1, '12037756': 1, '16516645': 1, '20658635': 1, '32879662': 1, '20182344': 1, '24163668': 2} | {'3672127-1': 1} |
163,801 | 3806675-1 | 24,163,646 | noncomm/PMC003xxxxxx/PMC3806675.xml | Induction of Eosinophilic Esophagitis by Sublingual Pollen Immunotherapy | A 44-year-old female presented at our center with increasing dysphagia for 4 weeks. At the time of presentation, she reported having dysphagia for the first time in her life which occurred every day. Prior to this episode, the patient had never experienced any esophageal symptoms. Difficulties with swallowing required her to adapt her eating habits such as drinking liquids after swallowing food (dysphagia score 7 on a scale from 0 to 9). Her medical history revealed pollinosis since childhood and additional allergic asthma at the age of 22 years which improved for several years after subcutaneous immunotherapy. A deterioration occurred at the age of 42 years. At this time a total serum IgG of 757 U/ml was documented. Prick testing and specific serum IgE identified grass, rye, hazelnut, birch alder and oak as major allergens. Her family history was positive for pollinosis (mother and brother).\nFour weeks before the onset of dysphagia, the patient had begun SLIT with ORALVAC Compact (Bencard Allergie GmbH, Munich, Germany), a commercially available treatment considered to be safe []. The SLIT contained specific soluble allergens (hazelnut, birch, alder) according to previous specific serum IgE testing, administered sublingually as prescribed by the manufacturer's instructions. Upper endoscopy showed confluent whitish exudates and longitudinal red furrows in the proximal and the distal esophagus (fig. ). Biopsies from these lesions revealed a predominantly eosinophilic inflammation with a peak infiltration of 164 eosinophils per high power field (fig. ), which confirmed the diagnosis of EoE. Immediately after upper endoscopy, the patient discontinued SLIT, which led to complete resolution of dysphagia within 4 weeks without any other medical intervention. A follow-up endoscopy 4 weeks after withdrawal of SLIT demonstrated a macroscopically normal esophagus (fig. ). Biopsies from the proximal and distal esophagus revealed normal mucosa without any eosinophilic inflammation (fig. ). During a follow-up of 12 months the patient remained free of any esophageal symptoms. | [[44.0, 'year']] | F | {'29356936': 1, '33207848': 1, '33204114': 1, '29676066': 1, '31058677': 1, '33016307': 1, '26552776': 1, '34639170': 1, '29332138': 1, '21195949': 1, '30364207': 1, '31616174': 1, '22236725': 1, '27103556': 1, '29617351': 1, '31748971': 1, '25789989': 1, '34947981': 1, '26059636': 1, '8749233': 1, '34059605': 1, '29413330': 1, '30855279': 1, '28154800': 1, '23532243': 1, '23799220': 1, '29680987': 1, '19925501': 1, '21477849': 1, '30032346': 1, '30201096': 1, '22391333': 1, '27000314': 2, '22310220': 1, '22921871': 1, '32469176': 1, '7603570': 1, '26855813': 1, '29909507': 1, '16792600': 1, '22994460': 1, '15087094': 1, '30903437': 1, '29980277': 1, '28822054': 1, '24803874': 1, '28774845': 1, '29545433': 1, '34809686': 1, '24163646': 2} | {'4802852-1': 1} |
163,802 | 3806676-1 | 24,163,672 | noncomm/PMC003xxxxxx/PMC3806676.xml | New-Onset Refractory Status Epilepticus Mimicking Herpes Virus Encephalitis | A 41-year-old man presented with a parainfectious syndrome characterized by low-grade fever and vomiting. Within 3 days, he experienced increasingly complex partial epileptic seizures, rapidly changing from tonic-clonic seizures to generalized SE, requiring intubation and admission to the intensive care unit. The patient had borderline intellectual functioning, possibly the expression of very mild perinatal posthypoxic encephalopathy. Clinical testing at the time of admission (as compared with neuroimaging and electroenchephalograpic studies which had been performed when the patient was a child) did not disclose any anatomic brain changes, pathology, or abnormal electric activity. No seizures were ever reported until the onset of SE.\nThe neurological examination, performed in the intensive care unit, revealed no cranial nerve or focal changes, or meningism. Because first-line anticonvulsants were not able to achieve the clinical remission of SE, intravenous anesthetic anticonvulsants were required. Intravenous infusions of propofol or thiopental were used to maintain the patient in an electrographic burst-suppression pattern, while enteral antiepileptic medications were titrated to therapeutic doses (e.g. valproic acid, clobazam, topiramate, phenobarbital, carbamazepine, and levetiracetam) [, ]. Extensive laboratory analyses, including virological, immunological, paraneoplastic, mitochondrial and endocrine tests were performed on blood and CSF with no evidence of infectious, inflammatory, mitochondrial, autoimmune, neoplastic and paraneoplastic pathology. No elevated proteins or pleocytosis were detected in CSF. Brain MRI, carried out 3 days after SE onset, showed signal hyperintensity of the temporal lobe bilaterally and symmetrically in T2 and FLAIR sequences, with involvement of both the cortex and white matter, deep into the hippocampus and pulvinar (fig. ). Signs of laminar necrosis were detected in the superior and medium temporal giri bilaterally (fig. ). Magnetic resonance diffusion-weighted images, including apparent diffusion coefficient mapping, permitted us to identify the presence of vasogenic edema (fig. ). Although some brain MRI findings strongly suggested herpes simplex virus (HSV) encephalitis (i.e. topography of lesions and cortical involvement), the absence of MRI signs of parenchymal hemorrhagic necrosis along with the absence of pleocytosis and hyperproteinorrachia in CSF and viral HSV1 and HSV6 RNA in blood and CSF did not permit the confirmation of that diagnosis. Therefore, a presumptive diagnosis of encephalitis with SE was considered, and acyclovir was empirically added to antibiotics (ceftriaxone, vancomycin) and steroids.\nDuring the following days, each time the tapering of the maximal dose of intravenous anesthetic anticonvulsants was tried, SE began again. Follow-up brain MRI studies, performed within 4 weeks, demonstrated an unvaried neuroradiological picture, but with a reduction of vasogenic edema in the temporal lobes (fig. ) and more evident involvement of the pulvinar bilaterally (fig. ).\nThe patient died 41 days after the onset of SE and an autopsy was not performed. Written informed consent could not be obtained from the deceased patient. Nonetheless, we acquired written informed consent from the patient's parents for the publication of this case report and the accompanying images. | [[41.0, 'year']] | M | {'21883180': 1, '18486818': 1, '20028339': 1, '12892002': 1, '16469483': 1, '25580311': 2, '22004046': 1, '8304844': 1, '19013586': 1, '17369598': 1, '17370636': 1, '20345937': 1, '20308685': 1, '15832606': 1, '12915084': 1, '24163672': 2} | {'4281438-1': 1} |
163,803 | 3806677-1 | 24,163,680 | noncomm/PMC003xxxxxx/PMC3806677.xml | Pattern Dystrophy of the Macula in a Case of Steinert Disease | A 41-year-old Hispanic female diagnosed with type 1 myotonic dystrophy (Steinert disease) was referred for ophthalmologic examination with the chief complaint of progressive vision loss. Her best-corrected visual acuity was 20/32 in her right eye and 20/40 in her left eye. Ocular motility was normal. She had bilateral ptosis with abnormal elevator function. Slit lamp examination revealed the presence a bilateral polychromatic cataract with posterior subcapsular component.\nDilated fundus examination was remarkable for macular pigmentary changes with multifocal yellowish depigmented patches within the macular area in both eyes (fig. ). Fundus autofluorescence highlighted a branching linear pattern of mixed hyper- and hypoautofluorescence limited to the macular area in both eyes (fig. ).\nOptical coherence tomography images showed diffuse subretinal hyperreflective material between the photoreceptor layer and the RPE in both eyes. Larger focal vitelliform lesions were also evidenced. No subretinal or intraretinal fluid was found in association with the deposits (fig. ). | [[41.0, 'year']] | F | {'20447109': 1, '18808764': 1, '20176601': 1, '15370544': 1, '20346890': 1, '22411247': 1, '2037285': 1, '8337494': 1, '23411896': 1, '19568364': 2, '22892517': 1, '34051736': 2, '1546325': 1, '24163680': 2} | {'2694290-1': 1, '8164789-1': 1} |
163,804 | 3806678-1 | 24,163,655 | noncomm/PMC003xxxxxx/PMC3806678.xml | Unusual Images of Mass-Forming Intrahepatic Cholangiocarcinoma | A 78-year-old Japanese woman, with no particular physical indications like abdominal pain, generalized itching, weight loss, fever or jaundice, who was incidentally found to have changes in liver function tests, particularly an elevated level of alkaline phosphatase (368 U/l), was admitted to our hospital for investigation and treatment. She had no history of HBV or HCV infection or of excessive alcohol intake.\nUltrasonography revealed a solid liver tumor. Computed tomography also showed a large, heterogeneous and hypovascular tumor in the anterior segment; the tumor margin was smooth, clear and demonstrated ring enhancement and low density within the tumor both in early and delayed phase, suggesting degeneration, necrosis or a cystic lesion inside the tumor. Magnetic resonance imaging confirmed the presence of a mass lesion that was isointense on T1-weighted images and minimally hyperintense on T2-weighted images, with slightly lower intense fringe. The tumor was hyperintense on diffusion-weighted imaging. After the injection of intravenous contrast, the T1-weighted image showed peripheral ring enhancement on both early (fig. ) and delayed phases.\nEnhanced magnetic resonance imaging showed that the tumor border was obvious; the tumor was isointense on T1-weighted imaging and showed slightly higher intensity than round on T2-weighted imaging and high intensity on diffusion-weighted imaging (fig. ).\nContrast-enhanced ultrasonography showed a tumor with isoechoic or mixed pattern; a dynamic study showed pycnomorphous tumor margin in the early phase, and the center of the tumor was heterogeneous and hypoechoic in the late phase. Defect re-perfusion imaging showed that the solid part of the tumor was hypervascular (fig. ). 3D volumetric analysis showed that the total liver volume was 1,041 ml (right lobe 660 ml, left lobe 381 ml); the tumor volume was 24 ml (fig. ).\nLaboratory testing showed normal liver enzymes, except for ALP (368 U/l): AST 18 U/l, ALT 15 U/l, total bilirubin 1.0 mg/dl and direct bilirubin 0.1 mg/dl. Complete blood count was normal (WBC 7,100/μl, RBC 4.30 × 106/μl, PLT 343 × 103 and INR 1.0). Tumor markers were all within normal limits, e.g. CEA 4.2 ng/ml, CA19-9 14 U/ml, AFP 3 ng/ml, PIVKA-II 21.0 mAU/ml, etc.\nAlthough the laboratory and radiological findings were not typically pathognomonic for any specific hepatic tumor, the lesion was resected on the basis of a high degree of suspicion for malignancy and submitted for pathologic evaluation. Grossly, a 5.5 × 4.0 × 3.0 cm well-defined and non-encapsulated solid mass was identified (fig. ). Microscopically, the neoplasm was a moderately differentiated adenocarcinoma with abundant fibrous stroma, consistent with a mass-forming CC (fig. ). The patient's postoperative course was generally unremarkable. | [[78.0, 'year']] | F | {'16397610': 1, '10489176': 1, '15185025': 1, '19750567': 1, '11045707': 1, '16214602': 1, '11373220': 1, '8000995': 1, '2834769': 1, '1329455': 1, '12063953': 1, '12933488': 1, '15218306': 1, '24163655': 2} | {} |
163,805 | 3806679-1 | 24,163,653 | noncomm/PMC003xxxxxx/PMC3806679.xml | Infected Walled-Off Pancreatic Necrosis following EUS-Guided Drainage Successfully Treated Using Multiple Stents in Different Sites Technique | We experienced the case of a 40-year-old female who was referred and diagnosed with a WOPN sized 13 × 9 × 7.4 cm that developed 2 weeks after an episode of acute severe pancreatitis. She was initially admitted due to acute severe epigastric pain. Her blood workup showed leukocytosis 2.73 × 103/µl (reference range 4.0–11.0 × 103/µl) with 91% neutrophils (reference range 40–74%) and serum amylase 1,309 U/l (reference range 0–220 U/l); liver chemistry showed total bilirubin 1.9 mg/dl (reference range 0.3–1.2 mg/dl), direct bilirubin 0.5 mg/dl (reference range 0.0–0.5 mg/dl), AST 126 U/l (reference range 0–40 U/l), ALT 343 U/l (reference range 0–40 U/l) and alkaline phosphatase 104 U/l (reference range 32–92 U/l). She underwent endoscopic retrograde cholangiopancreatography which showed only common bile duct sludge. She did not need intensive care but developed high-grade fever with abdominal pain 14 days after admission. A CT scan showed pancreatic necrosis with fluid collection at the pancreatic body. She had high-grade fever even after intravenous antibiotics for another 7 days. She underwent EUS-guided drainage with a 10 Fr × 7 cm double pigtail stent, and prophylactic antibiotics were prescribed for 7 days.\nHowever, she was re-admitted 1 week later because of severe abdominal pain and sepsis. A CT scan of the upper abdomen showed enlargement of the pancreatic collection to 15 × 7 × 14.5 cm with increased enhancement of the rim, septation and some air inside (fig. ). She was scheduled for repeat EUS-guided drainage of the infected WOPN. The procedure was performed with the patient in the left lateral decubitus position using a curvilinear echoscope (GF UC-140P, Olympus, Tokyo, Japan). Endoview showed a partially clogged stent (fig. ) and echoview showed a large collection with turbid content and some air inside (fig. ). We punctured the abscess using a 19-gauge needle (EchoTip® Ultra, Cook Ireland, Limerick, Ireland) at a different site under EUS guidance. The aspirated fluid was noted grossly to be purulent and was sent for culture. After contrast injection, 8.5 and 10 Fr tapered tip Teflon catheters were used for dilatation, and a 10 Fr × 7 cm double pigtail stent was subsequently inserted. Since the collection was multiseptated with thick and turbid pus, we decided to place two additional stents into the abscess for better drainage via a different puncture site using the same technique (fig. ). The patient received an extended course of intravenous antibiotics and was discharged after 33 days of hospitalization without complications. A follow-up MRI 6 weeks later showed only a small pancreatic fluid collection (fig. ). | [[40.0, 'year']] | F | {'21612778': 1, '18563416': 1, '21274380': 1, '19691744': 1, '17522520': 1, '18291387': 1, '17095841': 1, '24163653': 2} | {} |
163,806 | 3806680-1 | 24,163,661 | noncomm/PMC003xxxxxx/PMC3806680.xml | Displacement of Malignant Cells into the Portal Triad of the Liver Results in Reduced Liver Perfusion, Mimicking Segmental Fatty Liver | We report the case of a 69-year-old male patient who was suffering from a right-sided non-small cell bronchial cancer. The initial PET/CT showed a localized tumor in the right upper lung with 1 PET-positive lymph node in the right and left hili (R 10, L 10), which was confirmed histologically after transbronchial biopsy. There was also 1 histologically proven bone metastasis in the right iliac bone, but no signs of further distant metastasis in the liver or abdomen. The initial stage was cT3, cN3, M1. EGF receptor and K-ras mutation were negative. At the onset of the known disease 4 months earlier, the liver, especially in a routine CT scan, showed no pathological signs or liver metastasis (fig. ). The patient was treated with systemic chemotherapy and was in a generally good condition. Four months later, a sudden elevation of liver enzymes was documented, while 4 months earlier they had been within the normal range. There was an elevation of serum lactate dehydrogenase (636 U/l), carcinoma embryonic antigen (147 U/l), Y-GT (741 U/l) and alkaline phosphatase (645 U/l). At this time, the patient showed no sign of clinical symptoms, especially in the abdomen. A repeat CT of the abdomen was performed in order to investigate the elevation of the liver enzymes. Segmental hypointensity was found in the venous phase in segments 5 and 6, without any occlusion of the central portal vein and hepatic artery (fig. ). A precontrast scan was not performed, but the density in the portal venous phase was 32 Hounsfield units. Our first suspicion was inhomogeneous liver steatosis, but the distribution of this change was atypical and looked bizarre. Having doubts, we performed an ultrasound scan with the application of a contrast medium. The normal B-mode ultrasound shows discrete hyperechogenic regions (fig. ). The additionally performed power Doppler showed reduced vessels in the periphery of segments 5 and 6 (fig. ). After applying a contrast medium, there were clear signs of perfusion deficiency in the early arterial phase without washout in the late phase (fig. ). Because we had problems in making a definitive diagnosis, a core biopsy was performed within this area.\nTo our surprise, histology showed infiltration of the portal triad, which surrounds small portal veins and the hepatic artery within the portal triad. There were also some small metastatic cells within the small portal veins (fig. ). There were no signs of classical liver metastasis or steatosis. Chemotherapy was intensified, but the local changes in the liver did not change at any time, as documented by subsequent CT scans. | [[69.0, 'year']] | M | {'11961152': 1, '9547102': 1, '6934563': 1, '19238392': 1, '16100085': 1, '17402991': 1, '17102041': 1, '21318585': 1, '1393413': 1, '24163661': 2} | {} |
163,807 | 3806681-1 | 24,163,660 | noncomm/PMC003xxxxxx/PMC3806681.xml | Management of Two Cases of Recurrent Anal Carcinoma | A 58-year-old female presented for consultation at our center with a prior medical history of recurrent anal/rectal carcinoma first diagnosed 3 years earlier when a poorly differentiated infiltrating squamous cell carcinoma at the distal anorectal junction was found during colonoscopic evaluation performed to investigate symptoms of pain, bleeding and poor bowel function unresponsive to laxative treatment of 5 months’ duration. The patient tested negative for human papilloma virus (HPV). The first recurrence 9 months later presented as an infiltrating poorly differentiated squamous cell carcinoma in the anorectal resection specimen. Lymph nodes and resection margins were negative. A biopsy of a 2-cm mass 11 months later revealed a second local recurrence of a keratinizing and nonkeratinizing anal carcinoma with basilar features. A positron emission tomography-computed tomography (PET-CT) scan of the pelvic/abdominal region revealed a new opaque mass at the anorectal junction with increased focal activity consistent with local recurrence of a primary anal carcinoma. Pathology reports at the time of the second recurrence revealed malignant metastatic squamous cell carcinoma of the anus and left retroperitoneal lymph node. The patient was staged as T2, N1 based on endoscopic ultrasound examination.\nTreatment included chemoradiation therapy and concomitant cisplatin/capecitabine at the time of initial diagnosis followed by anal resection at the first recurrence. Cisplatin/capecitabine was repeated following gamma knife surgery of the anus at the time of the second recurrence.\nWhen presenting to our center 1 year following the second recurrence, a third recurrence was suspected. A CT-guided periureteral core biopsy obtained 6 months after the initial consult confirmed the presence of a third recurrence presenting as poorly differentiated squamous cell carcinoma. The patient had additionally developed ambulatory difficulty and was dragging her left foot. Her performance status was rated as ECOG 3. An MRI revealed a small disk herniation at C6–C7 and bulging disks at L3–L4 and L4–L5 but no evidence of metastasis, and the differential diagnosis at the time was sacral plexopathy following an electromyogram study. Leg pain was eventually diagnosed as secondary to foraminal disk herniation at L3–L4 exerting compression on the exiting L3 nerve.\nThe patient was treated with radiation therapy for the second time (concurrent with weekly carboplatin). There was a short interval of response observed by PET scan, but after 3 months further evidence of disease progression was demonstrated.\nMolecular profiling was performed on the initial pathology specimen at diagnosis. The patient expressed a wild-type genotype for K-RAS and BRAF, no epidermal growth factor receptor (EGFR) amplification by fluorescent in situ hybridization analysis, high RRMI expression by immunohistochemistry, low PTEN expression by immunohistochemistry, and ERCC-1 underexpression by immunohistochemistry.\nApproximately 3 months after the chemoradiation with carboplatin and after discussion with the patient who wished to pursue an ‘aggressive approach’ to her cancer management, treatment with irinotecan plus cetuximab was initiated. The regimen was reasonably well tolerated with occasional mild diarrhea and a stable rash. Imaging studies revealed stable disease and the treatment was continued for a total of 4 cycles followed by observation. However, when there was radiographic evidence of disease progression 2 months later, the treatment program was reinitiated for several additional cycles. Of note, the time to subsequent disease progression after the documentation of a third recurrence of the anal carcinoma was 17 months. Unfortunately, with progression the patient experienced a decline in her performance status, was referred to a hospice and eventually succumbed to the disease. | [[58.0, 'year']] | F | {'15217974': 1, '9164216': 1, '21095071': 1, '8823332': 1, '18430910': 1, '12599225': 1, '19336010': 1, '8256774': 1, '17925552': 1, '17252287': 1, '12453851': 1, '8424915': 1, '29147423': 2, '22295202': 1, '20459770': 1, '24908401': 1, '11669560': 1, '19474385': 1, '8874455': 1, '22436791': 1, '16763788': 1, '19923868': 1, '12788191': 1, '24163660': 2} | {'3806681-2': 2, '5649953-1': 1, '5649953-2': 1} |
163,808 | 3806681-2 | 24,163,660 | noncomm/PMC003xxxxxx/PMC3806681.xml | Management of Two Cases of Recurrent Anal Carcinoma | A 64-year-old female presented to our center at the time of her third recurrence with a 6-year prior history of anal carcinoma. At this time, her ECOG score was 1. Her primary tumor had initially been treated with concurrent chemoradiation, mitomycin C and 5-fluorouracil (5-FU) and staged as T3NXMX. Notably, the tumor was negative for HPV. Recurrence in the right groin was noted 10 months later and managed with 7 months of cisplatin plus paclitaxel chemotherapy. She remained free of disease for approximately the next 5 years, but subsequently experienced a second recurrence in the right groin (pathology confirming poorly differentiated squamous cell carcinoma). Surgical resection was performed, with the patient experiencing a complication of deep venous thrombosis.\nUnfortunately, PET-CT scan demonstrated evidence of another recurrence. Further surgery and radiation were not believed to be good options at this time, and after extensive discussions the patient was treated with the combination of irinotecan plus cetuximab. Although she experienced morbidity (diarrhea, bone marrow suppression) of the treatment and advanced disease process (cellulitis, constipation), she remained without evidence of progression of the cancer for 14 months following the initiation of irinotecan plus cetuximab.\nAt this point, the patient was treated with additional local radiation, maintaining a stable clinical state for approximately 11 months.\nPemetrexed was subsequently initiated, based on a molecular profiling study which revealed that the tumor exhibited low expression of thymidylate synthetase. The patient continued on this agent with stable disease for 9 months until evidence of disease progression was demonstrated. | [[64.0, 'year']] | F | {'15217974': 1, '9164216': 1, '21095071': 1, '8823332': 1, '18430910': 1, '12599225': 1, '19336010': 1, '8256774': 1, '17925552': 1, '17252287': 1, '12453851': 1, '8424915': 1, '29147423': 2, '22295202': 1, '20459770': 1, '24908401': 1, '11669560': 1, '19474385': 1, '8874455': 1, '22436791': 1, '16763788': 1, '19923868': 1, '12788191': 1, '24163660': 2} | {'3806681-1': 2, '5649953-1': 1, '5649953-2': 1} |
163,809 | 3806682-1 | 24,163,671 | noncomm/PMC003xxxxxx/PMC3806682.xml | Growing Evidence about the Relationship between Vessel Dissection and Scuba Diving | A 52-year-old-man presented with headache and homolateral Horner's syndrome which had started 4 weeks previously.\nOn the day after scuba diving in cold water, the patient complained of a considerable and persistent neck pain which irradiated towards the left retroocular region. On the following morning, a left-sided facial edema appeared and lasted for a few days. The persistence of the headache, ptosis and miosis, which increased with the worsening of the neck pain, led the patient to seek a neurological evaluation. The examination revealed only the presence of an incomplete Claude Bernard-Horner syndrome (CBHS). Ultrasonography (US) of the carotid arteries did not show plaques or stenosis of the vessels. The fluid dynamic and velocity were normal. A chest X-ray was performed and revealed the presence of a thickening of the right pulmonary apex and several little nodules in the homolateral superior lobe, which were firstly attributed by the radiologist to an expression of a possible old lesion.\nThe patient's past medical history was characterized by benign arterial hypertension treated with Enalapril (20 mg/day), benign prostatic hypertrophy, tension headache attacks and bronchopneumonia at a young age. In his family, his father had died due to pulmonary cancer; his mother and his younger brother were in good health. He had a 19-year-old son with no medical problems.\nFour weeks after the beginning of the symptoms, the patient was admitted to our department. The neurological examination showed a left Horner's syndrome, with normal direct and consensual response to the light stimulus, and no signs of either fatigability or diplopia in any direction of gaze (fig. ). He also presented with a dysesthesic area in the left side of the head, particularly in the parietal and frontal regions, without a clear distribution in the territory of the V cranial nerve innervation. A left-sided deviation of the tongue, when protruded, was also detected (fig. ). No other neurological alterations were found. Head and neck pain had disappeared.\nA head CT scan was performed, but no abnormalities were detected. Because of the persistence of an incomplete CBHS and the family history of lung cancer, in order to exclude the presence of malignancy, we discussed the chest X-ray findings with a lung specialist, who confirmed the hypothesis that the right lobe nodules were scars of a previous disease. Since these lesions were also contralateral to the CBHS, no further investigations were carried out during hospitalization. A follow-up was recommended.\nThe ophthalmologic evaluation showed only a slight increase of the left eye tone and confirmed the presence of anisocoria with miosis in the left eye.\nDespite the normal US findings, we performed brain and vascular magnetic resonance imaging (MRI), aiming at a better investigation of both intra- and extracerebral circulation and potential parenchymal ischemic lesions. The examination did not show any infarctions. Otherwise, MRI revealed a dissection of the ICA in the precarotid region associated with a pseudoaneurysmatic deformation (fig. ). An aneurysm at the bifurcation of the left middle cerebral artery was also found. Cardiac disease could be excluded by echocardiogram.\nThe patient was treated with anticoagulant therapy (Aspirin 100 mg/day). In a follow-up brain and vessel MRI 1 month later (therefore, 2 months after the beginning of the symptoms), a slight decrease of both the dissection and the pseudoaneurysmatic lesion of the left ICA could be detected (fig. ). Parenchymal lesions were never visible. | [[52.0, 'year']] | M | {'20385736': 1, '12580717': 1, '12670119': 1, '169444': 1, '7802358': 1, '8757037': 1, '19557495': 1, '15228893': 1, '22301716': 1, '31008325': 1, '22218053': 1, '19200713': 1, '21282505': 1, '11596791': 1, '20798911': 1, '19017557': 1, '20655684': 1, '14586598': 1, '9251862': 1, '21364358': 1, '5135496': 1, '16373650': 1, '15984390': 1, '24163671': 2} | {} |
163,810 | 3806683-1 | 24,163,675 | noncomm/PMC003xxxxxx/PMC3806683.xml | Changes in Optical Coherence Tomography Findings in Acute Zonal Occult Outer Retinopathy | A 39-year-old Japanese woman presented with a complaint of photopsias and central scotoma in her right eye. Best corrected visual acuity (BCVA) was 0.7 and 1.2 in her right and left eyes, respectively. Intraocular pressure was 16 mm Hg in each eye. The patient had no specific past medical history. No inflammatory cells were observed in the anterior segment or vitreous of either eye, and there were no specific abnormal findings during a fundus examination (fig. ).\nOCT (RS-3000; Nidek, Japan) showed that while there was attenuation of the IS/OS line throughout the entire region of her right eye and the COST line (fig. ), no specific abnormalities were detected in her left eye (fig. ). mfERG (LE-4100; Tomey, Japan) findings showed markedly decreased amplitudes in the right eye (fig. ) and no abnormalities in the left eye (fig. ). The patient was followed without any treatment. BCVA improved to 0.9 in the right eye and OCT revealed there was no recovery of the IS/OS at the foveal area at 1 month after the initial visit (fig. ). After 2 months, BCVA improved to 1.2 in the right eye and OCT showed a partial restoration of the IS/OS line (fig. ); however, the COST line was still absent, and she had no change in mfERG findings. At 4 months, reappearance of the IS/OS line was detected by OCT (fig. ). However, the COST line was still absent, and she showed no improvement in the mfERG findings. Fluorescein angiography and indocyanine green angiography were not available in this case. | [[39.0, 'year']] | F | {'22105799': 1, '18385077': 1, '18439564': 1, '22125531': 1, '10636684': 1, '20661173': 1, '30042791': 1, '21503168': 1, '21056448': 1, '22402912': 1, '21966193': 1, '17846358': 1, '18778338': 1, '19684865': 1, '23467270': 1, '27755372': 1, '12208243': 1, '24163675': 2} | {} |
163,811 | 3806685-1 | 24,163,657 | noncomm/PMC003xxxxxx/PMC3806685.xml | Proliferating Trichilemmal Tumor: A Case on the Nose of a 70-Year-Old Man | A 70-year-old white man, born in Buenos Aires, Argentina, visited for a consultation about a localized swelling on the tip of his nose and an external orifice with serosanguineous discharge (fig. , fig. ). Our initial hypothesis was a furuncular myiasis, since the patient had been to a rural area and had lived in a heavily wooded area with a plantation. The patient was treated with a single dose of 18 mg ivermectin, which was repeated 1 week later.\nWhen he returned 2 months later, his clinical status was unchanged. Although it did not look like a sebaceous cyst, the orifice produced a sebaceous secretion. At this point, an excisional biopsy was performed, removing a large part of the lesion followed by curettage. Histopathology showed follicular hyperkeratosis and, in the dermis, prominent sebaceous glands, telangiectasic capillaries, and a diffuse mononuclear inflammatory reaction. Also, a ‘cystically’ dilated infundibular structure was observed, whose wall showed squamous cell proliferation with wide eosinophilic cytoplasm, pleomorphic nuclei, and prominent nucleoli as well as extensive dyskeratosis-forming masses of cells with areas of necrosis. This histopathological picture was interpreted as suggestive of adnexal neoplasia with pilar differentiation and a possible proliferating epidermoid cyst (fig. , fig. , fig. ).\nThe lesion had already relapsed 45 days later, and another surgery was performed (fig. ). This time, part of the alar cartilage was removed and the reconstruction was done with a dorsal nasal flap. Histopathology showed a complete excision of the lesion. The patient has been monitored since then without a recurrence of the lesion (fig. ).\nAfter the last surgery, prostate cancer was diagnosed, and the patient was submitted to radical prostatectomy and radiotherapy. After this surgery, he suffered from deep vein thrombosis and needed to take anticoagulants. He also had intestinal cancer, making the removal of 25 cm of the large bowel necessary. One year before the appearance of these 2 malignant tumors, the patient had developed a severe mental depression due to his mother's ill health and eventual death. | [[70.0, 'year']] | M | {'22068807': 1, '17760602': 1, '4181052': 1, '23197215': 2, '31579496': 2, '31644620': 1, '22470211': 2, '31750191': 1, '15841643': 1, '5938217': 1, '24163657': 2} | {'3699925-1': 1, '6755257-1': 1, '3312659-1': 1} |
163,812 | 3806686-1 | 24,163,682 | noncomm/PMC003xxxxxx/PMC3806686.xml | Reverse Optic Capture to Stabilize a Toric Intraocular Lens | A 38-year-old woman, with no known cause for premature cataract apart from a family history of early cataract surgery, underwent cataract extraction in the left eye with implantation of a 1-piece acrylic toric IOL (SN6AT4; Alcon Laboratories, Inc.), with a power of +17 D sphere, 2.25 D (IOL plane), and 1.55 D (corneal plane) toric power. She had undergone cataract surgery with spherical foldable IOL implantation in the right eye 1 year before. Apart from an immature cataract in the left eye, the rest of the ocular examination was unremarkable.\nThe preoperative manifest refraction in the left eye was −0.75 −1.25 × 148°. Her preoperative axial length was 24.8 mm and her keratometry values were 42.99 @ 158° and 44.76 @ 68° (1.77 D cyl) as measured by the IOL Master. According to the Acrysof IQ IOL calculator (), the recommended axis of implantation was 64° using a superior incision with zero-induced cylinder.\nPreoperatively, the horizontal axis was marked by the surgeon using a fine-tipped sterile marking pen under topical anesthesia (Surgeons marking pen 115; Medical Action Industries, Inc.). The marking was made at the 3 and 9 o’ clock positions on the limbus with the patient seated at the slit lamp, ensuring the 2 eyes were level with no head tilt. The 64° axis was marked under the operating microscope using the Cionni Reverse Bevel Mendez Fixation Ring (Mastel Precision). She underwent phacoemulsification under topical anesthesia using the chop divide and conquer technique through a superior conjunctiva sparing scleral tunnel incision []. A toric IOL was implanted with the axis aligned to 64°. After all the viscoelastic was aspirated the anterior chamber was reformed with balanced salt solution (BSS; Alcon Laboratories, Inc.), the wound and the paracentesis were hydrated, and the intraocular pressure brought to normal. The IOL was confirmed again to be at the 64° axis.\nOn the first postoperative day, the patient's uncorrected visual acuity was 20/70 with a manifest refraction of +0.75 −2.25 × 143°. The axis of IOL rotation was measured with pupils dilated using the slit lamp method with a thin slit beam aligned along the axis markings of the IOL, and also with an internal OPD map on the OPD-Scan refractive power/corneal analyzer system (Nidek). The axis of the IOL had rotated to 135°. The dilated OPD-Scan refraction showed an internal astigmatism of −1.41 at 120°. (fig. ). Because of the large degree of IOL rotation and refractive error, it was decided to not wait for capsule contraction before surgically repositioning the IOL. The repositioning procedure was done on the fifth day postoperatively. | [[38.0, 'year']] | F | {'21700100': 1, '19969211': 1, '14967291': 1, '18812110': 1, '30323689': 2, '30555960': 1, '21241943': 1, '19545827': 1, '20692553': 1, '23522584': 1, '24163682': 2} | {'6173176-1': 1} |
163,813 | 3806689-1 | 24,163,659 | noncomm/PMC003xxxxxx/PMC3806689.xml | Complete Response to Trastuzumab-Based Chemotherapy in a Patient with Human Epidermal Growth Factor Receptor-2-Positive Metastatic Salivary Duct Carcinoma ex Pleomorphic Adenoma | A 74-year-old man noticed a hard, painless mass in his right parotid gland 2 months before his initial visit to our institution. His past medical history included prostate cancer, which was treated with definitive radiotherapy 2 years and 8 months ago. There was no evidence of facial nerve paralysis. Fine-needle aspiration biopsy findings of the parotid mass were consistent with those of CXPA. Positron emission tomography (PET)-computed tomography (CT) revealed an enhanced mass in the right parotid gland, without enlarged cervical lymph nodes. A total right parotidectomy along with right neck dissection and facial nerve reconstruction using cervical nerves was performed. Macroscopically, the tumor measured 25 × 17 mm at its largest dimensions and had a cartilage-like whitish cut surface with focal invasion of the surrounding fat tissue (fig. ). The mass consisted of broad hyaline tissue with nests of tumor cells (fig. ). At least two tissue components were identified: high-grade carcinoma with a cribriform growth pattern and comedo-like necrosis in the nests and slit-like tubular epithelium with myoepithelial cells at the base (fig. ). CXPA with a predominant SDC component was diagnosed on the basis of the presence of a cartilaginous, hyaline, nodular background and benign pleomorphic adenoma in the nodule.\nCT performed 4 months after a radical surgery revealed recurrence in the right cervical nodes, which was treated by right neck dissection. The recurrent tumor was histologically diagnosed as SDC (fig. ). The primary tumor was positive (score 3+) for membrane-localized HER2/neu protein (Dako, HerceptestTM) (fig. ). Dual-color chromogenic in situ hybridization revealed that HER2 gene was highly amplified (Ventana, INFORM HER2 Dual ISH) (fig. ). Five months later, CT revealed multiple bilateral pulmonary metastases (fig. ), and systemic treatment with paclitaxel (175 mg/m2) and trastuzumab (8 mg/kg dose loading followed by 6 mg/kg every 3 weeks) was initiated every 21 days. All pulmonary metastatic lesions had regressed after 4 treatment cycles (fig. ), and CR was confirmed after 7 cycles. The patient was maintained on trastuzumab alone (6 mg/kg every 3 weeks), and no evidence of disease progression was observed at the last contact with the patient, which was approximately 13 months after initiation of therapy. | [[74.0, 'year']] | M | {'25136467': 1, '22486195': 1, '17972317': 1, '11431714': 1, '21317706': 1, '30087853': 2, '8625227': 1, '18544445': 1, '25349876': 1, '15900577': 1, '18405406': 1, '20504363': 2, '8380049': 1, '31213830': 2, '11248153': 1, '27103403': 1, '21380780': 1, '7688652': 1, '28680294': 1, '11569926': 1, '12907212': 1, '19574086': 1, '31281644': 1, '25859537': 1, '14987238': 1, '30687059': 2, '17563907': 1, '14663441': 1, '31609094': 1, '24163659': 2} | {'6341428-1': 1, '6341428-2': 1, '6538880-1': 1, '2889991-1': 1, '6066556-1': 1} |
163,814 | 3806691-1 | 24,163,667 | noncomm/PMC003xxxxxx/PMC3806691.xml | Marked Retroperitoneal Lymphadenopathy in Hairy Cell Leukemia: A Case Report | A 73-year-old male presented with a diagnosis of acute respiratory and renal failure, a large abdominal mass, ascites, a white blood cell count of 8.09 × 103/μl, a hemoglobin value of 12.5 g/dl, and a hematocrit value of 36.1%. His past medical history included splenectomy, hypertension, and a diagnosis of HCL from 12 years earlier. Prior to admission the patient had a 1-month history of positional discomfort, with occasional nausea and vomiting, and a 1-week history of painless jaundice. Abdominal axial computed tomography (CT) with intravenous and gastrointestinal contrast revealed a large retroperitoneal mass encasing the superior mesenteric artery, displacing the stomach and infiltrating into the liver (fig. ). The patient was transferred to the medical Intensive Care Unit for further management and placed on a ventilator. After discussion with the attending physician, the family requested the patient be extubated and pronounced ‘do not resuscitate’. The patient died the following day.\nAutopsy revealed moderate ascites consisting of serosanguineous fluid (550 ml) and 2 retroperitoneal masses. The first mass was 3.5 cm below the xyphoid process and measured 7.7 × 5.0 × 3.5 cm. The second mass was immediately below the first and measured 16.0 × 10.0 × 9.5 cm. Approximately 80% of the larger mass was removed and weighed 825 g. No nodal enlargement was found below the aortic bifurcation. Histologic examination of the mass by standard hematoxylin and eosin (HE) staining revealed extensive HCL cells (fig. ). Additionally, IHC analysis revealed that the tumor cells were CD20 and tartrate-resistant acid phosphatase (TRAP) positive (fig. ). The IHC analysis was performed in the LSU Health Shreveport Pathology Histology Immunohistochemistry Procedures Pathology Services using antibodies from Cell Marque (Rocklin, Calif., USA) following the manufacturer's recommended protocols. | [[73.0, 'year']] | M | {'1283078': 1, '17926010': 1, '32756468': 1, '6360496': 1, '18798068': 1, '34535326': 1, '8928422': 1, '7820038': 1, '8147223': 1, '23335087': 1, '13560561': 1, '29742076': 1, '26261698': 1, '5322749': 1, '21663470': 1, '23892906': 1, '24163667': 2} | {} |
163,815 | 3806692-1 | 24,163,663 | noncomm/PMC003xxxxxx/PMC3806692.xml | Rare Adult Masseteric Rhabdomyosarcoma and a Review of the Literature | A previously healthy 32-year-old male nonsmoker presented at our ENT (ear, nose and throat) outpatient clinic complaining of a painless swelling in the right parotid region, which had been increasing for 2 months. The macroscopic examination reported a firm mass measuring about 3.5 × 1.5 cm with shaded limits, while ipsilateral lymphadenopathy was also present. No other ENT diseases were identified during the physical examination. The preoperative baseline parameters and chest X-ray were normal. Hematological and infectious diseases were evaluated, but both pathologies were negative based on hematological and microbiological examinations.\nThe patient was submitted to neck ultrasound, which identified a hyperechogenic nodular mass measuring about 2.5 × 1.3 cm in the right parotid region, with concomitant ipsilateral enlarged cervical nodes.\nMultislice computed tomography (CT) detected a mass in the right masseter with a maximum diameter of approximately 2.2 cm with central necrosis and perifocal inflammatory reaction, which was associated with thickening of the masseter muscle. At the lower parotid pole, there was a coexisting area of high enhancement, while multiple enlarged cervical nodes were found in the level III and IV cervical nodes, with a diameter of 1–1.8 cm (fig. , fig. ).\nMagnetic resonance imaging (MRI) with paramagnetic contrast identified an oval mass in the right masseter muscle, which was mildly hyperintense in T1-weighted images and hyperintense in long repetition time (TR), with regular margins and high contrast intake. The concomitant low pole mass had a cystic appearance with regular margins and low intensity in T1-weighted images and a higher intensity in short tau inversion recovery (STIR). Right lymphadenopathy was confirmed (fig. ).\nThe patient was also submitted to 18F-FDG positron emission tomoscintigraphy (PET), which indicated a high pathological increase in the glucose metabolism in the intramasseteric right region [maximum standardized uptake value (SUV max) 10.5], right jugular nodes, right submandibular nodes (SUV max 6.6), and right cervical nodes (SUV max 6.7). These were all suspected neoplastic locations (fig. ).\nSurgical treatment was proposed to the patient, and he gave written informed consent for treatment and case report publication. Ethical approval was received by the Institutional Review Board of ‘Magna Graecia’ University of Catanzaro, Italy. Thus, the patient was treated surgically by removal of the masseteric mass and by modified radical ipsilateral neck dissection. During surgery, the tumor appeared irregularly limited and it was strongly adherent to the mandibular bone surface and the masseter, with a colliquative lower pole. Postoperative tests were regular and the patient was discharged on the 5th postoperative day.\nHistological examination identified alveolar RMS in the right masseter mass and 44 cervical nodes (superficial periparotid node, intraparotid node, and levels IIA–IIB–III–IV–V right cervical nodes), with small and intermediate-sized round tumor cells according to hematoxylin and eosin stain (fig. ) and widespread nuclear immunoreactivity to myogenin (fig. ).\nThe tumor was classified according to the Intergroup Rhabdomyosarcoma Study (IRS) postsurgical pathological system as Group IIa (table ).\nThe patient received radiochemotherapy with radiation at 45 Gy, while chemotherapy consisted of 14 cycles of vincristine, dactinomycin, and cyclophosphamide (VAC).\nThe patient received a strict follow-up protocol with 3-monthly checks. He was free of locoregional disease with no evidence of distant metastasis 1 year after diagnosis. | [[32.0, 'year']] | M | {'10867669': 1, '17090187': 1, '14752797': 1, '25859531': 1, '11314359': 1, '3049995': 1, '11241248': 1, '21873599': 1, '18240175': 1, '6830102': 1, '8625211': 1, '8275414': 1, '18202417': 1, '20659696': 1, '12124838': 1, '10337369': 1, '24163663': 2} | {} |
163,816 | 3806693-1 | 24,163,658 | noncomm/PMC003xxxxxx/PMC3806693.xml | Ustekinumab Treatment of Erythrodermic Psoriasis Occurring after Physical Stress: A Report of Two Cases | A 59-year-old man with a 19-year history of moderate-to-severe plaque psoriasis was referred to our department in August 2011 due to a flare of erythroderma involving approximately 100% of his body surface area and a Psoriasis Area and Severity Index (PASI) score of 59 (fig. ).\nHe had been previously treated with topical and systemic drugs, such as cyclosporine A and methotrexate that were interrupted for high blood pressure and loss of efficacy, respectively. Without therapy, his psoriasis worsened. Considering the severity of the skin clinical features and his intolerance of conventional systemic therapies, the patient was considered as ‘high need’ for biological drugs and was treated with efalizumab in December 2003. The patient withdrew from efalizumab treatment in March 2004 for ineffectiveness and the onset of erythroderma. Hospitalization was necessary, and etanercept (50 mg s.c./week) was administered with a good control of the disease from April 2004 until July 2011.\nIn July 2011, shortly following cataract surgery on the left eye, the patient developed generalized erythroderma with fever (38.5°C). The therapy with etanercept was discontinued, and the patient was treated with systemic corticosteroid therapy (prednisone 50 mg/day) obtaining an unsatisfactory disease control. In August 2011, severe erythroderma and fever associated with chills and pruritus (itching VAS: 90) occurred. Complete laboratory and instrumental tests were performed, including chest X-ray, ECG, QuantiFeron TB-Gold, complete blood count, complete liver profile, creatinine, auto-antibodies (ANA, anti-dsDNA, ENA, LAC, anti-cardiolipin, anti-citrullin), C-reactive protein, tumor markers, hemoculture, and urinoculture; no significant abnormal results were found. We therefore decided to start therapy with ustekinumab 45 mg s.c. (body weight was 82 kg).\nAfter 4 weeks of treatment, the patient showed an excellent and rapid improvement (fig. ) with a reduction of the PASI score to 10 and the absence of fever and itching. After 12 weeks of therapy, the patient showed complete resolution of the clinical picture with the presence of only mild scaling and a PASI score of 3 (fig. ). Currently, the patient has been undergoing treatment for 12 months, maintaining a PASI score of 75 with no adverse events. | [[59.0, 'year']] | M | {'20222926': 1, '2048897': 1, '34136373': 1, '28856115': 1, '21545503': 1, '17287478': 1, '22364316': 1, '2530253': 1, '32180204': 1, '16792768': 1, '18486739': 1, '18486740': 1, '26848234': 1, '24163658': 2} | {'3806693-2': 2} |
163,817 | 3806693-2 | 24,163,658 | noncomm/PMC003xxxxxx/PMC3806693.xml | Ustekinumab Treatment of Erythrodermic Psoriasis Occurring after Physical Stress: A Report of Two Cases | The second case we report is a 53-year-old woman suffering from plaque-type psoriasis since adolescence, developing joint involvement since the age of 40. Various topical therapies (e.g., tar, corticosteroids, vitamin D analogues) and systemic therapies, both traditional and biological, were discontinued due to the lack of efficacy or the occurrence of adverse events (e.g., renal failure, leukopenia).\nBecause of the worsening of joint symptoms, therapy with metrotexate was reintroduced for 3 months, but ultimately suspended because of the onset of erythroderma. Treatment with intravenous methylprednisolone and ranitidine hydrochloride temporarily improved her clinical condition, but an erythrodermic relapse (PASI score: 40) was observed despite the patient undergoing treatment with small doses of oral corticosteroids (fig. ).\nTherapy with ustekinumab at the dosage of 45 mg s.c. was started as monotherapy, and after only 2 weeks (fig. ), the patient experienced an improvement of her clinical features with a visible reduction of erythema and scaling, achieving an improvement of her PASI score from baseline exceeding 75% (PASI score: 8.4). A second dose was administered 4 weeks later, and after 3 months, the patient showed a PASI score of 0 with a satisfactory control of articular symptoms, using ketoprofen as needed (fig. ). To date, the patient has been treated for 64 weeks, maintaining a PASI score of 90 with no reported side effects. | [[53.0, 'year']] | F | {'20222926': 1, '2048897': 1, '34136373': 1, '28856115': 1, '21545503': 1, '17287478': 1, '22364316': 1, '2530253': 1, '32180204': 1, '16792768': 1, '18486739': 1, '18486740': 1, '26848234': 1, '24163658': 2} | {'3806693-1': 2} |
163,818 | 3806694-1 | 24,163,674 | noncomm/PMC003xxxxxx/PMC3806694.xml | Malignant Hemispheric Cerebral Infarction Associated with Idiopathic Systemic Capillary Leak Syndrome | In January 2012, a 40-year-old man was admitted to our hospital because of shock. Three days before admission, a flu-like illness that included nausea, general malaise, lower abdominal pain, and severe diarrhea was observed. At the previous hospital, 500 ml of 5% albumin and 1,500 ml/day of saline were administered. Three days later, the patient's consciousness had deteriorated, and right hemiparesis appeared. He was then referred to our hospital.\nPhysical examination revealed a temperature of 36.0°C, blood pressure of 95/72 mm Hg, pulse of 160 beats/min, and respiratory rate of 25 breaths/min. His SpO2 was 100% using a 10-liter/min O2 mask. The jugular vein was collapsed. The bilateral radial artery pulses were insufficiently palpable, and the extremities were cold. A whole-blood sample was coagulated easily and considered to be in a state of hyperviscosity. Laboratory data indicated polycythemia, hypoalbuminemia, severe leukocytosis, and elevated creatinine. Serum electrolytes were normal, but severe metabolic acidosis was found (table ). Influenza virus types A and B were shown to be positive using a rapid diagnostic kit. Pericardial effusion and a collapsed inferior vena cava were revealed in heart echocardiograph and chest computed tomography (CT) examinations (fig. ). Magnetic resonance (MR) angiography showed the occlusion of the division of the left M2 segment of the middle cerebral artery (MCA). Diffusion-weighted MR imaging revealed high signal intensity in the MCA territory (fig. ), suggesting acute cerebral infarction. Due to the midline shift of the head on CT after 20 h of hospitalization, external and internal decompression surgery was performed (fig. ). Postoperative intracranial pressure was 9 mm Hg, but gradually exceeded 25 mm Hg with cerebral edema progression. Excessive cerebral edema rapidly developed on the ischemic lesion in the leak phase, and internal decompression was added 12 h after the initial decompressive surgery. The main cause of the hypoproteinemia and hemoconcentration was thought to be intravascular volume depletion due to increased vascular permeability, with extravasation of albumin. It was consistent with the pathology of ISCLS. Mechanical ventilation and massive fluid resuscitation (10 liters/day) were implemented on the first day (fig. ).\nSwelling, redness, and heat sensation were noted in the lateral surfaces of the legs bilaterally. Pretibial compartment syndrome was diagnosed and bilateral calf fasciotomy was performed (fig. ). All samples were negative, including pan cultures of blood, sputum, and urine, and were analyzed for aerobic, anaerobic, atypical mycobacteria, and fungi. Toxic shock syndrome, sepsis, anaphylaxis, acute adrenal insufficiency, drug reactions, and polycythemia vera were considered as differential diagnoses, but there was no evidence suggesting its pathology.\nSevere right hemiparesis and Broca's aphasia persisted, and the patient was unable to walk without assistance at the 2-month follow-up. Two hundred milligrams of theophylline were administered twice daily as prophylaxis against ISCLS. Despite compliance with the prescribed medications, 7 attacks of ISCLS were documented during the first 12-month follow-up, with 2 severe episodes requiring fasciotomy (fig. ). Appropriate fluid resuscitation has resulted in no observed stroke recurrence. A monoclonal immunoglobulin (IgG kappa) was found in the clinical course using immunoelectrophoresis, though plasmacytosis was not found in bone marrow aspiration. The patient was also given an intravenous infusion of immunoglobulins, corticosteroids, and immunosuppressive therapy. | [[40.0, 'year']] | M | {'20634497': 1, '9646773': 1, '18552679': 1, '20643990': 1, '9347824': 1, '19486705': 1, '9428835': 1, '29619573': 1, '10375339': 1, '21464348': 1, '27752564': 2, '870792': 1, '11591575': 1, '28012935': 1, '13693909': 1, '11328338': 1, '21119178': 1, '17575386': 1, '7574220': 1, '27099745': 2, '17505178': 1, '24163674': 2} | {'5052828-1': 1, '4831401-1': 1} |
163,819 | 3806695-1 | 24,163,664 | noncomm/PMC003xxxxxx/PMC3806695.xml | Malignant Transformation from Endometriosis to Atypical Endometriosis and Finally to Endometrioid Adenocarcinoma within 10 Years | A 33-year-old woman (gravida 0, para 0) was referred to Osaka Central Hospital (Osaka, Japan) for gynecological, fertility-preserving laparoscopic surgery. According to her surgical history, two prior laparoscopic surgeries had been performed to treat endometriosis. At the age of 24, she underwent her first laparoscopic cystectomy for left ovarian endometrioma at a community hospital. When she was 29 years old, a second laparoscopic surgery (laparoscopic cystectomy for a right ovarian cyst) was performed at the same institution. The histological examinations of both specimens revealed benign endometriotic cysts. However, approximately 7 months following the second surgery, ultrasonographic and pelvic examinations revealed bilateral ovarian cysts. In response, we administered gonadotropin-releasing hormone agonist therapy (buserelin acetate, 900 μg/day) every 6 months. Upon termination of treatment, the cysts gradually enlarged. At 33 years of age, our patient got married. She desired children and was therefore referred to our institution for fertility treatment via laparoscopic surgery.\nUpon presentation to our hospital, both her ovaries were enlarged (left, 3 cm; right, 4 cm) because of endometrioma. MRI and ultrasound scans showed no solid component within the bilateral cysts. Initially, we considered terminating the hormonal therapy to allow for natural pregnancy. However, she did not become pregnant during a follow-up period of approximately 5 months. Therefore, our patient consented to a third laparoscopic procedure to improve her fertility.\nA preoperative MRI scan revealed a solid 2-cm component of her right ovarian endometrioma. Although the imaging was not enhanced, the possibility of malignancy could not be overlooked. Therefore, we recommended exploratory laparotomy to be performed at another institution. However, the patient and her husband rejected this recommendation and strongly insisted upon a third laparoscopic surgery at our institution. Our patient was fully informed of the treatment options and submitted written consent after which we agreed to perform the third laparoscopic surgery.\nNotably, the third laparoscopic surgery was performed at our institution approximately 10 years after the first surgery. The patient's cancer antigen 125 serum level was within the normal range and both ovaries, which were strongly adhered to surrounding tissues, were enlarged (right, 5 cm; left, 4 cm). The cul-de-sac was obliterated with dense pelvic adhesions. Laparoscopic cystectomy for both ovarian cysts and adhesiolysis were performed.\nThe patient had an uneventful recovery. A histological examination revealed a transition between the endometrioid adenocarcinoma and the directly adjacent endometriosis (fig. ). The cytological result of the small amount of ascites was negative. We reviewed the external slides of the previous two surgeries and confirmed the diagnosis of atypical endometriosis based on the second specimen (fig. ). The patient was diagnosed as having FIGO stage 1c(2), grade 1 ovarian endometrioid adenocarcinoma. Once informed of our diagnosis, our patient desired to attempt to preserve her fertility and rejected complete curative surgery for ovarian cancer.\nFor the fourth surgery, we performed laparoscopic salpingo-oophorectomy of the right ovary, biopsy of the left ovary and partial omentectomy. All specimens showed no pathological malignancy. Postoperatively, the patient underwent three courses of chemotherapy consisting of 175 mg/m2 of paclitaxel and carboplatin (AUC 5) every 3 weeks. A follow-up examination conducted 7 years after the fourth surgery showed no evidence of recurrence. | [[33.0, 'year']] | F | {'34681634': 1, '11349218': 1, '3417292': 1, '34066945': 1, '26413541': 1, '32920422': 1, '9088954': 1, '8852439': 1, '27123121': 1, '31279332': 2, '14675692': 1, '32110695': 1, '10785482': 1, '13087921': 1, '2304731': 1, '12818453': 1, '31013963': 1, '11002961': 1, '12383550': 1, '15307975': 1, '424103': 1, '906985': 1, '30792646': 1, '33598524': 1, '24163664': 2} | {'6612217-1': 1} |
163,820 | 3806696-1 | 24,163,654 | noncomm/PMC003xxxxxx/PMC3806696.xml | Toxic Megacolon and Acute Ischemia of the Colon due to Sigmoid Stenosis Related to Diverticulitis | A 40-year-old man presented to the accident and emergency department with severe diffuse abdominal pain which had started 8 h earlier. He also reported abdominal bloating, diarrhea and nausea. In his past medical history he had two episodes of acute diverticulitis over the past 2 years. Ten years prior to this presentation he had been hospitalized for a ruptured diverticulum in the sigmoid colon. As he refused to have surgery he was treated conservatively at that time.\nOn physical examination his temperature was 38.8°C and his heart rate was 120 beats/min. Blood pressure and oxygen saturation (while breathing ambient air) were normal. He had abdominal distension and tenderness on deep palpation on the left lower quadrant without peritoneal signs. Rectal examination revealed no stool in the vault. Laboratory examination revealed: hemoglobin 15.9 g/dl, WBC 19.120 (NEUT 80.2%), CRP 270.6 mg/l, CPK 543 U/l, GLU 125 mg/dl, LDH 481 U/l, fibrinogen 4.4 g/l, Na 141 mEq/l, and K 5.2 mEq/l.\nAn abdominal CT scan showed located stenosis of the sigmoid colon and marked dilation of the descending (12 cm diameter), transverse (7.5 cm diameter) and ascending (12 cm diameter) colon and of the cecum (11 cm diameter) (fig. ). It is to be noted that in one of his prior admissions due to a crisis of acute diverticulitis 2 years earlier, CT scan had showed a stenotic lesion in the sigmoid colon with mechanical obstruction and prestenotic dilation of the colon. Before the latest admission he had experienced mild periodic discomfort in the abdomen but had not sought medical treatment.\nOver a period of 8 h the patient deteriorated with signs of sepsis, multiorgan failure, severe dyspnea and metabolic acidosis. A CT scan was performed which ruled out pulmonary embolism. He was then intubated because of respiratory muscle fatigue. Laboratory tests changed to the following values: CRP 318 mg/l, CPK 543 U/l, fibrinogen 6 g/l, creatinine 2.2 mg/dl, PT 28.20 s, INR 2.56, D-dimer 2,223.2 μg/l, Na 133 mEq/l, K 5.4 mmol/l, and P 5.4 mg%.\nThe above clinical and laboratory findings were compatible with toxic megacolon. A surgical assessment was performed and emergency laparotomy was decided. Surgery revealed extensive necrotic colon and total colectomy was implemented with protective loop ileostomy. After surgery the patient was transferred to the intensive care unit because of hemodynamic instability. He was extubated after 12 h and transferred to the ward where he stayed until his discharge 10 days later. Histological examination of the resected colon revealed resolving necrotic colon. The specimen was negative for malignancy. The loop ileostomy was reversed 3 months later. Today, 4 years later, the patient remains in good health. | [[40.0, 'year']] | M | {'17436142': 1, '12601205': 1, '10509950': 1, '19843713': 1, '10733108': 1, '23319717': 1, '9093173': 1, '1915133': 1, '22826630': 1, '18647926': 1, '20205505': 1, '3512358': 1, '30151448': 2, '15513359': 1, '15488845': 1, '17601511': 1, '8282262': 1, '18003962': 1, '18936653': 1, '26181875': 1, '20224374': 1, '22549495': 1, '16718822': 1, '8178252': 1, '21876861': 1, '24163654': 2} | {'6100695-1': 1} |
163,821 | 3806697-1 | 24,163,656 | noncomm/PMC003xxxxxx/PMC3806697.xml | Common Blue Nevus with Satellite Lesions Needs a Differential Diagnosis from Malignant Melanoma | A healthy 24-year-old Japanese man was referred to our hospital with a blue-black skin lesion on his left forearm. As confirmed by the patient, this lesion had developed after he accidentally pricked his forearm with a pencil 13 years earlier. Physical examination revealed a 10 × 7-mm, blue-black nodule with an irregular border, which was accompanied by 1–2-mm guttate macular satellite lesions (fig. ). Dermoscopic examination showed a homogeneous, blue-white structure in the absence of any other dermoscopic structures (fig. ). An excisional biopsy was performed with the suspicion of a common blue nevus versus a malignant melanoma. The lesion was excised with a 3-mm margin of surrounding normal skin down to the level of the superficial fascia. We recognized a black-colored restiform structure in the dermis during the operation and added another 3-mm margin. In the histopathological examination of the excised lesion, nevus cells were dispersed in the dermis, and hyperpigmented, spindle-shaped melanocytes infiltrated among the collagen bundles (fig. ). Periappendageal and perivascular concentrations of the nevus cells were observed (fig. ). Similar findings were observed in the satellite lesions as well (fig. ). There were no features suggestive of malignancy, such as cytological atypia, atypical mitoses or necrosis. A histological diagnosis of common blue nevus was then rendered. | [[24.0, 'year']] | M | {'22826721': 1, '19841410': 1, '11843220': 1, '19461250': 1, '29267439': 2, '10583181': 1, '10826091': 1, '24707253': 2, '22030018': 1, '24163656': 2} | {'5726670-1': 1, '3975198-1': 1} |
163,822 | 3806698-1 | 24,163,685 | noncomm/PMC003xxxxxx/PMC3806698.xml | Punctate Inner Choroidopathy: A Clinical Case Report | A 29-year-old Caucasian male presented to our emergency department with complaints of decreased central vision in his left eye (LE), detected a few hours before. Ten years before, he had undergone ophthalmic surgery with phakic lens implantation due to high myopia in both eyes. The patient was taking benzodiazepines and beta-blockers due to panic disorder. He denied systemic disease known to be associated with choroiditis, systemic symptoms or recent illness. There was no relevant family history.\nBest-corrected visual acuity (BCVA) in the LE was counting fingers at 50 cm. He described having blurred central vision in the LE tested on the Amsler grid. Fundoscopy of the LE evidenced multiple, round and yellowish lesions in the macula and nasal to the optic nerve, without signs of intraocular inflammation (fig. , left). BCVA in the right eye was 20/20, and ophthalmological examination showed slight changes of the RPE.\nOCT showed increased retinal thickness with detachment of the neuroepithelium and a slight RPE detachment in the LE (fig. , middle). FA revealed hyperfluorescent lesions with blurred borders in the macula (fig. , right).\nWe performed a chest X-ray and an analytic study to exclude autoimmune and infectious diseases. Afterwards an intravitreal injection of bevacizumab (1.25 mg/0.05 ml) was administered in the LE, showing a significant reduction of the neuroepithelial detachment (fig. ). Four months later, BCVA in the LE was 20/200 and no increased retinal thickness was seen on OCT.\nOne year later, the patient was reexamined and showed a BCVA of 20/40 in the LE. FA and OCT appearances confirmed no active lesions, and fundoscopy revealed a chorioretinal scar on papillomacular beam (fig. ). The same findings were also observed 2 years later. | [[29.0, 'year']] | M | {'20379284': 1, '16391624': 1, '20696997': 1, '28606070': 1, '22210152': 1, '8684800': 1, '26955337': 2, '9003340': 1, '6208783': 1, '28424992': 1, '25741523': 1, '21770809': 1, '20714365': 1, '18185141': 1, '20858403': 1, '31043958': 2, '17434588': 1, '21275596': 1, '17459318': 1, '24163685': 2} | {'6477474-1': 1, '4777951-1': 1} |
163,823 | 3806701-1 | 24,163,662 | noncomm/PMC003xxxxxx/PMC3806701.xml | Diffuse Abdominal Splenosis Mimicking Peritoneal Metastases in a 35-Year-Old Man with a Resectable Carcinoma of the Ampulla of Vater | A 35-year-old man had suffered from intermittent upper abdominal pain for approximately 1 month. An ultrasound of the abdomen revealed no pathology, and routine blood tests were normal apart from an elevated P-amylase of 374 U/l (approx. twice the upper normal limit). At elective gastroscopy 3 weeks later, the patient reported increasing fatigue and an unintended weight loss of 7 kg. On clinical examination, he was icteric. His bilirubin was 105 μmol/l (normal range 5–25 μmol/l), ALAT was 621 U/l (normal range 10–70 U/l) and alkaline phosphatase was 430 U/l (normal range 35–105 U/l). Slight anemia of 7.2 mmol/l (normal range 8.3–10.5 mmol/l) and thrombocytosis of 424 × 109/l (normal range 145–350 × 109/l) were also found. The patient's medical report included splenectomy following a motocross accident with blunt abdominal trauma and intra-abdominal bleeding 20 years earlier, and surgery for appendicitis the same year.\nThe gastroduodenoscopy showed a macroscopically malignant tumor located between the first and second part of the duodenum, involving almost the entire lumen. Biopsies showed an invasive, poorly differentiated adenocarcinoma of the intestinal type. A CT scan with intravenous and peroral contrast (fig. ) revealed a tumor in the ampulla (arrow) involving the whole circumference of the duodenal lumen, but with no apparent involvement of major blood vessels or surrounding organs. In addition, multiple nodular tumors were seen in several intra-abdominal locations, giving rise to the suspicion of peritoneal metastases (fig. ). The nodules varied in size from a few millimeters up to 60 mm (A arrows). Surgical clips from the patient's prior splenectomy were also seen (B arrow). After these findings, the patient was referred to the multidisciplinary team conference for discussion of palliative chemotherapy.\nAt the multidisciplinary team conference, the patient's medical history and signs of previous surgery, including absence of the spleen and presence of multiple surgical clips in the abdominal wall, as well as the uncharacteristic appearance of the intra-abdominal lesions, raised the suspicion of diffuse posttraumatic splenosis. In support of this diagnosis, the CT scan showed slightly hypervascular lesions, with soft tissue attenuation and homogeneous enhancement in the portal venous phase. A core needle biopsy of 1 lesion showed characteristic morphological and immunohistological appearances of benign ectopic splenic tissue.\nA radical pancreaticoduodenectomy ad modum Whipple was performed following laparoscopy. The presence of splenosis was confirmed macroscopically and with frozen biopsies during surgery. The resected tumor was a poorly differentiated adenocarcinoma, originating from the papilla of Vater, with intravascular and perineural growth. Two of 22 lymph nodes contained metastatic adenocarcinoma. The TNM stage was pT2 pN1 M0 R0.\nThe postoperative CA 19-9 was normal (2.4 IU/l). After discussing the option with the patient, adjuvant treatment was offered consisting of gemcitabine 1,000 mg/m2, 3 weeks on, 1 week off, for 6 months. He tolerated the treatment well and is without any signs of recurrence at follow-up, 18 months after surgery. | [[35.0, 'year']] | M | {'8372748': 1, '17161039': 1, '34179460': 2, '19957058': 1, '14550459': 1, '12544129': 1, '26941863': 1, '19123935': 1, '17591312': 1, '22076204': 1, '8124888': 1, '21446083': 1, '9669351': 1, '24163662': 2} | {'8221843-1': 1} |
163,824 | 3806702-1 | 24,163,673 | noncomm/PMC003xxxxxx/PMC3806702.xml | Intracranial Hypertension due to Cerebral Venous Sinus Thrombosis following Head Trauma: A Report of Two Cases | The patient was a 13-year-old female who was hit by a car while riding a horse. She was described as having a Glasgow coma scale score of 9 and intubated prior to transport to the neurosurgical department at Umeå University Hospital. During clinical examination with a low dose of propofol, the patient showed withdrawal to painful stimuli in all extremities and the pupils were of normal size and responsive to light. A CT scan showed unremarkable findings with only some minimal contusions and otherwise visible sulci on the convexities and open basal cisterns (fig. ). There was no visible skull fracture. The ICP, measured by an intraparenchymal pressure monitor (Codman MicroSensor; Johnson & Johnson), however, was 30 mm Hg. Despite sedation with phenobarbital and the placement of an external ventricular drainage for intermittent drainage of cerebrospinal fluid, the ICP was 30–35 mm Hg. To exclude venous thrombosis, an angiography was performed 2 days later that showed thrombosis in the right transverse sinus (TS) and contrast stagnation in cortical veins, including the vein of Labbé, as a sign of impaired venous drainage (fig. ). The right femoral vein was catheterized and a microcatheter (Renegade; Boston Scientific) was inserted into the right TS in an attempt to perform a mechanical thrombectomy. This maneuver, however, did not provide a lasting effect; 20 mg of tissue plasminogen activator was instead administered locally as a bolus. Angiographic imaging showed a partial resolution of the thrombus with flow in the TS (fig. ), whereas the ICP increased to 70 mm Hg. A CT scan showed newly formed subarachnoid haemorrhage, acute subdural haematomas bilaterally and progress of frontal contusions (fig. ). Evacuation of acute subdural haematomas and a bifrontal hemicraniectomy were performed immediately, and the postoperative ICP remained stable at <20 mm Hg (fig. ). The patient was then treated with dalteparin (2,500 U) daily during 5 additional days in the ICU until she could be extubated. The patient's recovery following a cranioplasty 2 months later was excellent, and there were no neurological deficits. | [[13.0, 'year']] | F | {'16703896': 1, '20402748': 1, '19877797': 1, '22920956': 1, '8539371': 1, '22551588': 1, '14999484': 1, '21799156': 1, '20413766': 1, '17600510': 1, '9950487': 1, '14974030': 1, '16002765': 1, '31156540': 1, '19509620': 1, '24163673': 2} | {'3806702-2': 2} |
163,825 | 3806702-2 | 24,163,673 | noncomm/PMC003xxxxxx/PMC3806702.xml | Intracranial Hypertension due to Cerebral Venous Sinus Thrombosis following Head Trauma: A Report of Two Cases | This patient was a 20-year-old male with a history of drug abuse. The patient had tried to commit suicide by jumping from the second floor of a building and landed on concrete. He was reported to have a Glasgow coma scale score of 9 on admission to hospital. A CT scan showed multiple non-dislocated fractures in the posterior fossa and cerebral contusions in the right cerebellar hemisphere and bifrontally (fig. ). The patient was intubated and transferred to the neurosurgical department at Umeå University Hospital. A clinical examination with a low dose of propofol revealed that he showed withdrawal to pain in all extremities and that the pupils were of normal size and reactive to light. An intraparenchymal pressure monitor was inserted (Codman MicroSensor; Johnson & Johnson) that showed an initial ICP of 50 mm Hg that soon increased to 80 mm Hg. A new CT scan showed only slight progress of contusions compared to the initial investigation. The patient was brought to the operating room, and a large bifrontal hemicraniectomy was performed. There was profuse venous bleeding from the bone and the dura during the procedure and there were clear signs of venous congestion of the cortical veins. At the end of the procedure, the ICP was approximately 25 mm Hg; however, it soon increased to 50 mm Hg. A new CT scan showed a substantial progress of cerebral oedema and frontal contusions, whereas a CT venography showed a thrombosed sigmoid sinus on the right side, a fractured jugular foramen and a thrombus extending down to the jugular vein (fig. ). The ICP further increased to 80 mm Hg and the patient subsequently died of circulatory arrest.\nWe received consent from the surviving patient in this case report. For obvious reasons, it was not possible to obtain such consent from the patient who died. There was no study protocol that needed approval from an ethical committee. | [[20.0, 'year']] | M | {'16703896': 1, '20402748': 1, '19877797': 1, '22920956': 1, '8539371': 1, '22551588': 1, '14999484': 1, '21799156': 1, '20413766': 1, '17600510': 1, '9950487': 1, '14974030': 1, '16002765': 1, '31156540': 1, '19509620': 1, '24163673': 2} | {'3806702-1': 2} |
163,826 | 3806704-1 | 24,163,670 | noncomm/PMC003xxxxxx/PMC3806704.xml | Progressive Multifocal Leukoencephalopathy in an Immunocompetent Patient? | A 72-year-old female was admitted to her local hospital because of right-sided hemiparesis and dysphasia. She had a history of well-regulated hypertension and total alopecia at age 40 years with spontaneous improvement. She had no known risk factors for immunosuppression. Her mother had suffered a stroke at the age of 70 years and no other family history of disease was reported. Three months prior to admission, the patient noted fluctuating small, red, itchy skin eruptions without fever or other accompanying infection signs. CT of the brain showed a hypodense lesion in the left parietal region, considered to be of vascular genesis. Acetylsalicylic acid and simvastatin were added to her antihypertensive medication.\nOne month later, a gradual worsening occurred. Three months after the initial neurological signs, a new CT scan revealed an enlarged hypodense lesion in the left parietal region and a minor lesion in the right dorsal parietal region. The patient's condition deteriorated considerably with increasing neurological symptoms, personality changes, aphasia, apraxia and right-sided hemiplegia.\nLaboratory tests showed a normal hemoglobin level and white blood cell and neutrophil counts. The lymphocyte count was low (12–15%; normal range 21–43) with low levels of serum IgG (4.7 g/l; normal range 6.1–14.9) and IgM (0.2 g/l; normal range 0.4–2.1), but a normal IgA level and no monoclonal component were seen. C-reactive protein, SR level, antinuclear antibodies, antineutrophil cytoplasmic antibody, double-stranded DNA, cardiolipin antibodies and rheumatoid factors were normal. No kidney, liver or thyroid abnormalities were observed. Cancer marker tests were normal. Serological tests for Epstein-Barr virus, cytomegalovirus, borrelia and syphilis were all negative. An HIV test was not performed. CSF analysis revealed a normal cell count and normal protein and glucose levels; there was no sign of intrathecal immunoglobulin synthesis. PCR for neurotropic viruses (herpes simplex virus, varicella zoster virus, cytomegalovirus, Epstein-Barr virus and enterovirus) and borrelia were negative. The electroencephalogram showed bilateral theta and delta waves, but no epileptic activity.\nA whole-body CT scan revealed bilateral kidney cysts, but no sign of malignancy or other pathological findings. MRI of the brain showed widespread white-matter lesions in both hemispheres, more extensively on the left side involving the frontal, parietal and occipital lobes (fig. ). The lesions were localized in the subcortical white matter. Examination revealed several small foci on contrast-enhancement in the right parietal lobe. Restricted diffusion was not noted. Magnetic resonance spectroscopy performed with multivoxal chemical shift technique over the right frontoparietal lobe showed unspecific changes with an elevated choline-to-creatine ratio and reduced N-acetylaspartate levels.\nThe patient deteriorated and the planned stereotactic brain biopsy was not performed because of her poor condition. She gradually progressed to a vegetative state. She passed away from the cardiopulmonary complications of bilateral bronchopneumonia 5 months after the first signs of disease.\nThree days later an autopsy was performed. The bilateral bronchopneumonia, moderate coronary atherosclerosis, bilateral kidney cysts and cholecystolithiasis were confirmed. A 13-mm tumor in the ileum without atypia was detected on histopathological examination. The brain was macroscopically atrophic, most prominently in the frontal and parietal lobes. Multiple confluent demyelination foci were described in both hemispheres, but not in the brainstem or the cerebellum. The microscopic examination revealed areas with demyelination, a variable number of macrophages, enlarged purple-stained oligodendroglial nuclei and massive gliosis with gemistocytic astrocytes, some with bizarre nuclei (fig. ). Electron microscopy showed intranuclear inclusions, and the in situ hybridization confirmed JC virus. The autopsy diagnosis was consistent with PML. | [[72.0, 'year']] | F | {'11049808': 1, '30863734': 2, '4104715': 1, '16862584': 1, '19828476': 1, '23614603': 1, '15883345': 1, '27273076': 1, '5102141': 1, '11357954': 1, '22661423': 1, '9675474': 1, '21227915': 1, '28669032': 1, '27529042': 2, '5462240': 1, '19258267': 1, '20298967': 1, '32522746': 1, '25489887': 1, '15550673': 1, '27042682': 1, '24163670': 2} | {'6394363-1': 1, '4978838-1': 1} |
163,827 | 3806705-1 | 24,163,676 | noncomm/PMC003xxxxxx/PMC3806705.xml | Putative Corneal Neuralgia Responding to Vitamin D Supplementation | The patient is a 29-year-old female of Indian origin who first reported to our clinic in November 2012 with a month-long complaint of intermittent severe left eye irritation triggered by wearing her soft contact lenses for prolonged periods of time (up to 14–16 h/day). Symptoms included photophobia and a mild foreign body sensation. She used VisineTM a few times daily and reported that this therapy relieved some of the irritation. She had also noticed that the left eye was often red.\nAt that visit, the patient's past medical history was significant for gastroesophageal reflux controlled with omeprazole (on an ‘as needed’ basis). Her past ocular history was significant for the treatment of high myopia with LASIK 6 years prior to the first visit and prophylactic peripheral cryopexy on both eyes. The patient reported enjoying an uneventful postoperative course after LASIK surgery. She was a −10 myope prior to the surgery. In addition, she developed mild myopia 4 years after LASIK surgery, for which she used contact lenses or glasses.\nHer family's medical history was significant for high myopia, but her social history was negative for smoking, alcohol or illicit drug use. The patient had no food, drug or environmental allergies.\nWith her current correction, the patient's vision was 20/20–2 OD and 20/30–2 OS. Color vision was normal (10 of 10 Ishihara plates correctly scored). The physical exam revealed normal pupillary findings, visual fields by confrontation and extraocular movements. The intraocular pressure (Goldmann) was 8 and 9 in the OD and OS, respectively.\nA slit lamp examination revealed mild blepharitis and meibomian gland dysfunction. There were mild conjunctival papillae OU, but neither injection nor lesions of the conjunctiva otherwise. The corneas bilaterally demonstrated mild epithelial punctate staining. The LASIK flap scar was bilaterally visible and the flaps were well positioned. The anterior chambers, irides and lenses were bilaterally normal.\nDilated fundoscopic exam bilaterally confirmed normal optic nerves, each with a cup to disc ratio of 0.5, as well as normal vitreous and maculae. There were areas of far peripheral retinal findings consistent with atrophy and previous cryopexy.\nThe patient was diagnosed with contact lens overwear in the left eye and was instructed to use preservative-free artificial tears up to 6 times/day and artificial tear ointment at bedtime as well as to decrease contact lens use to a maximum of 6–8 h/day. The patient was offered a follow-up appointment in 1 month if still symptomatic or after 6 months if not. Corneal topographic measurements were suggested for the follow-up visit.\nThe patient returned to our clinic 3 months later with continuing complaints of severe left eye irritation, worse in the wind. She completely discontinued contact lens wear 2 weeks prior to this visit, but suffered persistent left eye pain and blurred vision. She reported that the left eye had been red and that she had been told that she sleeps with her eyes ‘slightly open’.\nHer medical history changed. She reported that she was undergoing an endocrinologic workup because she noted hair loss, one episode of galactorrhea and 4 days of spotting outside the time of her usual menses. We also learned that her mother was treated for hypothyroidism.\nThe patient's family doctor sent a battery of blood tests, including a pregnancy test, transferrin/Fe/TIBC, vitamin B-12, RBC folate, thyroid-stimulating hormone, DHEA-S, free testosterone, prolactin, ferritin, ANA, anti-hepatitis B surface antigen antibody, hepatitis C antibody screen, hepatitis B surface antigen, Treponema pallidum antibody, vitamin D (25-OH), D2, D3, luteinizing hormone, follicle-stimulating hormone, complete blood count with differential and HIV antibody test. The anti-hepatitis B antibody was positive, consistent with the patient's history of vaccination. Free testosterone was slightly elevated. The follicle-stimulating hormone and luteinizing hormone were considered within normal range for a woman during the luteal phase of her menstrual cycle. Vitamin D 25-OH was 15 ng/ml; the normal range is between 30–100 ng/ml, indicating a deficiency in our patient. The patient was told that vitamin D deficiency is common among people of the Indian ethnicity.\nHer vision at this second visit with correction was 20/25 OD and 20/40 OS, improving with pinhole to 20/20. The remainder of the physical exam was unchanged, including the presence of mild blepharitis, meibomian gland dysfunction and punctate staining on both corneas.\nThe patient was brought to the attention of our corneal service, where she was examined and diagnosed with possible exposure keratopathy. Notably, the findings between the two eyes were identical, while the patient confirmed that the complaints were only in the left eye. The patient was instructed to continue aggressive lubrication with preservative-free artificial tears 6–8 times/day and was prescribed erythromycin ointment 4 times/day.\nWe remained in communication with the patient. She reported that she tried oral nonsteroidal anti-inflammatory medication for the pain, but this did not help. She added that the lubricating eye ointment at bedtime helps with the morning dryness, and sleeping later than usual exacerbates this feeling. In addition, she felt that the additional lubrication helped the blurred vision OS. However, the patient reported that the burning pain in the left eye persisted and questioned whether her vitamin D deficiency could be the problem. Thereafter, the patient started taking oral vitamin D supplementation, 1,000 IU/day and within 4 days reported being completely free of the burning pain. We remained in e-mail communication with the patient; at 4 weeks, she was much more comfortable and no longer needed eye drops. Three months after her last visit, she was still free of pain without topical therapy and could even tolerate wearing her contact lenses for short periods of time, but only if she used topical lubrication. Although the patient returned to her hometown 3 months after her last visit, a recent e-mail 5 months after her last visit confirmed that her situation remained improved. The patient returned to her hometown in May and we were not able to schedule a final follow-up. Her family doctor did not have the opportunity to obtain a follow-up serum vitamin D level.\nAt this point, we made a putative diagnosis of corneal neuropathic pain. This condition has been described by patients as burning, stinging, scratchiness or just pain, and this pain is usually severe []. It can mimic symptoms of dry eye and blepharitis, and the objective findings at the slit lamp are disproportionately benign compared to the complaints; patients seem to not respond to topical therapies as it appeared to be the case in our patient. Hyperesthesia with abnormal sensitivity to wind or light can be reported by patients, including our patient. Therapies that have been recommended for this condition include lubrication, anticonvulsants, tricyclic antidepressants and serotonin reuptake inhibitors, a scleral reservoir lens and evaporation-prevention goggles.\nCorneal neuralgia has also been reported in patients after refractive surgery [], although we do not presume to suggest that our patient's pain was related to her relatively remote history of LASIK.\nA limitation of this report is that we did not have the opportunity to examine our patient again once her symptoms resolved. In addition, we do not know the degree to which the vitamin D supplementation reversed the deficiency discovered by serum testing. We did note that our patient's exam findings were extremely mild and that they did not change between her two visits despite her good compliance with suggested interventions. We believe it is also noteworthy that the patient was able to discontinue all topical lubrications soon after the vitamin D therapy was initiated.\nNotably, there is a published case report indicating that correction of vitamin D deficiency reversed diabetic neuropathic pain []. Furthermore, low levels of vitamin D have been shown to be an independent risk factor for diabetic neuropathy [, ]. In patients suffering from Sjögren's syndrome, neuropathy has been associated with low levels of vitamin D [], and in pediatric patients with unexplained limb pain, vitamin D insufficiency has been reported frequently [].\nIt is unclear how vitamin D might be associated with the relief of pain. It has been reported that hypovitaminosis D causes hyperinnervation of nociceptors in skeletal muscle tissue []. Vitamin D also reduces nitric oxide production []; nitric oxide is believed to be a nociceptive transmitter and cause nociceptive hypersensitivity [].\nThe metabolism of vitamin D in the cornea is not completely understood. Calcitriol (the active form of vitamin D), calbindin D-28k (a vitamin D-dependent calcium-binding protein) and a plasma membrane calcium pump have been immunolocalized to the human corneal endothelium and basal epithelium []. In addition, calbindin 2 is reported to be expressed in the corneal epithelium, stroma and endothelium []. Vitamin D metabolites were found in human corneal limbal epithelial cells after irradiation with UV-B, suggesting that these cells were capable of synthesizing these products []. Finally, vitamin D has been shown to enhance corneal epithelial barrier function [].\nWe recognize that our diagnosis of corneal neuralgia for our patient was a putative one. In addition, pain is subjective and we cannot rule out a placebo effect. However, given the literature regarding neuropathic symptoms associated with vitamin D deficiency, it may be reasonable to consider assessing vitamin D levels and appropriately supplementing deficiencies thereof in patients who present with recalcitrant corneal/ocular surface pain with disproportionately mild findings on clinical examination. | [[29.0, 'year']] | F | {'27980879': 1, '22835660': 1, '27698364': 1, '26904676': 1, '22827868': 1, '20709057': 1, '22632164': 1, '22050401': 1, '21715350': 1, '22330055': 1, '7539352': 1, '20712970': 1, '34129211': 2, '25724179': 1, '21726279': 1, '25257359': 1, '23304571': 1, '19635651': 1, '21436345': 1, '24163676': 2} | {'8319231-1': 1, '8319231-2': 1, '8319231-3': 1} |
163,828 | 3806706-1 | 24,163,665 | noncomm/PMC003xxxxxx/PMC3806706.xml | Multimodality Imaging of Right-Sided (Tricuspid Valve) Papillary Fibroelastoma: Recognition of a Surgically Remediable Disease | A 61-year-old Hispanic woman presented with recurrent paroxysmal pleuritic chest pain and severe dyspnea. Between episodes, the patient was normally functional and asymptomatic. There was no prior history of structural cardiac, coronary, pulmonary, or systemic disease. Pulmonary CT angiography did not reveal any emboli. Transthoracic and transesophageal echocardiography showed a mobile mass of moderate size and shimmering edges, measuring 1.3 × 0.9 × 1.1 cm, attached to the septal tricuspid valve (TV) leaflet. Pulmonary pressure was minimally elevated at 35–40 mm Hg. Anticoagulation with rivaroxaban (oral factor Xa inhibitor) was initiated. A pedunculated mass with peripheral shimmering frond-like appearance and stalk attached to the septal TV leaflet was seen prolapsing through the TV with tricuspid regurgitation (fig. ). CT pulmonary angiography did not show gross filling defects to suggest pulmonary embolism (PE) but revealed a mobile mass visible in the orthogonal image planes (fig. ). Cardiac MRI revealed a mobile mass measuring ≥1 cm in multiple dimensions, showing hyperintensity on T2-weighted and inversion recovery sequences (fig. ). A differential diagnosis of papillary fibroelastoma (PF) versus cardiac myxoma was entertained. Cardiac surgery was advised due to size (>1 cm), symptomatology, and the established recurrent embolic potential of the tumor. At surgery, shave excision of the sessile mass, and TV repair using a 30-mm Medtronic Contour ring was performed. Gross pathology revealed a friable mass with surface fronds on a short pedicle, with the typical sea anemone appearance of a PF. Microscopic findings showed avascular branching filamentous fronds with a single endothelial cell covering. Each frond had a fibrous core with loose connective tissue rich in mucopolysaccharide (fig. ). Postoperatively, the patient continued anticoagulation for 8 weeks. To date, the patient remains asymptomatic at rest and exercise. | [[61.0, 'year']] | F | {'12947356': 1, '16714684': 1, '23793590': 1, '15227497': 1, '27904982': 1, '1953134': 1, '22626753': 1, '30746328': 2, '16242444': 1, '24163665': 2} | {'6341851-1': 1} |
163,829 | 3806707-1 | 24,163,669 | noncomm/PMC003xxxxxx/PMC3806707.xml | Clinical Outcome of a FIGO Stage IV Gestational Choriocarcinoma | In October 2012, a 37-year-old female patient presented with a 7-day history of lower abdominal pain, vaginal bleeding and a raised β-hCG level (44,565 IU/l). In anamnesis, she had two normal antecedent term pregnancies. Within 1 year after the second pregnancy, choriocarcinoma developed. In December 2010, the patient was treated for choriocarcinoma with lung metastasis with three courses of EMACO chemotherapy. Hysterectomy with preservation of the adnexa was performed. In May 2011, she developed clinical manifestations of brain metastasis, which was treated successfully through surgery (extirpation of the tumor in the parieto-occipital region of the brain), radiotherapy and 4, 5 and 6 courses of chemotherapy. Thereafter, she was closely followed up by a gynecologist and a neurologist. Her regular therapy was carbamazepine at a dosage of 800 mg daily.\nThe patient was in remission from July 2011 to October 1, 2012 when she addressed herself to our Institute. A vaginal examination revealed vaginal bleeding and a palpable mass in the lesser pelvis behind the site of the hysterectomy scar. Her physical examination was otherwise normal and, apart from β-hCG units with a tendency to rise, her laboratory analyses were without pathological findings too. An MRI scan of the abdomen and pelvis revealed a tumor of 7.0 × 7.6 × 9.3 cm in size, infiltrating local tissues and indicating a relapse of choriocarcinoma (fig. ). The MRI scan also showed multiple metastases in the right lung. A computed tomography (CT) of the chest showed multiple metastases (fig. ), but the brain CT was normal. Previously, the patient was at FIGO stage IV and had a WHO score of 13, both indicating that she was a high-risk patient with poor prognosis []. Considering the local tumor infiltration of the tissue, surgery was not an option. Instead, she was introduced to 9 courses of EMACO chemotherapy. Her vaginal bleeding persisted and was stopped by vaginal tamponade. Upon therapy, the patient became highly febrile (39°C). Her laboratory findings revealed elevated enzymes because of an acute-phase inflammation [C-reactive protein 361 mg/l, erythrocyte sedimentation rate 150/mm/h (2–10), fibrinogen 10 g/l (2–4), aspartate transaminase 130 IU/l (14–50), alanine aminotransferase 102 IU/l (21–72) and lactate dehydrogenase 546 IU/l (180–360)]. A blood analysis showed pancytopenia [white blood cell count: 3.7 g/l (0–132); red blood cell count: 1.89 ×1012/l (4.10–5.10); hemoglobin 53.5 g/dl (115–165); platelet 125 g/l (150–400)]. The hemostasis tests were within normal ranges. The patient was treated with cephalosporin, ertapenem, metronidazole, ciprofloxacin, neupogen and 4 doses of blood infusion. Three days after the introduction of antibiotics, the patient developed convulsive tonic-clonic seizures, which were partly controlled by carbamazepine. A repeated brain CT did not show metastasis. The patient was transferred to a neurosurgical clinic, where she died from liver failure and infection due to tumor necrosis on the second day after admission. | [[37.0, 'year']] | F | {'26788218': 1, '26622776': 1, '22587615': 1, '17425677': 1, '18946601': 1, '18928664': 1, '34703509': 1, '22640711': 1, '22195336': 1, '22925191': 1, '19322933': 1, '22244665': 1, '22705360': 1, '24163669': 2} | {} |
163,830 | 3806709-1 | 24,163,647 | noncomm/PMC003xxxxxx/PMC3806709.xml | Incidental Finding of Isolated Colonic Neurofibroma | A 70-year-old woman was referred to our gastroenterology clinic for colon cancer screening. She denied abdominal pain, nausea, vomiting, heartburn, irregular bowel habits or hematochezia. She had undergone colonoscopy 10 years prior at an outside facility which according to her had been unremarkable. Her past medical history included migraine, hypertension, coronary artery disease and osteopenia. Her home medications included aspirin, hydrochlorothiazide, metoprolol, simvastatin, calcium, vitamin D and alendronate. Her family history was significant for stomach cancer in a sister, lung cancer in a brother and thyroid cancer in a daughter. She denied any family history of neurological tumors and cutaneous neurofibromas. She had a 40-pack-year smoking history, which she quit for 12 years. Physical examination revealed an overweight woman with a body mass index of 29. Her abdomen was soft with no tenderness or palpable masses. She did not have any skin lesions or pigmented/hypopigmented spots. Abdominal and neurological exams were within normal limits. Laboratory data revealed a hemoglobin level of 13.9 g/dl, a white blood cell count of 8,100/μl, a platelet count of 251,000/μl and a serum creatinine of 0.9 mg/dl. Basic metabolic panel, liver function tests and coagulation profile were within normal limits. Hepatitis serology was negative.\nAs part of routine screening, colonoscopy was performed up to the cecum. Findings included a 20-mm pedunculated polyp with a stalk measuring 0.6 cm in length and 0.4 cm in diameter in the ascending colon (fig. ), and an 8-mm polyp in the transverse colon removed with polypectomy and a 3-mm polyp in the ascending colon removed with biopsy forceps. Other findings were diverticulosis of the entire colon and internal hemorrhoids. The 8-mm transverse colon polyp revealed tubular adenoma on histopathology, and the 3-mm ascending colon polyp revealed colonic mucosa. Histologically, the pedunculated ascending colon polyp revealed bland spindle cell proliferation in the submucosa (fig. , fig. ). Immunohistochemical stains showed that the tumor cells were immunoreactive to S100 protein (fig. ) and were non-reactive to CD117, SMA and desmin antibodies. These findings were consistent with a diagnosis of colonic submucosal neurofibroma. The patient continued to be followed up in our outpatient clinic. She remains asymptomatic without any systemic signs of neurofibromatosis even after 9 months of follow-up. | [[70.0, 'year']] | F | {'20606732': 1, '16222760': 1, '31984122': 2, '11087058': 1, '9653918': 1, '7719404': 1, '13663747': 1, '11142587': 1, '1916682': 1, '22423240': 1, '27366045': 1, '4374669': 1, '27577727': 1, '9305312': 1, '19030214': 1, '3927657': 1, '19065103': 1, '212258': 1, '23622184': 1, '18744831': 1, '8731581': 1, '9749504': 1, '10868203': 1, '10813133': 1, '12389695': 1, '32518783': 2, '4962547': 1, '24163647': 2} | {'6943092-1': 1, '7262705-1': 1} |
163,831 | 3806710-1 | 24,163,649 | noncomm/PMC003xxxxxx/PMC3806710.xml | Adult Colocolic Intussusception and Literature Review | A 63-year-old Caucasian female with no significant past medical history presented with a 1-month history of intermittent right upper quadrant pain radiating to the umbilicus after 1 h of eating food. She also had decreased appetite, with an unintentional weight loss of 20 lbs within the past 6 months. In addition, she had had 1 year of nonbloody diarrhea with no history of travelling. She denied any chills, fevers, nausea or vomiting. Her surgical history included appendectomy, with no family history of colon cancer but significant for Crohn's disease.\nAt the time of presentation to the emergency room, her temperature was 98.1°F, blood pressure 175/83 mm Hg, pulse 76 beats per minute, respiratory rate 16 breaths per minute and oxygen saturation 99% while breathing ambient air. At abdominal examination she had appreciable bowel sounds with a right lower mild tender and palpable abdominal mass but no rebound tenderness. Laboratory test were within the normal range: blood cell count 8,800/µl, hemoglobin 9.5 g/dl and hematocrit 40.6% g/dl. However, she had an elevated CEA level of 78 µg/l with abdominal CT scan that showed considerable edema of the intussusception of the proximal colon into the mid-transverse colon, due to a tumor measuring 4.1 × 6.3 cm, with no obstruction. The small bowel loops were normal in caliber, but there was significant edema from the distal transverse colon almost to the splenic flexure (fig. ). Colonoscopy was performed to further evaluate the lead point of the intussusception, which was a tumor located at 65 cm in the transverse colon, causing partial obstruction. A biopsy was obtained at 60 cm, which showed colonic mucosa with focal erosion, congestion and focal hyperplastic changes.\nBased on these findings we diagnosed the patient with colocolic intussusception caused by colonic tumor. We performed an exploratory laparotomy that revealed an ascending 4.7 × 3.5 × 2.0 cm tumor as the lead point of intussusception into the proximal transverse colon, with palpable mesentery lymph nodes and no liver lesions (fig. ). The patient underwent right hemicolectomy with side-to-side ileocolic anastomosis. The postoperative course was uneventful, and she was discharged home after 6 days in good general condition. Histopathological examination of the tumor revealed high-grade mucinous adenocarcinoma with signet ring cells with 12 out of 12 lymph nodes negative for metastasis (fig. ). The final pathology staging was T3N0M0 or stage II. | [[63.0, 'year']] | F | {'16773257': 1, '32009867': 2, '30733177': 1, '9074370': 1, '9464437': 1, '5433296': 1, '19486100': 1, '20951844': 1, '28144618': 1, '29531876': 2, '7469558': 1, '15729613': 1, '19399931': 1, '9296505': 1, '17846839': 1, '2662787': 1, '25861510': 2, '5557762': 1, '30363296': 1, '29201755': 2, '30546977': 2, '10195723': 1, '19598308': 1, '24163649': 2} | {'4377455-1': 1, '4377455-2': 1, '6289586-1': 1, '6984140-1': 1, '5578591-1': 1, '5578591-2': 1, '5837297-1': 1} |
163,832 | 3806712-1 | 24,163,688 | noncomm/PMC003xxxxxx/PMC3806712.xml | Delayed Development of Pulmonary Hemorrhage in a Patient with Positive Circulating Anti-Neutrophil Cytoplasmic Antibody: A Clinical Dilemma | A 50-year-old male visited our hospital in October 1996 because of abnormalities detected in a medical checkup. Urinary protein and occult hematuria had been documented in medical checkups over the previous few years, with marked proteinuria of up to 3.8 g/day being a prominent feature of his clinical presentation. Renal biopsy performed in December 1996 revealed segmental sclerosis in 1 of 7 glomeruli and deposition of immunoreactive substances into glomeruli, including IgM and complement. Therefore, a diagnosis of FSGS was made on the basis of the results of a renal biopsy. Also, chest computed tomography (CT) delineated interstitial changes accompanied by cystic lesions in the lung and pleural thickening (fig. ), along with chest X-ray abnormalities that had been noted in a past medical checkup. He had worked as a demolition worker and smoked approximately 30 cigarettes a day since he was 18 years old. Work- and smoking-related lung conditions were therefore the most likely causes of the pulmonary lesions. An annual chest CT showed little change over several years, in contrast to progression of the renal disorder. Pleural thickening strongly suggested concomitant TB based on epidemiological reports showing a strong association of TB with pneumoconiosis [], although mycobacterium species were not detected by sputum culture tests that were repeatedly performed over a couple of years.\nCyclosporine A (CsA) was administered at doses of 50–100 mg per day under therapeutic drug monitoring (the trough level was usually around 50 ng/ml) in lieu of steroid therapy [] to reduce the risk of excessive immunosuppression, but the serum creatinine (Cr) level showed a rapid elevation in 2000, at approximately 3 years after biopsy (fig. ). He had presented with persistent microscopic hematuria, which is inconsistent with the clinical presentation of FSGS, since the first visit. By contrast, a temporary decrease in proteinuria (down to 1.3 g/day) was observed afterward, unlike with treatment-resistant FSGS. Rapidly progressive glomerulonephritis was suspected despite the biopsy findings, and circulating ANCA was measured (this test has been clinically available since 1998 in Japan). Elevation of the MPO-ANCA titer (168 EU) was found, along with an altered clinical presentation. However, potent immunosuppressive therapies such as glucocorticoids were still withheld due to the possibility of an underlying infection (TB). Apheresis was alternatively conducted in an effort to avoid decreased immune competence, but initiation of HD was required in September 2001 because of end-stage renal disease (ESRD). Thrice-weekly HD was performed uneventfully for several years, and there were also no changes in pulmonary signs. An annual CT checkup had shown little change (fig. ), and elevation of serum KL-6 [] had not been documented. In contrast, circulating MPO-ANCA had ranged from 10.5 to 32.5 U/ml, even in the dialysis period, indicating possible AAV (fig. ). However, steroid therapy was postponed due to the unconfirmed diagnosis, presumed TB, and lack of problematic clinical events.\nAbruptly, the patient developed gross hemoptysis accompanied by severe cough at night in bed and was transported to our facility by ambulance in October 2010. Chest CT showed infiltrative shadows in the bilateral lung fields (fig. ). Under a presumptive diagnosis of alveolar hemorrhage associated with AAV, steroid therapy comprising 3-day intravenous infusion of 500 mg methylprednisolone followed by daily oral administration of 20 mg prednisolone (PSL) was launched. A preventive dose of 100 mg isoniazid per day was also prescribed. As expected, the hemorrhagic shadows almost disappeared as early as 2 days after hospitalization (fig. ), and the serum MPO-ANCA titer subsequently fell to normal (fig. ). The patient was discharged after 17 days and has had no recurrence of hemoptysis. At present, PSL has slowly been tapered to a daily dose of 5 mg, but there has been little change over time in the serum MPO-ANCA level and follow-up CT. | [[50.0, 'year']] | M | {'11257154': 1, '11757762': 1, '9507222': 1, '18676500': 1, '21798892': 1, '18799054': 1, '21928092': 1, '22948120': 1, '19815703': 1, '16497860': 1, '12427162': 1, '15373919': 1, '12595614': 1, '12090888': 1, '20884728': 1, '16859597': 1, '12631105': 1, '19533266': 1, '26309421': 1, '24163688': 2} | {} |
163,833 | 3806723-1 | 24,163,648 | noncomm/PMC003xxxxxx/PMC3806723.xml | Biliary Cast Syndrome in an Opium Inhaler | A 52-year-old man, who was a known case of opium addiction, presented with the chief complaint of epigastric pain for 1 week prior to admission. Physical examination showed moderate right upper quadrant tenderness. There were no significant disorders in his past medical history. Routine laboratory evaluation revealed cholestatic liver enzyme elevation with alkaline phosphatase 1,810 IU/l (reference range 80–306 IU/l), total bilirubin 0.5 mg/dl (reference range 0.1–1.2 mg/dl) with normal aminotransferases, high erythrocyte sedimentation rate (90 mm/s) and normal prothrombin time. Serum levels of fasting blood sugar, blood nitrogen urea, creatinine, triglyceride, total and low-density lipoprotein cholesterol and uric acid as well as thyroid function tests were in the normal range.\nUltrasound demonstrated a dilated common bile duct. An abdominal CT scan demonstrated dilated intrahepatic and extrahepatic bile ducts (the common bile duct measured 11 mm). Magnetic resonance cholangiopancreatography showed a distended gallbladder and a dilated bile duct with the conclusion of ampullary and periampullary lesion (fig. ). Endoscopic retrograde cholangiopancreatography showed a linear filling defect in the intra- and extrahepatic duct (fig. ). A long biliary cast was successfully removed using an extractor balloon (fig. ).\nThe patient was discharged without any complication. After removal of the biliary cast he is receiving ursodeoxycholic acid (UDCA) 750 mg per day and does not report any problem 4 months after treatment. His last laboratory evaluation revealed a significant decrease in erythrocyte sedimentation rate (30 mm/s) and a mild decrease in alkaline phosphatase (1,423 IU/l). | [[52.0, 'year']] | M | {'16635387': 1, '23121103': 1, '23423962': 2, '23190361': 1, '20213831': 1, '11316181': 1, '18522886': 1, '23242023': 1, '16929156': 1, '12655251': 1, '18777601': 1, '168674': 1, '17554188': 1, '12907345': 1, '8365616': 1, '10781781': 1, '10697662': 1, '12655263': 1, '18496388': 1, '24163648': 2} | {'3572362-1': 1} |
163,834 | 3806998-1 | 24,175,048 | noncomm/PMC003xxxxxx/PMC3806998.xml | Nephrectomy for a Renal Metastasis of Undiagnosed Hepatocellular Carcinoma Arising From an Orthotopic Liver Transplant Undertaken for Cryptogenic Cirrhosis | A 70-year-old man presented with an incidental right renal mass after magnetic resonance cholangiopancreatography (MRCP) for investigation of abnormal results of liver function tests (LFTs), which suggested an obstructed biliary tree. The patient had undergone OLT in 2000 after extensive preoperative investigations for cryptogenic liver cirrhosis including serology and radiology. Post-OLT histopathology showed that the native liver had nodules of varying sizes consistent with cirrhosis with no evidence of carcinoma. The patient was started on immunosuppressive therapy with tacrolimus, which was subsequently changed to sirolimus in 2005, and he was followed up quarterly by the liver transplant service at our center.\nOn routine follow-up, the patient was found to have obstructive (cholestatic) LFT results in late 2009. An MRCP was performed and a diagnosis of choledocholithiasis was made, but incidentally a right renal mass was also found. No biliary tree obstruction or liver lesions were noted on this scan. A triple-phase computed tomographic (CT) scan of his abdomen and pelvis further confirmed the presence of a lobulated enhancing mass (55 mm×45 mm in diameter) in the right upper pole extending into the perinephric fat and abutting the right hemidiaphragm () but with a clear plane between the liver and the mass. Again, the hepatobiliary system had no lesions present. He was otherwise asymptomatic with all staging negative for metastatic disease. His case was reviewed at a multidisciplinary meeting where consensus dictated that the mass was likely to represent a primary renal tumor that should be resected. Partial nephrectomy was offered but declined by the patient.\nThe patient underwent a right open radical nephrectomy via a flank approach and resection of part of the hemidiaphragm requiring repair with a synthetic mesh (Gore-Tex patch). There were no obvious liver lesions on careful inspection and palpation. The procedure resulted in 500 mL of blood loss and no perioperative complications. Histology of the specimen revealed a tumor with hepatoid morphology () invading the upper pole of the kidney, perinephric fat, and diaphragm. Immunohistochemical staining (positive for HepPar 1 and polyclonal carcinoembryonic antigen) was also suggestive of HCC. The patient was discharged but 5 months later it was noted that his serum alpha-fetoprotein levels were significantly elevated and abnormal serum baseline liver function was declining. An ultrasound demonstrated six previously undetected focal liver lesions. A CT scan further confirmed the liver lesions, which continued to enlarge (). At restaging, new pulmonary lesions were also noted (). After a multidisciplinary meeting, the patient was commenced on the tyrosine kinase inhibitor sorafenib in a bid to control his overt metastatic disease, which at 3 months has stabilized. | [[70.0, 'year']] | M | {'14501871': 1, '12004349': 1, '18813102': 1, '17561170': 1, '16713550': 1, '1142495': 1, '32582519': 1, '9873096': 1, '32637169': 1, '8727613': 1, '9305716': 1, '24175048': 2} | {} |
163,835 | 3806999-1 | 24,175,049 | noncomm/PMC003xxxxxx/PMC3806999.xml | Missed Spermatic Cord Torsion in an Old Man | A 63-year-old man presented with right scrotal pain and swelling. A couple of weeks previously, he had experienced right scrotal pain when he woke up. The scrotal swelling and dull scrotal pain had gradually increased over a few days. He was then seen by a primary care physician. However, the physician failed to find any abnormalities other than epididymal enlargement on scrotal ultrasonography. The patient was then referred because his symptoms did not improve despite empirical antibiotics use. He denied having any history of trauma to the testis, strenuous exercise, sexual activity, or febrile illness. He also had no known sexually transmitted diseases. On physical examination, a swollen, edematous, and erythematous change in the right hemiscrotum was noted. The right testis was enlarged, hard, consistent, and somewhat tender on palpation compared with the intact left testis. The results of a complete blood count, chemistry profile, and urinalysis were normal. Serum levels of α-fetoprotein and β-human chorionic gonadotropin were in the normal range. Gray-scale ultrasonography of the scrotum demonstrated heterogenous echotextures in the right testis that were combined with a thickened scrotal wall and hyperechoic supratesticular mass (). Color Doppler sonography revealed that blood flow was present in the asymptomatic left testis, but absent in the right testis. An increased blood flow in peritesticular structures adjacent to the nonperfused testis was identified (). Torsion of the right spermatic cord was strongly suspected judging from the sonographic findings. Although very rare, a few cases of intrascrotal torsion of a testis tumor have been reported []. Therefore, we could not absolutely exclude the possibility of a testis tumor and thus planned to perform radical orchiectomy of the symptomatic right testis.\nThe patient was taken for surgical exploration of the right testis through a right inguinal incision. Severe adhesion and inflammation around the torsed testis were found. Radical orchiectomy was done in the usual manner. The frozen section examination of the right orchiectomy specimen revealed testicular infarction with suppurative inflammation. Hence, left transscrotal orchiopexy was done to prevent contralateral torsion at a later date. An underlying anatomic abnormality, the bell-clapper deformity, was found in the left testis. In the cut section, the right testis was 4.3 cm×3.2 cm×4.2 cm in size and had reddened parenchyma rimmed with several scattered lesions of dirty yellow pus-like exudates. A twisted intravaginal spermatic cord was identified (). Final histopathological examinations revealed a total hemorrhagic infarct of the testis and diffuse chronic inflammation of the peritesticular soft tissues (). | [[63.0, 'year']] | M | {'20407849': 1, '28058232': 1, '8212449': 1, '11956451': 1, '17162068': 1, '3219547': 1, '10930945': 1, '24175049': 2} | {} |
163,836 | 3807010-1 | 24,167,418 | noncomm/PMC003xxxxxx/PMC3807010.xml | A Case of Thyrotoxic Myopathy with Extreme Type 2 Fiber Predominance | A 55-year-old woman was admitted to our hospital with two years of progressive weakness of both legs. Initially, she had difficulty in climbing stairs and rising from a chair, but she felt no problem when she walked on flatland. Both legs weakness was progressed and she lifted up her both legs when going up stairs and walking on flatland at three months before visiting our clinic. Over the previous 1 year she had lost 2 kg in weight and become increasingly nervous, vulnerable to heat and shortness of breath on exertion. She had noticed tremor of the outstretched fingers and hyperhidrosis over the previous four months. However, there were no weakness of upper extremities, sensory symptom, myalgia, dysarthria and dysphagia. Physical examination revealed a mild degree of bilateral exophthalmos and diffuse enlargement of thyroid gland. The arterial blood pressure was 189/93 and the pulse was regular tachycardia and the frequency 118 per minute. Motor examination showed proximal muscle atrophy with MRC grade 4/5 in proximal limbs and grade 4+/5 in distal limbs. She showed Gower sign when trying to stand up from squatting but toe gait and heel gait were intact. Motor power of both upper extremities was normal and deep tendon reflexes were normal. Cranial nerve examination was intact and there was no sensory loss. No fasciculation or myotonic reactions were present.\nThe following laboratory test showed normal results: complete blood cell count, hemoglobin, C- reactive protein, erythrocyte sedimentation rate, serum electrolyte, calcium, urinalysis, blood urea nitrogen, creatinine, chest x-ray and liver function test. Serum creatine phosphokinase (CPK), lactate dehydrogenase (LDH), fluorescent antinuclear antibody (FANA) and rheumatoid factor were also normal. She was diagnosed with hyperthyroidism by thyroid function studies which showed free T4 9.02 (0.7-1.8 ng/dl), T3 680 (87-184 ng/dl) and thyroid stimulating hormone (TSH) 0.05 (0.4-4.1 µIU/ml). In thyroid autoantibodies studies, TSH receptor antibody 31.69 (0-1 IU/L) and antithyroid microsomal antibody 1,478 (0-60 U/ml) were increased. Tc-99m thyroid scan showed diffuse enlargement with evenly increased uptake (40.8%).\nElectromyography showed motor unit potentials of reduced amplitude and short duration (30%) in left vastus lateralis, tibialis anterior, peroneous longus and gastrocnemius muscles with early recruitment, but no spontaneous activity. These findings suggested a myopathic pattern. Muscle specimens were obtained from the vastus lateralis. Sections were stained with the modified Gomori trichrome and processed for the nicotinamide adenine dinucleotide-tetrazolium reductase (NADH-TR) reaction. Muscle fiber typing was done using the pH 9.4 myofibrillar adenosine triphosphatase (ATPase) reaction and cytochrome C oxidase (COX-2) immunohistochemistry staining. When examined by light microscopy and electron microscopy, size of myofibers was slightly variable and there were a few atrophic myofibers. There were no inflammatory infiltrates or blood vessel abnormalities (). There was extreme predominance of type 2 fibers (fast twitch) in the analysis of NADH-TR reaction, ATPase reaction and COX-2 immunohistochemistry staining ().\nFor treatment of hyperthyroidism and thyrotoxic myopathy, methimazole 15 mg/day was administered orally. After 1 month, hands tremor, shortness of breath, nervous and weakness of both legs were improved. She has continued methimazole treatment presently. | [[55.0, 'year']] | F | {'32606523': 2, '3065602': 1, '4162369': 1, '17479722': 1, '22048': 1, '26451739': 1, '5490661': 1, '25866834': 1, '509876': 1, '274725': 1, '4177247': 1, '4818413': 1, '24167418': 2} | {'7313581-1': 1} |
163,837 | 3807946-1 | 24,167,404 | noncomm/PMC003xxxxxx/PMC3807946.xml | Lipoma arborescens associated with osseous/chondroid differentiation in subdeltoid bursa | A 43-year-old, right-handed woman presented with complaints of pain and discomfort in her right shoulder. She had no history of previous injury or minor problems with her shoulder. The symptoms had begun after labor related to institutional food service for 1½ years. She had occasionally experienced a catching sensation and aggravated pain in the shoulder with labor activity. Symptoms were not alleviated by rest or non-steroidal anti-inflammatory drugs. Physical examination revealed positive findings for Neer's sign and Hawkins impingement test, Speed test and O’Brien's test. Patient's rotator cuff muscle strength was normal and no musculature atrophy was observed. The active range of motion (ROM) of the shoulder joint was mildly restricted during flexion, abduction and internal rotation, but passive ROM showed full range. The laboratory investigations including erythrocyte sedimentation rate and serology showed no significant results. Plain radiograph of shoulder demonstrated multiple rounds and ring like calcifications at the right glenohumeral joint with entheophyte at greater tuberosity of right humeral head []. Magnetic resonance imaging (MRI) of the shoulder showed a fluid-filled paralabral ganglion cyst that originated at the posterior superior labrum, forming a large cystic mass located at suprascapular and spinolgenoid notch around the spine of scapula [Figure and ]. The cyst originated at a tear of the superior labrum and extended to the posterior aspect of biceps long head origin [Figure and ]. The axial MRI also revealed fatty mass, which showed iso-signal intensity to the subcutaneous fat on all sequences, under intermuscular space located between anterolateral cortex of the humeral head and anterior belly of the deltoid muscle []. Another encapsulated mass was found in intermuscular space between infraspinatus and the deltoid muscle []. Abundant villous projection on the medial portion of the mass was located with multiple rings like or round low intensities on all pulse sequences. It showed background low signal intensity on T1-weighted image and high signal intensity on T2-weighted image, representing calcification arising from chondroid matrix [Figure and ]. Arthroscopy revealed a type II SLAP lesion with mild synovitis, but the articular cartilage of the humeral head and glenoid was intact. The detached posterior-superior labrum was fixed with sutures by insertion of two metal anchors. Patient subsequently underwent a separate incision laterally around the acromion and medially along the lateral one-third of the spine of the scapula. The origin of the deltoid was detached from the acromion and from the exposed part of the spine of the scapula. We retrieved LA and lipoma respectively. Lipoma size was 1.8 cm × 2.2 cm × 1.7 cm. LA size was 7.1 cm × 2.8 cm × 2.6 cm in the form of encapsulated mass. Opening the capsule revealed villous projection of fatty synovial tissue associated with central large whitish cartilaginous nodules attached to villous synovium []. Histologic examination demonstrated that diffuse papillary proliferation of the synovium with near total replacement of subsynovial tissue into mature fat tissue. Extensive area of osteochondral metaplasia in villous fat tissue was also seen [Figures and ].\nPost-operatively, the arm was placed at the side in a sling for 3 weeks. Passive motion including external rotation of the shoulder and ROM of the elbow were started immediately. This was followed by a home-based rehabilitation program of progressive ROM. Strengthening exercises for the rotator cuff, scapular stabilizers and deltoid were started 6 weeks post-operatively. She achieved full recovery in her affected shoulder within 3 months of surgery. At 2-month follow-up, the ultrasonogram demonstrated complete removal of LA, lipoma and cyst. She was asymptomatic and showed no recurrence of calcification on plain radiographs at a final follow-up 3 years after surgery. | [[43.0, 'year']] | F | {'2388216': 1, '7593260': 1, '18460687': 1, '12632038': 1, '30038543': 2, '15371618': 1, '7543810': 1, '12395279': 1, '31903223': 2, '7735751': 1, '10424336': 1, '19734739': 1, '18270682': 1, '9247000': 1, '8911186': 1, '25973368': 1, '12811424': 1, '33327323': 2, '3343272': 1, '20237127': 1, '15483537': 1, '11430745': 1, '21447530': 1, '27563476': 1, '1400636': 1, '16981949': 1, '16235076': 1, '24167404': 2} | {'7738011-1': 1, '6053968-1': 1, '6923803-1': 1} |
163,838 | 3807952-1 | 24,167,336 | noncomm/PMC003xxxxxx/PMC3807952.xml | Role of Sadyo Vamana in dental abscess (danta arbuda) | A 24-year-old, unmarried male was presented with pus filled dental abscess inside the left cheek, severe, persistent, throbbing toothache and sensitivity to the pressure of chewing orbiting, fever, swelling in cheek, foul-smell from mouth, tender, swollen lymph nodes under the jaw and neck since 15 days. He was on antibiotic and analgesic for 10 days before being presented, but there was no relief either in fever or in dental abscess. The patient was given SadyoVamana. External oleation and sudation given locally prior to administration of emetic drug to facilitate proper expulsion of morbid factors as mentioned in .\nInformed consent was obtained from the patient for documenting and publication.\nRoutine hematology (hemoglobin, total count, differential count and erythrocyte sedimentation rate [ESR] investigations were normal. ESR was high.\nPathya: The patient was advised to eat only light, hot and easily digestible food.\nApathya: The patient was advised not to take head bath, and was advised to avoid drinking cold water and eating curds, cold food. | [[24.0, 'year']] | M | {'22408299': 1, '22408302': 1, '23723669': 1, '24501448': 1, '23723640': 1, '24167336': 2} | {} |
163,839 | 3808021-1 | 24,174,760 | noncomm/PMC003xxxxxx/PMC3808021.xml | Sinus lift tissue engineering using autologous pulp micro-grafts: A case report of bone density evaluation | A male M.B., 45 years old, was selected in the Department of Oral Surgery, Don Orione Hospital, Bergamo, Italy. Informed written consent approved by the local Ethics Committee was obtained from patient to use his data for research purpose.\nThe patient had an unremarkable medical history, no other oral diseases, and he wanted to rehabilitate the upper right maxilla with dental implant-prosthetic therapy. He was taking no medications and denied any allergies. Before the surgery he underwent sextant scaling with ultrasonic and hand instruments. The same patient presented a third molar with advanced bone resorption but healthy for caries. We decided to extract the upper right third molar and extract the pulp to produce micro-gratfs for bone tissue regeneration of the upper left maxilla. | [[45.0, 'year']] | M | {'31636677': 1, '27826462': 1, '29021982': 1, '32992850': 1, '11689957': 1, '17931932': 1, '34712658': 1, '18300003': 1, '11087820': 1, '26967938': 1, '32420971': 1, '17452570': 1, '19908196': 1, '33457454': 2, '26620980': 1, '17625255': 1, '17524678': 1, '32536230': 1, '14574412': 1, '17409736': 1, '17347663': 1, '18215674': 1, '16873765': 1, '18211282': 1, '16953068': 1, '30400946': 1, '17764674': 1, '17565721': 1, '14574413': 1, '16222704': 1, '15085046': 1, '16622855': 1, '15270704': 1, '27738884': 1, '19065566': 1, '29924768': 1, '17432951': 1, '20228973': 1, '27126653': 1, '16007337': 1, '32398041': 1, '24174760': 2} | {'7782279-1': 1} |
163,840 | 3808022-1 | 24,174,761 | noncomm/PMC003xxxxxx/PMC3808022.xml | Multicentric peripheral ossifying fibroma: A case report and review of the literature | A healthy 11-year-old boy presented to the Postgraduate Department of Periodontics and Oral Implantology, with ‘slow-growing, painless, soft tissue masses in the maxillary posterior regions bilaterally’ that enlarged gradually for two months. The lesions started as small papules one year back. According to the patient, the lesions had been present for approximately two months and his mother stated that it had just recently become visible between the teeth [Figures and ]. Totally there were approximately five lesions, three in the maxilla and two in the mandible. In the mandible, the lesions were present between the lower right first premolar and deciduous first molar and on the left side between the deciduous first and second molar. As reported by the patient, the lumps were interfering with his bite and felt uncomfortable. Occasionally, bleeding occurred when he brushed his teeth.\nThe lesions initially occurred on one side of the mouth and in a subsequent course of time involved both sides. Both the maxillary and mandibular gingivae were affected and the growths appeared as nodular masses, with erythematous and ulcerated surfaces. The growths were sessile and firm in consistency measuring anywhere between 5 mm and 3 cm in diameter. The lesions appeared reddish-pink in color and were slightly pedunculated, with what appeared to be a broad-based attachment. The lesions were not fluctuant, nor did they blanch with pressure, but had a rubbery consistency. The lesions were tender to firm pressure, but not to light palpation.\nPanoramic radiographs were obtained []. The radiographs did not reveal any abnormality and there was no finding pertaining to the multiple exophytic lesions.\nThe laboratory tests performed included, a complete blood hemogram and lipid and thyroid profiles. All the test results were within normal limits except for the total leukocyte count, which was slightly more than normal (12800/mm3 of blood).\nOn histopathological examination, upon low power magnification (4x), the lesional tissue exhibited a keratinized stratified squamous epithelium (gingiva), overlying a fibrous connective tissue stroma exhibiting dense interlacing bundles of collagen and numerous ossifications []. High power magnification (40x) showed pink homogenous calcified tissue (ossification), with a presence of osteocytes entrapped in the lacunae []. The histology for all the lesions was the same. The picture is consistent with the clinical diagnosis of POF.\nUnder local anesthesia, the lumps were excised completely using a scalpel. The tissue was submitted to the Oral Pathology Division for histopathological diagnosis. The deciduous teeth present in the lesion were also removed and included in the biopsy specimen. The adjacent teeth were scaled to remove any local irritants.\nThe patient presented for a follow-up examination 20 days postoperatively. The surgical site appeared to be healing well [Figures and ]. There was no evidence of recurrence of the lesion and the child was asymptomatic. | [[11.0, 'year']] | M | {'8708123': 1, '9866149': 1, '11495143': 1, '26556782': 1, '3472146': 1, '4626993': 1, '17220623': 1, '6422375': 1, '9526731': 1, '2216359': 1, '12657032': 1, '2120653': 1, '15553980': 1, '11500629': 1, '19212524': 1, '6750498': 1, '10793367': 1, '6936553': 1, '5223950': 1, '11447957': 1, '4199101': 1, '15855714': 1, '5248843': 1, '2926546': 1, '1940738': 1, '24174761': 2} | {} |
163,841 | 3808023-1 | 24,174,762 | noncomm/PMC003xxxxxx/PMC3808023.xml | Peripheral odontogenic myxoma of maxillary gingiva: A rare clinical entity | A 41-year-old female patient was referred to our department with history of a slowly enlarging gingival mass in the anterior maxilla of 6 months duration. There was no associated history of trauma, pain, or tooth extraction. Intraoral examination revealed a solitary, non-tender swelling on the labial gingiva of the left maxilla in relation to 21 and 22, measuring about 1 × 2 cm []. The lesion was firm in consistency and the mucosa covering the lesion was normal in color; no mobility of the regional teeth was seen. The rest of the clinical head and neck examination was unremarkable. No radiographic changes were seen associated with the lesion []. Based on the overall findings, provisional diagnosis of fibroma was made.\nThe lesion was surgically excised under local anesthesia and subjected to histological examination. Microscopic examination of Hematoxylin and Eosin stained section demonstrated atrophic, parakeratinized stratified squamous surface epithelium []. Underlying stroma showed abundant loose myxoid tissue containing few collagen fibrils. The tumor was composed of loosely arranged spindle- and stellate-shaped fibroblasts with small round nuclei suspended in a delicate network of collagen fibrils [Figures and ]. Small blood vessels were also present and no noticeable odontogenic islands were seen. A diagnosis of peripheral OM was made. Six months of follow-up showed no evidence of recurrence. | [[41.0, 'year']] | F | {'27994429': 2, '28770159': 1, '8445469': 1, '16827840': 1, '10982957': 1, '8307237': 1, '12800761': 1, '3456413': 1, '15145033': 1, '16367860': 1, '18642035': 1, '23449257': 1, '18245926': 1, '18088737': 1, '2037972': 1, '8509916': 1, '8600281': 1, '24174762': 2} | {'5141676-1': 1} |
163,842 | 3808024-1 | 24,174,763 | noncomm/PMC003xxxxxx/PMC3808024.xml | An unusual clinical presentation of gingival melanoacanthoma | A 13-year-old male patient attended the Department of Periodontics, Mahatma Gandhi Post Graduate Institute of Dental Sciences, Pondicherry, in May 2011 for gingival enlargement and difficulty in mastication. The patient was otherwise healthy. He first noticed enlargement 6 months earlier along the buccal aspect of tooth 26, which increased in size slowly to the present clinical picture. The clinical examination was significant for the presence of pigmented diffuse gingival enlargement along buccal and palatal aspects of 24, 25, 26, 27 and lingual aspects of teeth 34, 35, 36, 37 []. Gingival enlargement was extending up to middle third of the crown of tooth 24, partially covering the occlusal surface of teeth 25, 26 and completely covering the tooth 27 [] and extending up to occlusal surface of teeth 34, 35, 36, 37. The gingival enlargement was firm in consistency, painless, brownish black in color with well-defined borders and there was no associated erythematous background.\nOther significant dental findings included root canal treated fractured tooth 21 and congenitally missing tooth 23. Patient's oral hygiene was deemed satisfactory. There was no significant medical history. Patient was not having any associated cutaneous pigmentary changes. Based on the clinical findings, provisional diagnosis of idiopathic gingival enlargement was made and gingivectomy was planned for the treatment.\nPatients’ parents provided oral consent for treatment prior to the initial and additional tests and the dental treatment that followed. Routine blood investigations were found to be within normal limits. Gingivectomy was performed under local anesthesia on the buccal aspect of II quadrant [] and the excised tissue was sent for biopsy []. One week later, gingivectomy was performed on the palatal aspect of II quadrant followed by lingual aspect of III quadrant after 1 week. Kirkland knives were used for incisions on the facial and lingual surfaces. Orban periodontal knives were used for interdental incisions. Patient experienced an uneventful post-operative recovery [] at 1 year recall examination there was no recurrence of gingival enlargement at the surgical sites []. Patient will continue to be monitored on a 6 month basis and any new gingival enlargement/lesion will undergo histopathologic investigation.\nHistopathological examination revealed numerous dendritic melanocytes distributed in basal and suprabasal layers of acanthotic epithelium. Melanocytes did not display any cytologic atypia []. The connective tissue was normal except for the presence of occasional eosinophils. There was no spillage of melanin pigment/melanocytes in subepithelial zone []. Histopathologic diagnosis of oral melanoacanthoma was rendered. | [[13.0, 'year']] | M | {'19254138': 1, '17767102': 1, '27398186': 1, '31110620': 2, '18173514': 1, '11763954': 1, '18254569': 1, '21465013': 1, '2179347': 1, '3378373': 1, '32313756': 2, '19776516': 1, '3467289': 1, '12544093': 1, '15530266': 1, '15357676': 1, '3422293': 1, '3056992': 1, '6581460': 1, '24174763': 2} | {'7164714-1': 1, '6522109-1': 1} |
163,843 | 3808025-1 | 24,174,764 | noncomm/PMC003xxxxxx/PMC3808025.xml | Six year follow-up of a root coverage procedure on a lower molar tooth with lateral pedicle flap | A 62-year-old female patient, presented to the dental clinic with a chief complaint of bad breath along with bleeding gums, difficulty in mastication and inability to maintain deposit free teeth in relation to the right lower back region. On clinical examination, there were local factors present and she had faulty tooth brushing practice. An isolated Miller's Class III recession defect[] was observed in relation to the mesial root of 46 []. Tooth 45 was missing and un-replaced. The edentulous space was slightly collapsed due to mesio-buccal tilting of 46. There was visible food impaction in between 46, 47 and 48. Dental caries was diagnosed distal to 46 and 47. Patient was systemically healthy without any deleterious habits.\nPhase 1 therapy consisting of thorough oral prophylaxis and root planning was performed on 46 and caries was restored. Vitality check showed a non-vital 47. Root canal treatment was done for 47. Oral hygiene practice was corrected and the patient was recalled after a month. Patient maintained a good oral hygiene. LPF was planned for the root coverage and was explained to the patient and an informed consent was obtained.\nThe gingival recession was in relation to the mesial root of 46 and was measured. The dimensions were 4 mm wide and 8 mm deep. Donor site was adjacent edentulous area in relation to 45. There was sufficient width, length and thickness of keratinized tissue present. Oral hygiene and patient maintenance was satisfactory.\nNumber 15 blade was used to make a crestal incision on the adjacent edentulous area in relation to 45 and was extended to make a crevicular incision that crossed the apical area around the gingival recession. Vertical releasing incisions were performed on both sides, one distal to the mesial root of 46 and the other distal to 44. The pedicle flap size was 1.5 times wider than the area of the recession. Vertical incisions were extended to the alveolar mucosa so that the pedicle flap could be reflected sufficiently to enable the lateral displacement without tension. A full thickness flap was then reflected sufficiently from the donor site and displaced without tension at the recipient site. Suturing was done using 4-0 non resorbable silk suture. Area was cleaned and Coe pack applied [Figures –]. Cap Amoxicillin 500 mg tid, tablet meftal forte tid and chlorhexidine mouth wash thrice daily for 5 days were prescribed. Patient was advised to have a soft diet and avoid brushing in the area of surgery. Sutures were removed after 10 days. Healing was satisfactory.\nAfter completion of the procedure, approximately 7 mm of recession attained clinical attachment gain and adequate width of attached gingiva was appreciated []. After 6 months, coverage increased to 8 mm probably due to creeping attachment []. On review the periodontium looked healthy and the maintenance was satisfactory even after the 3rd year. Hence the next phase of treatment was started.\nFollowing crown preparation, a 4-unit bridge was constructed from 44 to 47 []. Follow-up visits were scheduled 2 months post-operative and subsequently after 4, 5 and 6 years [Figures –]. Maintenance was satisfactory and the gingiva maintained the same level of attachment throughout 6 years without any clinical sign of inflammation. | [[62.0, 'year']] | F | {'7823274': 1, '33144774': 1, '8229627': 1, '20142945': 1, '10972649': 1, '5282573': 1, '3546673': 1, '24174764': 2} | {} |
163,844 | 3808026-1 | 24,174,765 | noncomm/PMC003xxxxxx/PMC3808026.xml | Intentional replantation of periodontally compromised hopeless tooth | Systemically healthy 24-year-old male patient came to Department of Periodontics, with the complaint of unaesthetic appearance of upper central teeth because of forwardly placed maxillary left central incisor since 6 months. Patient gave history of extraction of supernumerary tooth, which was placed palatal to 11 and 21, 3 months back. 21 had gradually come to the present position over 6 months []. Patient was also complaining about functional problems of the upper central teeth because of loss of biting ability due to forwardly placed and mobile tooth. During the clinical examination, approximately 6 mm of periodontal pocket were observed with 21. Radiographic examination was revealed moderate alveolar bone resorption reaching to the middle third of the tooth []. Mobility of the tooth was Grade II.\nPatient demanded not to loose any teeth because of psychological reasons during the treatment plan phase. Considering patient's demands and the clinical situation, the treatment plan of upper anterior teeth (21) decided as Phase I periodontal therapy and intentional replantation and relocation of maxillary left central incisor followed by periodontal splint. Oral hygiene motivation, scaling and root were as the initial periodontal therapy. At the 4th week after the initial therapy, a considerable improvement in oral hygiene and gingival health and slight reduction in periodontal pocket depths were observed during the clinical examination. Endodontic treatment was performed prior to intentional replantation in three visits.\nAfter giving local, gingival attachments of central teeth were removed by periotome and sulcular incisions. Left upper central tooth was gently and atraumatically extracted []. Granulation tissues in the extraction sockets were removed by gentle curettage and the sockets were rinsed with sterile saline []. All irritants and necrotic cementum were removed from the root surfaces with periodontal curettes carefully. Extruded tooth was put into position by preparing the reimplantation site [], at the apical end of the socket to accommodate the tooth in the new position. Tooth was then placed into the socket in an adequate position contacting their roots directly to the alveolar bone []. The replanted tooth was then splinted with composite splint [].\nPatient was advised not to eat stiff foods using maxillary anterior teeth at least for 3 months. Patient was prescribed amoxicillin 1 g. Bid for 5 days along with an analgesic and also recommended to use interdental brush at the replantation site, in addition to the routine oral hygiene attempts. Chlorhexidine mouthwash 0.2% was prescribed twice daily for 14 days. Regenerative therapy was carried out 3 months later. Patient was placed in a maintenance recall program every month for the first 3 months and every 3 months thereafter [] 6 months post-operative showing bone fill [] following regenerative therapy. The necessary oral prophylaxis was done, oral hygiene instructions were reinforced and splint integrity was checked along with clinical parameters at every recall visit.\nPatient is under continued supportive periodontal therapy and has not shown any untoward effects of root resorption or mobility other than slight papillary recession at 14 months follow-up as per clinical and radiographic evaluation [Figures and ]. | [[24.0, 'year']] | M | {'9776033': 1, '12656855': 1, '30131630': 2, '9248694': 1, '6928908': 1, '24716000': 2, '8206180': 1, '24174765': 2} | {'6077966-1': 1, '6077966-2': 1, '3970054-1': 1} |
163,845 | 3808027-1 | 24,174,766 | noncomm/PMC003xxxxxx/PMC3808027.xml | Management of chronic luxated central incisor with hopeless prognosis | A 16-year-old boy reported, with a chief complaint of mobile upper front teeth. His dental history revealed history of trauma 8 months back. Trauma led to avulsed maxillary right central incisor (11), extrusively luxated displaced out of the arch with Grade III mobility maxillary left central incisor (21), fractured (Ellis Class III) left lateral incisor (22) [].\nPulp sensibility was performed and both left central and lateral incisor (21, 22) were found to be nonresponsive. Intraoral radiographs revealed severe bone loss with respect to maxillary left elicited with right lateral incisor (12). Fremitus test was found to be negative. Case was diagnosed as primary endo and secondary perio lesion. The prognosis of tooth (21) appeared to be hopeless. Hence, extraction was advised for the left central incisor (21), which was extruded, non-responsive and had severe bone loss. Various replacement options such as RPD and implant were suggested to patient, but patient was keen on retaining his natural tooth and had financial constraints.\nHence, intentional replantation was considered as a treatment option. The probable outcome of treatment and complication were explained to patient and written consent was obtained.\nThe main goal of treatment was to achieve a conservative approach and thereby fulfill the individual's requirement. Treatment plan consisted of Phase I therapy followed by endodontic treatment, which was to be followed by intentional replantation.\nPhase I therapy was performed and patient was posted for endodontic treatment. Calcium hydroxide dressing was given for 2 weeks followed by obturation with Gutta percha.[] Surgery was planned 1 week after completion of endodontic treatment.\nLocal anesthesia (2% lignocaine HCl with 1:80000 adrenalines) was administered. Full thickness mucoperiosteal flap was reflected. On flap reflection, severe bone loss extending more than 2/3rd root length on palatal aspect was seen []. Tooth was atraumatically extracted and was immediately placed in a solution of tetracycline (500 mg of tetracycline dissolved in 20 ml saline) for a period of 5 min[] and was then transferred to a solution of sodium fluoride (0.05% w/v) for a period of 5 min [Figures and ]. After degranulation and curettage, PRF was prepared.\nA total volume 10 ml of blood was withdrawn, which was immediately centrifuged at 3000 rpm for preparation of PRF.[] PRF obtained was mixed with nano hydroxyapatite (HA) crystals and was placed in the tooth socket and bony defect. The tooth was replanted and aligned []. Flap was repositioned immediately and sutured using 3-0 silk sutures. Fiber reinforced composite resin splinting was done, periodontal pack was applied. Patient was put on amoxicillin 500 mg tid for 5 days and a combination of aceclofenac and paracetamol bid was given for 3 days. Mouthwash containing 0.2% chlorhexidine was advised from the day following surgery. Patient was recalled after 1 week for suture removal, revealed satisfactory healing was seen.\nIntraoral periapical radiograph (IOPAR) using long cone technique was taken to ascertain alignment of the tooth [Figures and ]. Oral hygiene instruction was reinforced and strict instruction not to bite on anterior teeth was given. Patient was put on regular recall visits.\nPatient was recalled after 2 months and it was observed that there was a significant reduction in in probing pocket depth. Radiograph taken revealed radiopacity in periapical area suggestive of periodontal repair or regeneration [].\nIn 3rd month, IOPAR has taken revealed significant radiopacity in periapical area []. Splint was removed. Mobility was found to be remarkably reduced to Grade I with a significant reduction in probing pocket depth. As mobility was reduced and patient was comfortable, esthetic correction was planned. Right central incisor (11) had avulsed and the left central incisor (21) had migrated toward midline so, a composite buildup of right lateral incisor (12) was performed. This was followed by restoration of Ellis Class III fractured 22, using post-placement followed by composite buildup []. Furthermore, lingual splint was placed in the region of 22 and 21 [].\nPatient was satisfied with the esthetic outcome. Patient has been followed-up for 6 months and so far the treatment outcome has been found to be esthetically and functionally satisfactory. | [[16.0, 'year']] | M | {'3459127': 1, '27504421': 1, '30131630': 2, '6928908': 1, '17511843': 1, '1723382': 1, '19958903': 1, '17546867': 1, '21564520': 1, '2984404': 1, '14708652': 1, '16504852': 1, '15025689': 1, '7641620': 1, '16504850': 1, '20881816': 1, '20373539': 1, '19089687': 1, '21284545': 1, '14708651': 1, '12656855': 1, '22051114': 1, '16504861': 1, '2559181': 1, '19589702': 1, '18173657': 1, '8724716': 1, '24174766': 2} | {'6077966-1': 1, '6077966-2': 1} |
163,846 | 3808033-1 | 24,174,771 | noncomm/PMC003xxxxxx/PMC3808033.xml | Self-limiting symptomatic peri-ictal bradyarryhthmia due to junctional AV rhythm | A 66-year-old gentleman had generalized tonic-clonic seizures (GTCS) since the age of 14 years, which was well controlled for nearly two to three decades with antiepileptic drug (AED) viz., phenytoin – 300 mg/day and phenobarbitone – 120 mg/day. Cranial CT scan was reported to be normal. For the last 10 months, there was recurrence of seizures. The seizure frequency was 1-2 episodes per month in spite of polypharmacy with valproate (900 mg/day), carbamazepine (800 mg/day) and phenobarbitone (120 mg/day). He did not have any comorbid illnesses such as ischemic heart disease, diabetes mellitus or hypertension.\nHe was presented to us 3 days following an episode of GTCS with a confusional state. Initial examination revealed a disoriented patient with gait ataxia, fine tremor of outstretched hands, pes cavus and hammer toes and diminished ankle jerks. There were no other neurological or systemic deficits. Routine investigations including hemogram were within normal limits. Routine ECG on admission was normal. Scalp EEG at admission showed generalized slowing in theta range and there was no epileptiform activity. Routine serum biochemical parameters including liver and renal function tests and electrolytes were normal. Plasma ammonia was slightly raised (76.8 μmol/L; range: 11-35 μmol/L). MR imaging of brain carried out showed mild generalized atrophy with a cystic lesion secondary to gliosis of the left anterior temporal region []. The serum levels of phenobarbitone was elevated [53.35 μg/ml; reference range: 15-40 μg/ml], while that of carbamazepine was 7.11 μg/ml [range: 4-12 μg/ml] and valproate was 33.58 μg/ml [range: 50-100 μg/ml] were within therapeutic limits. A possibility of chronic uncontrolled symptomatic localization related secondary generalized epilepsy due to gliosis in the left temporal region with phenobarbitone toxicity was considered after evaluation. Tablet phenobarbitone was tapered and levetiracetam was initiated (1000 mg/day).\nOn the third day of hospitalization, the patient had a generalized seizure. During the immediate postictal period, he was drowsy and diaphoretic, with shallow respiration, bradycardia [pulse rate: 52/min, feeble radial pulse] and hypotension [systolic blood pressure: 60 mmHg]. There was no cyanosis. An electrocardiogram obtained at this time showed a heart rate of 43/min, with p-wave coming after QRS complex suggestive of junctional AV rhythm []. He was given supportive treatment with nasal oxygen (3 L/min), intravenous fluids and dopamine (10 μg/kg/min). About 40 minutes later, the heart rate normalized to 72 per minute and blood pressure rose to 100/80 mmHg. The 2-D echocardiogram showed only a mild left ventricular hypertrophy. The serum creatine kinase-MB [21 U/l; normal 9-25 U/l) and Troponin-I done after 4 hours was 0.6 ng/ml (ref: Up to 0.1). Repeat Troponin-I was 0.6 ng/ml. A repeat ECG carried out 2 hour later was normal []. He recovered completely and at the time of discharge 11 days later, he did not have any neurological deficits.\nThis event led to a possibility of self-remitting in-hospital symptomatic ictal bradyarrythmia (junctional AV rhythm) and hypotension during a generalized seizure. After 6 months of follow-up, he was asymptomatic and seizure free on levetiracetam and valproate. | [[66.0, 'year']] | M | {'20132291': 1, '19909325': 1, '19171456': 1, '3947265': 1, '12458028': 1, '16952443': 1, '24741239': 1, '9818844': 1, '22698381': 1, '17664402': 1, '22637287': 1, '16005188': 1, '19909329': 1, '8112246': 1, '11467468': 1, '24174771': 2} | {} |
163,847 | 3808034-1 | 24,174,772 | noncomm/PMC003xxxxxx/PMC3808034.xml | The role of lumbar puncture and pressure-lowering therapy for transverse dural sinus thrombosis | An 11-year-old girl with no significant past medical history presented to the ED complaining of 2 days of worsening headache, vomiting, and double vision. Approximately 2 weeks earlier, the patient was seen by her primary care physician (PCP) for evaluation of flu-like symptoms, headache, and left-sided neck pain. Examination at that time revealed an erythematous right tympanic membrane. The patient was diagnosed with AOM and started on oral amoxicillin/clavulanate. The patient continued to complain of worsening headache for 7 days following PCP evaluation, at which point she developed diplopia, nausea, and vomiting. She was subsequently taken to the ED for evaluation.\nNon-contrast CT revealed an asymmetrically hyperdense right transverse sinus []. Brain MRI demonstrated a thrombus in the right transverse sinus as well as fluid within the right mastoid air cells consistent with mastoiditis [Figures -]. A filling void in the right transverse sinus, consistent with a right transverse sinus thrombosis, was found on MRV [].\nNeurology evaluation did not reveal any focal abnormalities but ophthalmic examination was incomplete; LP was not recommended. The patient was admitted to the pediatric intensive care unit where heparin drip and intravenous antibiotics were started. Hypercoagulablity studies were negative. Ophthalmology consultation found a small right esotropia in primary gaze; optic disc edema bilaterally; and nerve fiber layer hemorrhages more pronounced in the right fundus than left. The patient was diagnosed with papilledema and palsy of the right cranial nerve VI, secondary to increased ICP.\nThe patient was discharged on oral cefdinir without performing an LP or ICP-lowering therapy. Outpatient ophthalmology follow-up 2 weeks later found worsening headache, persistent papilledema, and esotropia in primary and right-gaze. Formal visual field testing revealed enlarged blind spots bilaterally. The patient was referred to the ED for LP which revealed an opening pressure of 310 mm H2O (upper limit of normal 210 mm); the patient was started on oral acetazolamide. CSF studies were otherwise unremarkable. Follow-up examination 2 weeks later revealed improvement in headache and complete resolution of diplopia and esotropia. | [[11.0, 'year']] | F | {'17058373': 1, '20402748': 1, '15746223': 1, '18533553': 1, '20561500': 1, '17097444': 1, '18184940': 1, '14976332': 1, '9313731': 1, '10534264': 1, '24174772': 2} | {} |
163,848 | 3808035-1 | 24,174,773 | noncomm/PMC003xxxxxx/PMC3808035.xml | Occult spontaneous lateral intrasphenoidal encephalocele: A rare presentation | A 37-year-old male patient presented with complaints of transient loss of consciousness and persistent headache after minor head injury. He had no past history of head injury or brain surgery. Neurological examination was normal and there was no stigma of neurofibromatosis. Plain CT head did not show any brain parenchymal or bony injury. Contrast-enhanced 3-mm axial and coronal CT images of paranasal sinuses [Figure and ] revealed a large (approximately 12 mm in size) defect in the right lateral wall of the sphenoid sinus with herniation of a part of the right mesial temporal lobe through the defect, to occupy the ipsilateral lateral recess of the sphenoid sinus. The remaining part of the right sphenoid sinus showed mucosal thickening. The bones around the defect and encephalocele showed remodeling and appeared thinned out [Figure and ]. There was no evidence of meningitis or any other intracranial abnormality. CT cisternography was not performed as there was no history of nasal discharge. Further evaluation of the lesion with MRI was not possible because the patient was claustrophobic and refused to undergo sedation.\nThe surgical exploration confirmed the CT finding of a large bony defect in the right lateral wall of the sphenoid sinus, lateral intrasphenoidal encephalocele occupying the lateral recess with otherwise intact dura. Mild ipsilateral sphenoid sinus mucosal thickening was also documented. Endoscopic transpterygoid approach was used and the herniated brain tissue with intact dura was gently pulled up and the bony defect was closed to prevent future risk of CSF leak, ascending meningitis or brain abscess. The abnormal mucosal thickening was stripped off and space within the right sphenoid sinus was filled with free fat graft. The patient had a good postoperative recovery and was advised cross-sectional follow-up study after six months to confirm the integrity of the repair. | [[37.0, 'year']] | M | {'8588663': 1, '29732314': 1, '11077102': 1, '8972647': 1, '12368619': 1, '24174775': 1, '16169229': 1, '31528393': 2, '19881112': 2, '5059344': 1, '24174773': 2} | {'2797748-1': 1, '6743700-1': 1} |
163,849 | 3808038-1 | 24,174,776 | noncomm/PMC003xxxxxx/PMC3808038.xml | Giant cavernous carotid aneurysm with spontaneous ipsilateral ICA occlusion: Report of 2 cases and review of literature | A 65-year-old lady presented with 3-month history of facial numbness and occasional pain involving the left half of the forehead and left cheek and left sided ptosis. The symptoms were insidious in onset and not associated with any history suggestive of a subarachnoid hemorrhage. Clinical examination revealed complete ophthalmoplegia and hypoesthesia in the ophthalmic and maxillary divisions of the left trigeminal nerve.\nShe was evaluated with an MRI [Figure and ] which showed a giant partially thrombosed aneurysm in the left ICA cavernous segment. She was planned for a DSA with possible balloon test occlusion. DSA revealed complete occlusion of left ICA, without any filling of the aneurysm [Figure and ]. There was excellent cross-flow through anterior communicating artery, which was supplying the entire left hemisphere. There was no filling of the aneurysm through the right ICA or vertebral artery injection. MRA [] revealed lack of flow through the left ICA and the cavernous aneurysm.\nThe patient was managed conservatively and was put on aspirin to prevent further progression of the thrombus. At 6 month follow-up, the patient was doing well, her ophthalmoplegia had completely improved however, the pain and numbness over the left half of the face persisted. | [[65.0, 'year']] | F | {'3810738': 1, '19409005': 1, '12686795': 1, '7054441': 1, '11593970': 1, '30937059': 2, '2362671': 1, '7422064': 1, '12450106': 1, '1403108': 1, '10447280': 1, '28761512': 1, '11130752': 1, '15605203': 1, '2219219': 1, '1891762': 1, '19547823': 1, '24174776': 2} | {'3808038-2': 2, '6417339-1': 1} |
163,850 | 3808038-2 | 24,174,776 | noncomm/PMC003xxxxxx/PMC3808038.xml | Giant cavernous carotid aneurysm with spontaneous ipsilateral ICA occlusion: Report of 2 cases and review of literature | The second patient was a 55-year-old lady who presented with 2 episodes of generalized tonic clonic seizures 3 months prior to admission. She also developed visual deterioration in left eye, left ophthalmoparesis and left facial pain. Visual acuity in the left eye was perception of hand movements close to her face. She had paresis involving the left VI nerve, left relative afferent papillary defect and mild sensory loss in the left ophthalmic nerve distribution.\nMRI brain showed a 2.8 × 2.6 × 2.1 cm lesion in the cavernous sinus suggestive of giant ICA aneurysm [Figure and ]. DSA [Figure and ] revealed occlusion of the proximal ICA on the left side without any filling of the cavernous segment aneur ysm. On the right ICA injection, there was excellent cross flow across the anterior communicating artery, with a small aneurysm in the contralateral cavernous ICA.\nThis patient was also put on aspirin for stroke prevention. At 3-month follow-up, her visual acuity remained the same however, her ophthalmoparesis improved. | [[55.0, 'year']] | F | {'3810738': 1, '19409005': 1, '12686795': 1, '7054441': 1, '11593970': 1, '30937059': 2, '2362671': 1, '7422064': 1, '12450106': 1, '1403108': 1, '10447280': 1, '28761512': 1, '11130752': 1, '15605203': 1, '2219219': 1, '1891762': 1, '19547823': 1, '24174776': 2} | {'3808038-1': 2, '6417339-1': 1} |
163,851 | 3808039-1 | 24,174,777 | noncomm/PMC003xxxxxx/PMC3808039.xml | Isolated cysticercosis of the cauda equina | A 44-year-old housewife, born in Ecuador and otherwise healthy, was referred to us with a two years history of low back pain and left L5 radiculopathy complicated with more recent complaints of urinary incontinence and progressive paraparesis. Neurological examination disclosed muscle strength as grade — in both lower extremities with consensual diminished reflexes. Moreover, the patient presented hypoesthesia in the left L5 dermatome and saddle anesthesia. Magnetic resonance imaging (MRI) of the lumbar spine revealed two well-defined intradural cystic lesions, without contrast-enhancement, at L4-L5 level []. Our presumptive diagnosis was an intradural tumor of the cauda equina. This is why we did not perform any specific serologic or cerebrospinal fluid (CSF) tests. Therefore, the patient was subjected to L4-L5 laminectomy, but when the osteotomy was completed we had a surprise. The underlying dura appeared tough and tense with a spontaneous laceration in one point, through it a small cyst came out. After opening the dura the roots appeared tied up in bundle around two other lesions, not having been disclosed by preoperative MRI. By careful microsurgical dissection, the cystic masses were removed in toto, thanks to a clear cleavage plane []. The wound was irrigated with saline solution. The specimens were sent for histopathological analysis. Gross examination showed three transparent cysts and each one presented a small yellowish nodular area []. Histological examination demonstrated the cystic wall consisted of an outer cuticular layer with brush-like border, an epithelial-like intermediate layer, and an inner reticular layer made up of a canaliculi network. The scolex was not been identified []. Racemosus type of NCC was the final diagnosis. Post-operatively, the patient was treated with albendazole (15 mg/kg per day) for 4 weeks along with dexamethasone (4 mg\twice\daily for 1 week, then 4 mg per day for 10 days and every other day for 6 days). Clinically, the woman showed marked improvement in pain and motor strength, and a complete cranio-spinal MRI evaluation excluded any other cysticercosis lesions. The neuroradiologic follow-up studies, performed at 3, 6 months and 1-year after the operation [], demonstrated a complete resolution of the parasitic disease. The patient returned to her normal daily activities three months after the surgical procedure. | [[44.0, 'year']] | F | {'4012566': 1, '34926816': 2, '25540547': 1, '11105310': 1, '2849066': 1, '15926788': 1, '21722242': 1, '21430986': 1, '24174778': 1, '2264792': 1, '20118838': 1, '7650528': 1, '17719976': 1, '24174777': 2} | {'8674092-1': 1} |
163,852 | 3808041-1 | 24,174,779 | noncomm/PMC003xxxxxx/PMC3808041.xml | Fourth ventricular ependymoma with a distant intraventricular metastasis: Report of a rare case | A 23-year-old man presented with progressive swaying to either side while walking for five months and progressive headache associated with vomiting for four months prior to presentation. There was no history of seizures, diplopia or similar illness in family members. Examination revealed bilateral papilloedema and bilateral cerebellar signs. The patient was initially evaluated by a general practitioner at local hospital with computed tomography (CT) of the head. It revealed a midline posterior fossa mass lesion, isodense on non-contrast CT and enhancing heterogeneously on contrast injection with obstructive hydrocephalus. He was subsequently referred to our hospital. The patient was first seen at our hospital two months after the initial CT scan. Magnetic Resonance Imaging (MRI) of the brain done about 2 months after initial CT showed increase in the size of the tumor which was isointense on T1WI and T2WI and enhancing heterogeneously on gadolinium contrast injection. The lesion was completely intra-fourth ventricular []. Another lesion was noted in the septum pellucidum extending to the frontal horn of the left lateral ventricle causing obstruction of the foramen of Monro on the left side []. It had the same signal characteristics as that of the tumor. This lesion was not present in the initial CT scan [], which was done two months prior to the MRI. There were no other lesions seen on craniospinal MRI.\nIn view of severe symptoms of raised intracranial pressure, he initially underwent ventriculo-peritoneal shunt placement followed by midline sub-occipital craniectomy and near total excision of the tumor except for the part adherent to the brainstem. Post-operatively, he recovered well.\nHistopathological examination showed a cellular glial neoplasm consisting of proliferating ependymal cells arranged in compact sheets and several intervening perivascular rosettes. The cells exhibited brisk mitotic activity (6 to 7 in 10 high power fields) with areas of necrosis []. These features suggested a diagnosis of anaplastic ependymoma (grade III).\nThe patient was subsequently referred to radiation oncologist for adjuvant therapy. | [[23.0, 'year']] | M | {'12382522': 1, '19360419': 1, '11949823': 1, '29770253': 2, '18698591': 1, '8177398': 1, '18682894': 1, '26798226': 2, '3944630': 1, '19458954': 1, '26622745': 1, '16933138': 1, '7754745': 1, '15223962': 1, '6347998': 1, '17449478': 1, '30946332': 2, '24174779': 2} | {'6455983-1': 1, '4720801-1': 1, '5938895-1': 1} |
163,853 | 3808042-1 | 24,174,780 | noncomm/PMC003xxxxxx/PMC3808042.xml | Intra cranial hydatid cyst: A case report of total cyst extirpation and review of surgical technique | A 22-year-old unmarried female presented to our outpatient department with one and half year history of headache of mild to moderate intensity, dull in nature, with no variation with time. She had no complaint of vomiting, tinnitus, hearing or vision loss. There was no history of head injury. Fundoscopy revealed normal fundi. There were no lateralizing or localizing signs. Laboratory data showed mild leucocytosis without significant eosinophilia. Her liver function tests were within normal limits. Plain chest X-ray and ultrasound scan of the abdomen and pelvis did not show any abnormality. CT scan of brain demonstrated a single large, spherical, well-defined, thin-walled homogenous, iso-dense cyst in the frontoparietal region, with non-enhancing wall [Figures and ]. This cyst was causing a midline shift of 1 cm, as well as dilatation of ventricles. MRI showed unilocular isointense cyst without surrounding edema []. Hence the diagnosis of a hydatid cyst was made. The patient underwent right frontotemporoparietal craniotomy. Following removal of bone flap and opening the dura, a small corticotomy of 1.5 cm was made in the frontal lobe through which the cyst was identified. A 10 French drainage tube was passed between the cortex and the cyst wall. Normal saline was carefully pushed in through this tube (Dowling's technique) to deliver the cyst measuring 5.5 × 5.8 cm2 []. A hydatid cyst was confirmed on histopathology. A CT scan after 48 hours of surgery showed a large cerebrospinal fluid (CSF) filled space without any residual cyst []. Post-operatively, Albendazole 10 mg/kg twice daily was started and continued for four months. The patient was discharged on third post-operative day with close follow-up. On subsequent follow up visits the patient had no headache or seizures. | [[22.0, 'year']] | F | {'9085285': 1, '29744124': 2, '11595368': 1, '15608487': 1, '12434174': 1, '12389111': 1, '27994696': 1, '12640161': 1, '17765392': 1, '18230279': 1, '16494758': 1, '10602860': 1, '28127351': 1, '1175437': 1, '24174781': 1, '11338110': 1, '16679658': 1, '20013283': 1, '21845570': 1, '15389350': 1, '18342511': 1, '17803790': 1, '10883898': 1, '18485645': 1, '27695250': 1, '19439838': 1, '11778827': 1, '19431138': 1, '18518745': 1, '17434701': 1, '19585129': 1, '18082448': 1, '16374567': 1, '11151730': 1, '24174780': 2} | {'5934678-1': 1} |
163,854 | 3808069-1 | 24,174,807 | noncomm/PMC003xxxxxx/PMC3808069.xml | Primary malignant peripheral nerve sheath tumor at unusual location | A 35-year-old woman presented with 2-month history of rapidly progressive painless swelling in left orbitotemporal region with proptosis and blurring of vision leading to complete blindness. Physical examination revealed a lobular nontender, firm mass of size 15 × 7 cm extending from left orbit to the left temporal region. In addition to axial proptosis, the left eye showed restricted movement in all directions [Figure and ]. She was unable to perceive light in her left eye. Magnetic resonance imaging (MRI) of the orbits and brain showed left sphenoidal-based extra-axial marginated in homoginously enhancing mass at the lateral side of the left optic nerve buckling the ipsilateral anterotemporal lobe []. Other systemic observations of the patient were normal. Fine needle aspiration cytology came to be neurofibroma. Near total dissection of the tumor was done through a left lateral orbitozygomatic approach. The histopathology and immunohistochemistry of the lesion revealed MPNST [Figure and ]. Postoperatively, the patient recovered rapidly with improved cosmoses []. Vision in her left eye improved to finger counting at 1 m and extraocular movements were normal. She received local radiotherapy. On 6-month follow-up, the patient is doing well with no local recurrence or any distant metastasis. | [[35.0, 'year']] | F | {'15001982': 1, '11894862': 1, '8151527': 1, '8228608': 1, '21393901': 1, '1520949': 1, '1564550': 1, '21108617': 1, '2447857': 1, '16145592': 1, '28462660': 1, '14050005': 1, '27494873': 1, '33842103': 2, '18338507': 1, '21418642': 2, '3082508': 1, '6402292': 1, '28622765': 2, '32212796': 1, '23047517': 1, '31420428': 1, '22523517': 2, '17272904': 1, '28828137': 1, '20205747': 2, '21151396': 1, '24174807': 2} | {'3808069-2': 2, '2881068-1': 1, '5474051-1': 1, '3325436-1': 1, '8020617-1': 1, '3070674-1': 1} |
163,855 | 3808069-2 | 24,174,807 | noncomm/PMC003xxxxxx/PMC3808069.xml | Primary malignant peripheral nerve sheath tumor at unusual location | A 60-year-old male presented with rapidly enlarging painless swelling in back with lower limb weakness in a period of 2 month. On examination, lower motor type of paralysis was found in both the legs with power: 0/5 around all joints. Sensation of all modalities decreased below L3. A nontender hard lobulated mass of size 10 × 5 cm was found over left lumbar paraspinal area fixed to underlying structure []. MRI was suggestive of lumbar (L1-L4) extradural lesion with associated L3 vertebral body compressional collapse giving a picture of neurofibroma []. Near total excision of both intraspinal and paraspinal component was achieved. Histopathological examination and immunohistochemical staining confirmed the diagnosis of MPNST. Patient improved neurologicaly with power 2/5 around all joints in lower limb. On completion of local radiotherapy at 6-month follow-up, the patient was doing well with no local or systemic spread. | [[60.0, 'year']] | M | {'15001982': 1, '11894862': 1, '8151527': 1, '8228608': 1, '21393901': 1, '1520949': 1, '1564550': 1, '21108617': 1, '2447857': 1, '16145592': 1, '28462660': 1, '14050005': 1, '27494873': 1, '33842103': 2, '18338507': 1, '21418642': 2, '3082508': 1, '6402292': 1, '28622765': 2, '32212796': 1, '23047517': 1, '31420428': 1, '22523517': 2, '17272904': 1, '28828137': 1, '20205747': 2, '21151396': 1, '24174807': 2} | {'3808069-1': 2, '2881068-1': 1, '5474051-1': 1, '3325436-1': 1, '8020617-1': 1, '3070674-1': 1} |
163,856 | 3808070-1 | 24,174,808 | noncomm/PMC003xxxxxx/PMC3808070.xml | Cerebrotendinous Xanthomatosis: Report of two cases and a novel genetic mutation in an Indian patient | The second case was of a 28-year-old male who was born of a non-consanguineous marriage, had delayed psychomotor milestones with mental retardation, congenital cataract, and recurrent episodes of diarrhea since early childhood. He had history of progressive spastic diplegia, tremulousness in both upper limbs and scanning speech. The patient had impaired attention, vigilance, comprehension, and new learning ability. Pan-sensory impairment was noted below knee with impaired limb coordination in upper limbs.\nPatient's skin biopsy of swelling over Achilles confirmed xanthoma []. MRI brain showed altered signals in bilateral cerebral peduncles, ventral pons, both the middle cerebellar peduncles and medullary pyramids. Based on the clinical, radiological, and biopsy findings of the Achilles tendon swelling, diagnosis of CTX was confirmed. | [[28.0, 'year']] | M | {'26937392': 1, '14652454': 1, '17050932': 1, '17718147': 1, '21921005': 1, '14742951': 1, '10024088': 1, '7315872': 1, '22018287': 2, '5676919': 1, '18051740': 1, '19881113': 2, '20454938': 1, '16157755': 1, '24174808': 2} | {'2797749-1': 1, '3226568-1': 1} |
163,857 | 3808072-1 | 24,174,810 | noncomm/PMC003xxxxxx/PMC3808072.xml | REM sleep behavior disorder in Parkinson's disease: A case from India confirmed with polysomnographic data | A 55-year-old male presented with the complaints of non-refreshing sleep, excessive drowsiness during the day but, without experiencing irresistible sleepiness. He also had a history of nocturnal symptoms for the past 2.5 years manifesting as somniloquy and abnormal sleep behavior. On a recent visit to his attending neurologist (DG), his wife complained of increasing frequency of abnormal activity during sleep after which he was referred to a sleep specialist (RG).\nAccording to his wife, he followed a regular sleep schedule (bedtime: 11:00 pm and wake-time: 5:00 am). His wife reported that he used to have episodes of sleep talking (4-5 times/night), each lasting 10-15 minutes on most of the nights. At times, he also appeared enacting his dreams. During night-time acts his movements used to be a combination of sitting up in bed, kicking, searching, and picking. He had occasionally struck his wife and also fallen out of bed during these episodes. He himself reported having violent dreams during the night in which he was fighting with somebody. Content of the dreams varied and he reported being engaged in searching activity after losing some belongings in dreams. On few occasions, he woke up during these dreams and found that he was acting on his dreams. He snored (Grade II) but apneas were never witnessed by the bed-partner. Any kind of behavioral abnormality was never noticed during daytime. His Epworth Sleepiness score was 6 (normal < 10).\nHe had developed resting tremor in the right hand 8 years earlier back subsequent to an alleged insecticide exposure. He was then diagnosed as PD by a neurologist. Presently, the patient was suffering from stage-II (Hoehn and Yahr Staging). Since then he had been on treatment with a combination of drugs that included carbidopa/levodopa 10/100 mg bid, amantadine 100 mg bid and pramipexole 0.25 mg bid. He responded well to these drugs and symptoms of PD improved. It must be noted here that he changed the dose of levodopa/carbidopa on his own in spite of counseling and efforts by doctor and family members. In addition, many a times he had presented with dyskinesia. Hence, the dose of levodopa was kept low, but it is difficult to comment whether he was taking the prescribed doses or higher doses.\nThere was no history to suggest childhood parasomnias, restless leg syndrome, sleep-terrors, narcolepsy, closed head injury, seizures, alcohol use, consumption or therapy with antidepressants. Also, there was no history of PD or RBD in the family members.\nPhysical examination revealed that he weighed 65 kgs, was 165 cms tall (BMI = 23.9). He had Mallampatti grade III airway with neck circumference of 38 cms. Neurological examination was unremarkable except for postural tremors in his hands. MRI scan of brain was non-diagnostic. Diagnostic polysomnography was performed (see below) confirming the diagnosis of RBD after which he was treated with clonazepam 1.0 mg at bedtime. One week later, his wife reported a significant reduction in frequency of these episodes. The dose was escalated to 1.5 mg for optimal suppression of the behavior.\nStandard attended 17-channel polysomnography with video monitoring using Cadwell III Sleep Easy acquisition system (Cadwell Laboratories, Inc., Kennewick, WA.) was performed. Electrophysiologic sleep parameters included frontal, central, and occipital electroencephalogram, right and left electrooculogram, and submentalis electromyogram. Anterior tibialis electromyogram was recorded to assess limb movement activity. Airflow was detected by thermistors and respiratory effort was determined by measurement of chest and abdomen motion with piezoelectric sensors. The arterial oxygen saturation was measured by the Cadwell oximeter with a 4-beat averaging mode. Raw data was manually scored in 30-second epochs for sleep stages using standard criteria.[]\nResults of sleep measurements are shown in the . The hypnogram [] showed poor sleep continuity but total sleep time and REM duration that were adequate for evaluation. REM latency was longer than usual (170 minutes compared to normal approximately 90 minutes) but the amount of REM sleep was within normal limits (22% total sleep time; normal approximately 20-25%). Periodic limb movement index (PLMS) was mildly increased (12/hr; normal approximately 5/hr). Respiratory parameters were normal. The AHI measured 1/hr (normal < 5/hr) and there was no hypoxemia. Video monitoring depicted periods of frequent movements of the arms and legs associated with vocalizations and sitting up in bed developing strictly out of REM sleep []. In addition, excessive phasic activity was noted in the submentalis and anterior tibialis recordings with movement artifacts during REM sleep []. | [[55.0, 'year']] | M | {'3264148': 1, '20146689': 1, '20524706': 1, '20083800': 1, '20694845': 1, '32140765': 1, '18682443': 1, '21414715': 1, '20191945': 1, '20668263': 1, '21799880': 1, '20083010': 1, '12777365': 1, '18548830': 1, '20187236': 1, '19960644': 1, '24174810': 2} | {} |
163,858 | 3808073-1 | 24,174,811 | noncomm/PMC003xxxxxx/PMC3808073.xml | Chordoma of skull base presenting as nasopharyngeal mass | A 28 year-old female sought medical attention for pain in throat and difficulty in deglutition for past 2 months. On anterior rhinoscopy, a pale mass was seen occupying right nasal cavity. The left nasal cavity was normal. Oral cavity examination revealed a smooth bulge on right-sided soft palate and anterior pillar of right tonsil, because of which the right tonsil could not be visualized. Uvula was in the midline. Indirect laryngoscopy could not be done. On central nervous system (CNS) examination, bilateral occulomotor and right hypoglossal nerves were involved. Fibreoptic nasopharyngoscopy was done under local anesthesia. A mass was seen in superior part of nasopharynx. Other sites of nasopharynx including fossa of Rosenmuller, eustacian tube opening, and torus tubarius were unremarkable.\nComputed tomography (CT) scan of head and neck [Figure and ] showed that base of skull was eroded with extracranial extension of bilateral temporal lobes and occipital lobe. The mass was compressing and pushing brainstem and extending into orbit and bilateral pterygopalatine and infratemporal fossae. Biopsy of the mass was performed.\nHistological examination revealed round to oval cells with central nuclei and a vacuolated cytoplasm (physaliphorous cells) []. The cells stained positive with Periodic acid-Schiff (PAS) [] and monoclonal staining for epithelial membrane antigen (EMA) []. A histopathological diagnosis of chordoma was made.\nThe patient was advised RT but the patient did not comply and became lost to follow up. | [[28.0, 'year']] | F | {'30094043': 2, '33758665': 1, '18055855': 1, '24174812': 1, '19193749': 1, '27437234': 1, '26605267': 2, '12679315': 1, '31950468': 1, '31662933': 2, '19797798': 1, '8334623': 1, '14104636': 1, '7416673': 1, '28980142': 1, '26984125': 1, '20109225': 1, '15641104': 1, '24174811': 2} | {'6778900-1': 1, '6080053-1': 1, '4656887-1': 1} |
163,859 | 3808075-1 | 24,174,813 | noncomm/PMC003xxxxxx/PMC3808075.xml | Extracranially located PICA aneurysm presenting with supratentorial IVH: A rare event with diagnostic pitfalls | A 16-year-old female presented with sudden onset severe headache followed by transient loss of consciousness but no neurological deficits. She developed vasospasm on post-ictus day 9 with paraparesis, which improved gradually. Computed Tomography (CT), Magnetic Resonance Imaging (MRI), and Magnetic Resonance Angiography (MRA) of the brain performed at a regional center revealed intraventicular hemorrhage (IVH) in the lateral and fourth ventricles but did not reveal any aneurysm or arteriovenous malformation []. The patient was referred to us after one month with severe headache and improving paraparesis. Repeat CT showed non-communicating hydrocephalus, and a four-vessel digital subtraction angiography (DSA) showed extracranially originating right PICA harbouring a 9.5 × 3.6 × 5.2 mm saccular aneurysm directed posteriorly with a neck measuring 2 mm at the level of C1, which was missed on the initial brain MRI; as the aneurysm was extracranial []. In view of the raised intracranial pressure because of the hydrocephalus, the patient underwent a right ventriculo-peritoneal shunt followed by right far lateral sub-occipital craniectomy with C1-C2 right hemi-laminectomy for clipping the extracranially placed PICA aneurysm. The patient recovered without any neurological deficits. | [[16.0, 'year']] | F | {'19147205': 1, '3216980': 1, '8232818': 1, '9650904': 1, '19651470': 1, '9189879': 1, '20098024': 1, '24174770': 1, '7070615': 1, '16122213': 1, '33173421': 1, '24174813': 2} | {} |
163,860 | 3808169-1 | 24,174,881 | noncomm/PMC003xxxxxx/PMC3808169.xml | Membranous glomerulopathy and treatment with Acthar®: a case study | At an initial visit in September 2006, a 46-year-old white male presented with edema, blood pressure indicative of hypertension (144/94 mmHg), heart rate of 76 beats per minute, and creatinine of 1.4 mg/dL (123.76 μmol/L). He had experienced sudden onset of edema in his feet and legs 5 weeks prior to this initial visit, which caused him serious concern. At a height of 5 feet 8 inches (172.72 cm) and weighing 235 lbs (105.75 kg; up about 35 lbs [15.75 kg] from his usual weight), his body mass index was 35.7. He had not been on any medication regimen. Laboratory values included 24-hour urinary protein at >7,500 mg/dL (750.0 g/L) and cholesterol at 307 mg/dL (7.9513 mmol/L; low-density lipoprotein, 224 mg/dL [5.8016 mmol/L]). He was negative for cancer screening, hepatitis B and C panel, antinuclear antibody, rheumatoid factor, and rapid plasmid reagin. He was started on olmesartan medoxomil-hydrochlorothiazide 40/25 mg for hypertension and proteinuria and simvastatin 40 mg for elevated cholesterol.\nThe patient was scheduled for a kidney biopsy for nephrotic range proteinuria in October 2006, which resulted in a diagnosis of idiopathic membranous glomerulopathy. Lisinopril 40 mg twice daily was added to his medication regimen. At this time, his creatinine was at 1.3 mg/dL (114.92 μmol/L).\nThe patient’s membranous glomerulopathy progressed from October 2006 to July 2009, as revealed by laboratory results. During this period, he remained on an angiotensin receptor blocker (olmesartan medoxomil-hydrochlorothiazide) and angiotensin-converting enzyme inhibitor (lisinopril) treatment regimen. Since no improvement was observed, he then received cyclosporine A for 6 months, to which he was relatively adherent. No improvement was observed 3 months after initiation of cyclosporine A, so prednisone was added. Three months later, he developed shingles and was admitted to the hospital due to what was felt to be complications of cyclosporine A plus prednisone. Both cyclosporine A and prednisone were tapered off after the patient requested all immunosuppressive medications be stopped. Three months later, he agreed to be treated with mycophenolate, which he received for approximately 12 months but only during the last 3 months did he take it as prescribed.\nThe patient was agreeable to trying Acthar (80 USP U/mL) and received treatment from September 2009 to October 2010; his laboratory values during this period are summarized in . Acthar was self-administered subcutaneously at an initial dose of 40 U every 72 hours. After 3 months, the dose was increased to 80 U every 72 hours. In April 2010, his urinary protein levels rose to 9,520 mg/dL (952.0 g/L), and he required additional antihypertensive therapy. By July 2010, his urinary protein had dropped to 2,948 mg/dL (294.8 g/L). Thus, it took approximately 10 months of Acthar treatment to improve his urinary protein levels. By October 2010, his urinary protein levels had decreased further to 1,628 mg/dL (162.8 g/L). As shown in , in addition to the decline in urinary protein levels, the patient experienced decreases in creatinine and albumin levels, an increase in creatinine clearance, and modest weight gain while receiving treatment with Acthar.\nActhar treatment was stopped in October 2010 for several reasons. First, one year of ACTH treatment has been shown in European studies to be sufficient for resolving proteinuria.– In addition, the patient’s laboratory results indicated clinically significant improvement in his signs of membranous nephropathy. Finally, the patient reported that his quality of life had improved, and he was not experiencing any symptoms of membranous nephropathy. He felt well and was able to return to his previous lifestyle.\nThe laboratory results since halting Acthar are also shown in . Urinary protein levels continued to decline overall, from 407 mg/dL (40.7 g/L) in December 2010, with slight elevation to 451 mg/dL (45.1 g/L; still within normal range) in March 2011, to 189 mg/dL (18.9 g/L) in September 2011. His protein to creatinine ratio was 0.58 in January 2012, and at that time his medications were limited to an angiotensin-converting enzyme inhibitor (lisinopril) and angiotensin receptor blocker (olmesartan medoxomil-hydrochlorothiazide). As of May 1, 2012, his blood pressure was 124/78 mmHg, he weighed 199 lbs (89.55 kg), his heart rate was 81 beats per minute, and there was no evidence of edema. Current medications include olmesartan medoxomil-hydrochlorothiazide 40/12.5 mg once daily, lisinopril 40 mg once daily, and simvastatin 40 mg once daily. | [[46.0, 'year']] | M | {'27036111': 1, '19473632': 1, '27084801': 1, '27418857': 1, '30442868': 1, '21448451': 1, '16431252': 1, '15800117': 1, '10504505': 1, '16968719': 1, '15102969': 1, '24174881': 2} | {} |
163,861 | 3808791-1 | 24,167,514 | noncomm/PMC003xxxxxx/PMC3808791.xml | A Case of Arteriovenous Fistula after Renal Biopsy in an IgA Nephropathy Patient with Macroscopic Hematuria | A 27-year-old woman had a renal biopsy because of intermittent macroscopic hematuria and proteinuria after tonsillitis. When she was 24 years old, the first episode of macroscopic hematuria and proteinuria (1.0 g/g Cr) occurred just 1 day after tonsillitis with a high fever. After treatment with antibiotics, all symptoms disappeared except for microscopic hematuria. Because such episodes recurred several times and there was continued microscopic hematuria without proteinuria, the patient underwent tonsillectomy when she was 26 years old. However, even after tonsillectomy, microscopic hematuria persisted, and she repeatedly had episodes of macroscopic hematuria and proteinuria following pharyngitis with a high fever. She had a renal biopsy under real-time ultrasonographic guidance with a 16-gauge automated biopsy device and was diagnosed with IgA nephropathy. The histology showed crescent formations in 2 out of 16 glomeruli, but she refused steroid therapy. Before being discharged from our hospital, evidence of only slight renal subcapsular bleeding in the left kidney could be found on routine ultrasonography. Three months after the renal biopsy, she had sudden macroscopic hematuria without any symptoms, which lasted for 3 days. After that, the macroscopic hematuria disappeared but the amount of microscopic hematuria was clearly increased as compared to before her renal biopsy. In the urinary sediment, red blood casts were always present and comprised of 20–40% dysmorphic red blood cells. Since an enlarged left renal pelvis was newly recognized on ultrasonography, enhanced computed tomography (CT) was performed and she was diagnosed with an arteriovenous fistula (AVF) in the lower pole of her left kidney (fig. ). As the amount of microscopic hematuria had decreased again, she chose not to receive therapy. When she was 34 years old, our patient got married and was concerned about her future fertility. Since repeated ultrasonography showed an increased dilatation of the left renal vein (fig. ), she decided to undergo treatment with percutaneous intervention. An arteriogram confirmed an AVF with an enlarged draining vein and aneurysmal dilatation (fig. ). Selective embolization of the feeding arterial branch closed the AVF with 8 detachable coils (fig. ). Follow-up magnetic resonance imaging (MRI) performed 3 months after the intervention did not show any abnormalities, including the dilatation of the renal vein (fig. ). Microscopic hematuria disappeared within another 3 months and complete remission of IgA nephropathy had been achieved. | [[27.0, 'year']] | F | {'22417392': 1, '10364704': 1, '15847217': 1, '1482648': 1, '18495740': 1, '27406176': 2, '10534521': 1, '20586943': 1, '11906648': 1, '21081691': 1, '22537423': 1, '22837269': 1, '1395165': 1, '21034662': 1, '7634544': 1, '12213946': 1, '21778277': 1, '17222672': 1, '18335514': 1, '24167514': 2} | {'4942951-1': 1} |
163,862 | 3808792-1 | 24,167,512 | noncomm/PMC003xxxxxx/PMC3808792.xml | Initially Nondiagnosed Fabry's Disease when Electron Microscopy Is Lacking: The Continuing Story of Focal and Segmental Glomerulosclerosis | A kidney biopsy was performed in a 37-year-old man with proteinuria of 2.1 g/day, serum creatinine of 2.48 mg/dl and a glomerular filtration rate of 44 ml/min (table ). Optic microscopy revealed focal and segmental glomerulosclerosis (fig. ). The patient was started on meprednisone 40 mg/day, valsartan 320 mg/day and a gradual increase in aliskiren dose until 300 mg/day were reached. Low-sodium diet compliance was followed with urinary sodium excretion. One month later, serum creatinine increased to 2.7 mg/dl and proteinuria decreased to 0.8 g/day. Three months later, the steroid dose was tapered and the creatinine clearance improved to 54 ml/min and proteinuria remained steady for the following months (0.6–1 g/day). Twenty months later, while on dual blockade (valsartan had been lowered to 160 mg/day due to hypotension) and meprednisone 4 mg/day, proteinuria increased to 1.9 g/day. Steroids were restarted but proteinuria worsened to 6.8 g/day and creatinine clearance increased to 56 ml/min. A new kidney biopsy was performed and a test for α-galactosidase levels displayed low levels (0.7 ng/ml). A mutation [c.98A>G (D33G)] was identified in the gene of α-galactosidase A, diagnosed by sequential analysis. The kidney biopsy was consistent with secondary focal and segmental glomerulosclerosis and suggested Fabry's disease (fig. ). Electron microscopy and genetic studies confirmed the diagnosis (fig. ). The patient was started on agalsidase β (Fabrazyme, Genzyme Corp., Cambridge, Mass., USA) intravenously at 1 mg/kg body weight every fortnight and steroids gradually decreased, while the dual blockade was unchanged. Two months after diagnosis, his proteinuria decreased to 2.7 g/day, his creatinine clearance was 46 ml/min and steroids were discontinued. One month later, his proteinuria increased to 3 g/day and the creatinine clearance was 40 ml/min. As adjuvant therapy, meprednisone 10 mg was restarted and added to the regime. Proteinuria decreased to 2 g/day and creatinine clearance was 37 ml/min. | [[37.0, 'year']] | M | {'19876652': 1, '19965549': 1, '33490112': 1, '17656478': 1, '24959362': 2, '31847900': 2, '19900828': 1, '16079416': 1, '20504837': 1, '27733175': 1, '22579701': 1, '30775256': 1, '26312237': 2, '19039306': 1, '14750104': 1, '26064721': 2, '17353161': 1, '20941593': 1, '21541658': 1, '21160462': 1, '5451124': 1, '22085605': 1, '23007467': 1, '32997080': 1, '24167512': 2} | {'6918640-1': 1, '4544560-1': 1, '4544560-2': 1, '4544560-3': 1, '4443757-1': 1, '4052478-1': 1} |
163,863 | 3808793-1 | 24,167,513 | noncomm/PMC003xxxxxx/PMC3808793.xml | Disseminated Mucormycosis in a Patient with Recent Kidney Transplantation: A Case Report and Review of the Literature | A 47-year-old Hispanic man with a history of end-stage kidney disease secondary to diabetic nephropathy underwent deceased donor renal allograft transplantation. His immediate posttransplant course was unremarkable, with prompt functioning of his allograft and decreasing creatinine levels. His immunosuppressant regimen included tacrolimus, mycophenolate sodium and corticosteroids. Ten days after the transplant, he developed suprapubic abdominal pain that was thought to be due to the indwelling ureteral stent, necessitating its removal with complete resolution of his discomfort.\nApproximately 5 weeks following his transplant, the patient presented with fatigue, diarrhea and oligoanuria, without any associated fever or respiratory symptoms. He had significant allograft dysfunction with a creatinine level of 8.1 mg/dl up from a nadir of 2.7 mg/dl. Doppler ultrasound of the renal allograft showed an area of hypoperfusion affecting the upper pole of the renal allograft, with a moderate degree of hydronephrosis. A percutaneous nephrostomy tube was placed without any improvement in urine output or renal function. A renal allograft biopsy was then done to further elucidate the etiology of his graft dysfunction. This revealed diffuse C4d-positive staining in the peritubular capillaries suggestive of acute humoral rejection; however, the biopsy was also remarkable for numerous, broad, ribbon-like, nonseptate, fungal hyphae with wide-angle branching suggestive of Mucor infection. There was a focal cortical infarct accounting for approximately 10% of the overall biopsy, with focal small vessels containing fungal hyphae (fig. ). The patient was prepared for transplant nephrectomy and arteriovenous fistula thrombectomy. Postoperatively, his anti-rejection medications were discontinued, amphotericin B and micafungin were started and hemodialysis was initiated.\nA pathology exam performed after the nephrectomy (fig. ) showed significant cortical infarction involving more than half of the cortex, with patchy, widespread involvement of fungal hyphae that involved the ureteral lumen, ureteral wall, renal parenchyma and numerous large and small vessels. Chest CT showed a large right upper lobe cavitating mass measuring 4.9 × 2.8 cm, with scattered areas of smaller nodules present throughout both lungs (fig. ). Abdominal CT revealed a wedge-shaped area of hypodensity within the anterior spleen compatible with infarction, along with additional areas of hypodensity within the spleen. There was also a nonspecific hypodensity in the right hepatic lobe. Head and maxillofacial CT were normal. The patient underwent a CT-guided biopsy of the right upper lobe of the lung, and pathology confirmed the clinical suspicion of disseminated mucormycosis. Within 1 week of presentation, the patient became hemodynamically unstable, requiring a transfer to the intensive care unit for mechanical ventilation and vasopressor support. As his mental status showed significant decline, a repeat head CT was done. This revealed interval development of areas of subcortical hypoattenuation involving the bilateral frontal lobes, bilateral occipital lobes and bilateral cerebral hemispheres, suggesting multifocal cerebritis with no abscesses (fig. ). The patient's condition continued to deteriorate, and he developed supraventricular tachycardia and the inability to tolerate hemodialysis. His family elected for comfort care and the patient subsequently died.\nThe patient's records did not reveal any previous history of significant upper or lower respiratory symptoms, and his previous chest X-rays, including the one that was done just before his transplant surgery, were unremarkable. A renal allograft biopsy was done on the recipient of the donor-matched organ (the second donor kidney) and showed no evidence of fungal infection, which made it unlikely to be a donor-transmitted infection. | [[47.0, 'year']] | M | {'17654347': 1, '16925570': 1, '8889996': 1, '10455371': 1, '16080086': 1, '22583076': 1, '19435437': 1, '15776383': 1, '21508149': 1, '18611163': 1, '21622653': 1, '22000355': 1, '10852735': 1, '28386509': 2, '19659439': 1, '24167513': 2} | {'5366780-1': 1} |
163,864 | 3808796-1 | 24,191,181 | noncomm/PMC003xxxxxx/PMC3808796.xml | Brachymetatarsia of the Fourth Metatarsal, Lengthening Scarf Osteotomy with Bone Graft | A 16-year-old female was referred with unilateral shortening of the left 4th toe. The toe was not painful, however caused psychological distress when wearing opened toed footwear and whilst barefoot at swimming pools. Examination revealed a left 4th toe that was clearly short and sitting dorsally. Radiographs () showed a 4th metatarsal which was approximately 7 mm shorter that the 5th metatarsal with a dysplastic metatarsal head. The etiology of her deformity was unknown.\nA single stage lengthening metatarsal scarf osteotomy was performed. The rationale for a single procedure was to limit disruption from schooling. The 4th metatarsal was approached through a laterally based Z-plasty incision. A wide capsular release was performed and the metatarsal was elevated up and a lengthening scarf osteotomy performed. Two 1cm allograft cancellous cubes (RTI Biologics, United States) were used and the osteotomy held with one Omnitech® screw (Biotech International, France) (). Z lengthening of the short and long extensor tendons was performed.\nPost operatively, the patient remained heelweight bearing for 6 weeks. The patient had routine post-operative follow up () and the additional length of 9 mm (2 mm longer than 5th metatarsal) had been maintained, however, there was some scar contracture keeping the toe dorsally elevated by ten degrees. The patient remained satisfied with her overall increase in length of the 4th toe and was discharged at one year. | [[16.0, 'year']] | F | {'9393911': 1, '29207688': 1, '20058111': 1, '7615606': 1, '21400762': 1, '33532083': 1, '24191181': 2} | {} |
163,865 | 3808799-1 | 24,191,184 | noncomm/PMC003xxxxxx/PMC3808799.xml | Cement Embolism into the Venous System after Pedicle Screw Fixation: Case Report, Literature Review, and Prevention Tips | An 87-year-old man diagnosed with spondylolisthesis due to a non-traumatic osteoporotic compression fracture of the 3rd lumbar vertebra was admitted to our hospital with severe low back pain associated with load-dependent bilateral buttock pain radiating also bilaterally into the L4 dermatome. Because of the advanced age of the patient, a conservative treatment including physiotherapy and mobilization with a stabilizing orthosis accompanied by oral analgesia was firstly conducted.\nDue to progression of pain and vertebral slipping after 6 consecutive months of conservative therapy, a minimal invasive dorsal instrumentation under general anesthesia was ultimately performed.\nWe chose a percutaneous dorsal approach with 4 stab incisions to insert the pedicle screws and both rods. Admittedly, the BMD was preoperatively not measured. Intraoperatively, a very low bone quality was noted so that pedicle screw augmentation with polymethylmethacrylate (PMMA) cement was conducted to increase the implants stability. Two cc of PMMA per pedicle were injected into the distal tip of the preformed screw hole and along its entire length at the level of the 2ed lumbar vertebral body (VB) under lateral and intermittent anteroposterior fluoroscopy control. Then, 6.5-mm-diameter and 50-mm-long pedicle screws were inserted.\nThree cc of PMMA per pedicle were injected into the 4th lumbar VB in the same previous manner. Afterwards, 7.5- mm-diameter and 50-mm-long pedicle screws were inserted. The intraoperative simultaneous fluoroscopy showed no cement extravasations at any time of the procedure. Finally, 90-mm-long rod was inserted to the left side and 80-mm-long rod to the right side; both were then tightened with 2 locking nuts each.\nAfter this procedure, clinical improvements in the form of alleviation of pain and rapid postoperative mobilization were achieved. A routine high resolution computed tomographic scan revealed postoperatively presence of cement in a left laterovertebral lumbar vein extending into the inferior vena cava. A small asymptomatic vascular epidural leak was also observed ( and ). The origin of the leak arose at the level of the augmentation in the 4th lumbar VB.\nThe patient denied any chest pain or dyspnea and he was not in respiratory distress with respiratory rat of 20/min. Findings of the postoperative cardiopulmonary examinations as well as chest radiograph were age-appropriate within normal ranges.\nAs thrombosis prophylaxis, the patient received subcutaneously a weight-based low molecular weight heparin and 100 mg/d acetylsalicylic acid orally. No cardiac or respiratory dysfunctions were noticed over the entire treatment period and the patient was discharged 2 weeks postinterventional. Clinically, the patient showed an uncomplicated 1-year follow-up. | [[87.0, 'year']] | M | {'16373777': 1, '20922632': 1, '17208340': 1, '17633487': 1, '7846594': 1, '26261012': 1, '3956001': 1, '17877276': 1, '21284883': 1, '34754545': 2, '9403451': 1, '20675747': 1, '19893717': 1, '17881965': 1, '12440642': 1, '1395312': 1, '15385313': 1, '15167670': 1, '12480681': 1, '18781342': 1, '1862404': 1, '27678328': 1, '9259778': 1, '9654629': 1, '1566185': 1, '31030261': 1, '11795714': 1, '9657546': 1, '24696858': 1, '11940629': 1, '24191184': 2} | {'8571380-1': 1} |
163,866 | 3808805-1 | 24,167,515 | noncomm/PMC003xxxxxx/PMC3808805.xml | A Case of Malignancy-Associated Cryoglobulinemia | A 75-year-old male was referred to the nephrology service for evaluation of hematuria, proteinuria and an elevated serum creatinine. His past medical history was notable for type 2 diabetes mellitus.\nOn the initial assessment, he appeared unwell. He was hypertensive with pedal edema and had dipstick hematuria and proteinuria. His urinary protein leak approximated 2 g/day. His initial biochemical laboratory findings are summarized in table .\nHis antinuclear antibody was positive with a homogenous pattern and he was hypo-complementemic; however, his anti-double-stranded DNA was negative. Serum protein electrophoresis demonstrated a monoclonal IgG kappa band.\nA renal biopsy was performed, which demonstrated a diffuse endocapillary proliferative glomerulonephritis (fig. ). Capillary wall kappa, IgG, IgM and C3 were noted on immunofluorescence (fig. ) and there were scattered subendothelial electron-dense immune-type deposits on electron microscopy. There was a florid intimal arteritis involving the interlobular caliber arteries. Several arterioles contained eosinophilic material within the vessel wall consistent with cryoprecipitates.\nRemarkably, coincidental sampling of perinephric fat demonstrated infiltration by a monomorphic population of CD20-positive B lymphocytes, which was suggestive of a low-grade B cell lymphoma (fig. ).\nThe suspected diagnosis was type 1 cryoglobulinemia due to an underlying lymphopro-liferative disorder. Computed tomography of the thorax, abdomen and pelvis revealed moderate hepatosplenomegaly and enlarged lymph nodes in the anterior mediastinum. However, an initial attempt did not confirm the presence of serum cryoglobulin. Due to the strong histological evidence and supportive clinical, radiological and laboratory findings, further sampling was performed and, this time, was positive. A subsequent bone marrow trephine biopsy was consistent with a diagnosis of low-grade follicular B cell lymphoma.\nThe patient's initial clinical course was complicated by a nosocomial pneumonia and respiratory failure. Following stabilization, the patient underwent combination chemotherapy (rituximab, cyclophosphamide, vincristine and prednisolone).\nThree months after initiation of therapy, the patient was normotensive and euvolemic, without constitutional symptoms. His follow-up laboratory findings can be seen in table . | [[75.0, 'year']] | M | {'21868085': 1, '22484457': 1, '23196322': 1, '21594887': 1, '20040797': 1, '24167515': 2} | {} |
163,867 | 3808806-1 | 24,167,517 | noncomm/PMC003xxxxxx/PMC3808806.xml | Rosuvastatin-Induced Acute Interstitial Nephritis | An 83-year-old man was admitted to our unit for rapidly worsening renal function 3 weeks following angioplasty of the left internal carotid artery. During this 3-week period his serum creatinine increased from 2.0 to 5.4 mg/dl. The patient had suffered from hypertension within the last 20 years and had chronic kidney disease with unremarkable urinalysis and diffuse peripheral vasculopathy. At the time of admission, he was being treated with an angiotensin receptor blocker (ARB), a dihydropyridine calcium channel blocker, aspirin and rosuvastatin (20 mg/day), which was prescribed following the carotid angioplasty. At admission the patient was afebrile, eupneic and mildly hypovolemic, showed normal diuresis and had a blood pressure of 110/60 mm Hg and a heart rate of 88 bpm. Laboratory tests were normal except for elevated serum creatinine (5.4 mg/dl) and BUN (73 mg/dl). Urinalysis showed no active sediment with mild proteinuria (500 mg/day). ANA, ENA, C3, C4, CH50, ANCA, cryoglobulinemia, rheumatoid factor, serum and urine protein immunofixation and free light-chain concentrations were all within the normal range. Kidney ultrasonography showed elevated echogenicity of the parenchyma and an increased renal resistance index (0.76) in the absence of renal artery stenosis. The ARB was discontinued and the patient received intravenous crystalloids for the next 72 h. At this time, the possibility of atheroembolic renal disease was excluded since the recent carotid angioplasty was performed through a femoral artery catheter, during which both an ophthalmologic examination for retinal cholesterol crystal emboli and dermatological manifestations were negative and did not show eosinophilia. However, because renal function did not recover (serum creatinine: 5.9 mg/dl), an echo-guided biopsy of the left kidney was performed. Light microscopy showed interstitial edema with lymphocyte infiltrate associated with tubulitis (fig. ). Electron microscopy evaluation was negative. Immunofluorescence was aspecific and not consistent. Based on these results, a diagnosis of acute tubulointerstitial nephritis was made.\nSince rosuvastatin was the most recently introduced drug, a possible relationship between the drug and AIN was considered. Thus, rosuvastatin was withdrawn, and oral prednisolone (1 mg/kg/day) was prescribed but rapidly tapered over a period of 4 weeks. The patient was discharged with conservative therapy, and after 8 weeks renal function values returned to baseline (serum creatinine 2 mg/dl, BUN 30 mg/dl, proteinuria 150 mg/24 h and urinalysis at polarized light microscopy was unremarkable).\nOne month later, the same ARB was reintroduced and, because of the high cardiovascular risk of the patient, a different statin (atorvastatin 20 mg/day) was prescribed. The patient is being regularly followed up at our outpatient service and, 6 months after the beginning of atorvastatin, has not shown any deterioration in renal functions. | [[83.0, 'year']] | M | {'25684874': 2, '28974137': 1, '31517431': 1, '16581330': 1, '15340001': 1, '12612979': 1, '24167517': 2} | {'4323914-1': 1} |
163,868 | 3808859-1 | 24,174,964 | noncomm/PMC003xxxxxx/PMC3808859.xml | Endovascular Repair of Aortoiliac Aneurysm Using Bifurcated Stent Grafts with Sandwich Technique for Preserving the Internal Iliac Artery | A 76-year-old man with a history of hypertension, diabetes mellitus, benign prostate hypertrophy and tobacco use was presented with right flank pain. A retrograde pyelography revealed an extrinsic indentation of the right pelvic ureter. Computed tomography (CT) angiography demonstrated an AAA with bilateral CIA involvement (). The maximal diameter of the distal abdominal aorta was 34 mm and the diameter of the aorta at renal artery level measured 19.2 mm. The right CIA was 55 mm and the left CIA was 24 mm in their maximal diameters. The diameter of the right CIA at its ostium was 27 mm, whereas that of the left CIA was 11 mm.\nIn this patient, we decided to perform EVAR using a bifurcated stent graft. In order to preserve at least one IIA for pelvic perfusion, we planned to apply the sandwich technique. The right IIA was embolized using a 14 mm Vascular Plug (Amplatzer, St. Jude Medical, St. Paul, MN, USA) after the engagement of a 7 Fr sheath into the right IIA from the left common femoral artery. The main body of the bifurcated stent graft (Excluder 23-14-160 mm, Gore, Newark, DE, USA) was introduced through the left common femoral artery and deployed below the left renal artery origin.\nThereafter, a tubular-type stent graft (Viabahn 8×150 mm, Gore, Newark, DE, USA) was inserted into the left IIA through a 8 Fr Shuttle sheath from the left brachial artery. An iliac extender stent graft (Excluder 12×140 mm, Gore, Newark, DE, USA) was inserted through the left common femoral artery. The two distal stent grafts were deployed in parallel with the overlapping of the proximal main body stent graft and dilated synchronously by a kissing balloon method (). A contralateral limb (Excluder 12-140 mm, Gore, Newark, DE, USA) and an iliac extender (Excluder 12-100 mm, Gore, Newark, DE, USA) were inserted through the right CFA in order to cover the right CIA and the proximal segment of the right EIA sheath.\nAfter the procedure, angiography showed proper positions of the deployed stent grafts with good blood flow to the left IIA and minimal endoleaks (types Ib and III). Follow-up aorta CT scans taken at 3 days () and 8 months after the procedure showed patent stent grafts without significant endoleak. During the 8-month follow-up, the patient remained uneventful. | [[76.0, 'year']] | M | {'9587341': 1, '10834485': 1, '11013030': 1, '15978926': 1, '15978925': 1, '21314358': 1, '22321477': 1, '17924725': 1, '15615550': 1, '23336852': 1, '19156879': 1, '22484703': 1, '18338212': 1, '20801682': 1, '23210864': 1, '11496269': 1, '22176882': 1, '24174964': 2} | {} |
163,869 | 3808860-1 | 24,174,965 | noncomm/PMC003xxxxxx/PMC3808860.xml | A Case of Dilated Cardiomyopathy with Massive Left Ventricular Thrombus after Use of a Sibutramine-Containing Slimming Product | A 32-year-old man was admitted with progressively worsening dyspnea on exertion of 1 month duration. The patient was not known to have hypertension, diabetes or any other medical illness. He reported having taken the unauthorized health product, "Slim-30", for the last 7 months and had stopped taking it 2 weeks ago. Several medicines regulatory authorities are warning that this product contains an undeclared pharmaceutical ingredient, N-desmethyl sibutramine, an analogue of sibutramine, which has now been banned because of cardiovascular adverse effects. When the drug was first started, his body mass index was 26.3. From the outset the patient presented higher blood pressure and palpitation, therefore he had taken the pill at intervals of about 2 to 3 days. On admission, initial vital signs were as follows: blood pressure of 110/80 mm Hg, pulse rate of 130 beats/min, respiration rate of 20 breaths/min, and body temperature of 36.5℃. Upon physical examination, pitting edema in both lower extremities was noted and a S3 gallop sound was audible. Chest X-ray showed cardiomegaly (cardiothoracic ratio was 0.60) and no pulmonary edema (). The electrocardiogram showed sinus tachycardia with diffuse non-specific ST segmental changes. The cardiac enzymes were within the normal range with a Troponin-T level of 0.023 ng/mL (normal ≤0.100) and creatine kinase-MB level of 1.86 ng/mL (normal ≤4.94). However, pro-B-type natriuretic peptide level was elevated to 5404 pg/mL (normal ≤88). A complete blood cell count, coagulation profile, and thyroid function test were within normal limits. Liver enzymes were elevated with an aspartate aminotransferase level of 80 IU/L and alanine transaminase level of 120 IU/L. The transthoracic and transesophageal echocardiogram revealed dilated LV (end-diastolic diameter of 6.5 cm) with severely impaired systolic function {ejection fraction (EF) of 23%} and multiple hyperechoic, pedunculated masses attached to the LV apical wall, of which the largest measured 4.6×1.5 cm in size (). In the presence of severe LV systolic dysfunction, the mass-like lesions were suspected of thrombi. The patient was started on diuretics, angiotensin-converting-enzyme inhibitor (ACEI) and parenteral unfractionated heparin. He had a good clinical response to treatment and subsequent echocardiogram performed 10 days later showed that LV thrombi had nearly dissolved, although there was only a slight improvement in LV dilatation and contractility. Multi-detector computed tomographic coronary angiography, which was performed before discharge, showed normal a coronary artery (). He was discharged in a stable condition and prescribed a beta blocker, ACEI, and oral warfarin. At 1 month follow-up, echocardiogram demonstrated complete resolution of LV thrombi and markedly improved LV systolic function (EF of 45%) and dilatation (end-diastolic diameter of 5.6 cm) (). The patient is currently doing well and is being followed up via the outpatient department. | [[32.0, 'year']] | M | {'22547756': 1, '16542208': 1, '21219406': 1, '21751825': 1, '18728104': 1, '21525441': 1, '15771936': 1, '17548910': 1, '17984134': 1, '20818901': 1, '18687492': 1, '20731270': 1, '19471631': 1, '20109425': 1, '26157557': 1, '20144986': 1, '20446231': 1, '9758241': 1, '18788006': 1, '24174965': 2} | {} |
163,870 | 3808861-1 | 24,174,966 | noncomm/PMC003xxxxxx/PMC3808861.xml | Primary Cardiac Angiofibroma | A 57 year-old female without any medical history was admitted for a left ventricular (LV) tumor that was discovered incidentally. The tumor was found by echocardiography which was performed for the baseline evaluation of hypertension.\nThe echocardiography showed a round-shaped, immobile and echogenic mass attached at the LV apex. The valve and LV functions were normal ().\nCardiac MRI was performed to determine the tumor's tissue type and its relations to other cardiac structures. It showed a slightly high signal intensity on both T1 and T2 weighted images. The gadoliniumenhanced cardiac MRI showed a hypoperfused tumor core and peripheral enhancement ().\nIn addition, the lesion showed the centripetal enhancement pattern during the first-pass infusion of the gadolium-containing contrast (). The features of such are associated with the vascular tumors such as liver hemangioma.\nThe mass showed peripheral enhancement with the central sparing on the delayed enhanced imaging (). It suggested that the tumor had an abundant fibrous content as well as a vascular content.\nIn this patient, the initial preoperative diagnosis of the mass was fibrous tumor of the LV apex. The patient was referred to a cardiac surgeon for the removal of the cardiac mass. Intraoperatively, a whitish, solid mass was detached from the base of the anterolateral papillary muscle ().\nOn the histologic evaluation, it showed a somewhat well-demarcated collagenous mass arising from the myocardium (, arrows). The high-power view showed multiple irregular vascular channels () with intervening dense collagen deposition in the mass. The desmin immunohistochemistry and trichrome staining confirmed that the stroma consisted of dense collagenous tissue, not smooth muscle (). From these histologic findings, we diagnosed the mass as angiofibroma. The patient is currently doing well without any evidence of recurrence at the 2-year follow-up. | [[57.0, 'year']] | F | {'16953170': 1, '3023741': 1, '15608459': 1, '22423070': 1, '1939774': 1, '15811617': 1, '11550349': 1, '24174966': 2} | {} |
163,871 | 3808862-1 | 24,174,967 | noncomm/PMC003xxxxxx/PMC3808862.xml | A Case of Aorta-Right Atrial Tunnel Presented with an Asymptomatic Murmur | A 42-year-old female was transferred from private clinic with intermittent palpitation and cardiac murmur on July 2012. The patient had no specific medical history of illnesses such as hypertension or diabetes mellitus. There was no family history of aortic, collagen, vascular or congenital heart diseases. Vital signs were blood pressure of 109/64 mm Hg, pulse of 77 beats/min, respiration of 20 breaths/min, and body temperature of 36.5℃. Cardiac auscultation revealed continuous grade 3/6 murmur at the right 2nd and 3rd intercostal spaces. Heart size was normal according to the chest Xray and no apparent ST-segment and T-wave abnormalities were shown on the electrocardiography. The blood chemistries, including N-terminal pro-B natriuretic peptide, coagulation studies with fibrinogen, anti-nuclear antibody and complete blood cell counts, as well as cardiac enzymes and lipid profiles, were within normal limits. TTE and Doppler showed a tunnel-like structure with continuous Doppler signals from the left coronary sinus to the RA (). The pulmonary/systemic blood flow ratio was estimated at 1.3 : 1 measured by echocardiography. The left ventricle showed normal size and systolic function with an ejection fraction of 64%. Cardiac valves were also normal. Exercising treadmill tests showed negative finding. Although coronary angiography revealed the normal left coronary artery (LCA) (), there was a large tunnel-like structure beginning in the left coronary sinus, and terminating in the body of RA (). The tunnel showed aneurysmal dilatation, and the LCA arose separately from the tunnel (). Right coronary artery originates from right coronary cusp (). Cardiac-CT was performed in order to confirm the tunnel, and showed the tunnel taking its origin from the aortic root, passing posterior to the aortic root and entering the RA through a tortuous link (). Although we recommended a surgical treatment, the patient only wanted the surgery next year. | [[42.0, 'year']] | F | {'20844628': 1, '12771879': 1, '16256780': 1, '17353457': 1, '7431992': 1, '3713237': 1, '34327543': 1, '10735722': 1, '21801940': 1, '24174967': 2} | {} |
163,872 | 3809434-1 | 24,175,023 | noncomm/PMC003xxxxxx/PMC3809434.xml | The Usefulness of Brain Magnetic Resonance Imaging with Mild Head Injury and the Negative Findings of Brain Computed Tomography | A 53-year-old woman visited our hospital because of headache after pedestrian traffic accident. She had past medical history of hypertension and not taken any other medications. At the time of admission, GCS score was 14 points, and she had loss of consciousness. She showed normal level of coagulation factor on routine hematology examination. Except for scalp laceration, external wound of the other head parts was not observed. Initial brain CT scan which was taken at other institution did not show abnormal lesion, except scalp swelling. She had continuous headache and dizziness for 3 days. Thus, we performed brain MRI which showed hemorrhagic contusion at left frontal lobe (). After we managed with medication and closed observation, she was discharged without any neurologic deficit 1 week later. | [[53.0, 'year']] | F | {'16189365': 1, '20611043': 1, '15083871': 1, '22396839': 1, '16531845': 1, '16832279': 1, '8599485': 1, '10891517': 1, '25994196': 1, '20421059': 1, '16331165': 1, '15228461': 1, '11147578': 1, '1404507': 1, '16934645': 1, '15128116': 1, '17371884': 1, '23224915': 1, '12609645': 1, '19284234': 1, '15006561': 1, '19575576': 1, '10029032': 1, '3486260': 1, '12068346': 1, '24175023': 2} | {} |
163,873 | 3809438-1 | 24,175,027 | noncomm/PMC003xxxxxx/PMC3809438.xml | Glioma Mimicking a Hypertensive Intracerebral Hemorrhage | A 69-year-old woman visited our hospital presenting with nausea, vomiting, dysarthria, and right hemiparesis. The patient had been under medical treatment for hypertension for the previous 3 years. Brain computed tomography (CT) scans with contrast enhancement and CT angiograms demonstrated an acute intracerebral hematoma in the left basal ganglia, including the caudate nucleus, accompanied by a small amount of intraventricular hemorrhage, without any underlying enhanced lesion or vascular pathologies (). The patient was treated conservatively with anti-hypertensive drugs under a diagnosis of hypertensive basal ganglia ICH. Additional physical rehabilitation was performed, and the patient was discharged with improved motor function and mental status 6 weeks after admission. During follow-up as an outpatient, the patient was re-admitted for physical malaise and deteriorated mental status 6 weeks after discharge. Brain CT scans demonstrated asymmetric ventriculomegaly and low periventricular density (). Her mental status was temporarily improved and the ventricle size was decreased following a ventriculoperitoneal (VP) shunt operation. Three months after VP shunt placement, the patient's mental status deteriorated further and quadriparesis was noted. Brain magnetic resonance imaging (MRI) with gadolinium enhancement revealed an irregular, enhanced, round mass with multiple necrotic foci in the left basal ganglia, where the previous hemorrhage had occurred (). Navigation-assisted biopsy was performed, revealing an anaplastic astrocytoma (WHO grade III). The patient underwent radiotherapy, and repeat MR imaging revealed non-progression of the tumor (data not shown). However, she has been bed-ridden during 6 months of follow-up. | [[69.0, 'year']] | F | {'30948997': 1, '12513031': 1, '29844891': 2, '3316531': 1, '7367626': 1, '19779291': 1, '25957575': 2, '9883445': 1, '11086806': 1, '7099393': 1, '19847768': 1, '12604273': 1, '10582668': 1, '9309296': 1, '22277560': 1, '24175027': 2} | {'5937221-1': 1, '4489354-1': 1} |
163,874 | 3809439-1 | 24,175,028 | noncomm/PMC003xxxxxx/PMC3809439.xml | Anterior Dislodgement of a Fusion Cage after Transforaminal Lumbar Interbody Fusion for the Treatment of Isthmic Spondylolisthesis | A 51-year-old man presented with lower back and radiating pain to both legs. His symptoms had developed 5 years ago, but conservative treatments had failed. On admission, he had a limping gait and his pain was aggravated by posture. Neurological examinations showed grade 4/5 strength in extension of his left big toe. Plain radiographs and CT images showed L4-5 grade I isthmic spondylolisthesis with instability, a LSTV (Castellvi IIIa), and a dysplastic L5 vertebral body (). The anteroposterior length of the cranial endplate of the L5 body was relatively shorter than that of the L4 body, even though the surface was flat. Magnetic resonance images showed canal and foraminal stenosis and L4-5 disc degeneration. The bone mineral density measured by Dual-emission X-ray absorptiometry showed a T score of -2.1 for the lumbar spines.\nL4-5 decompression via bilateral paraspinal approaches was performed and a banana-shaped PEEK cage (WSH T-cage, WINNOVA CO., Ltd., Seoul, Korea) was inserted through an opening in the intervertebral disc on the left side, followed by bilateral pedicle screw fixation with reduction (VIPER™, DePuy Spine, Inc., Raynham, MA, USA). Local autograft and allograft cancellous bone chips were packed into the fusion cage and into the remaining intervertebral disc space posteriorly after the cage insertion. After surgery, the presenting symptoms significantly improved and the radiographs showed a good reduction (). The patient's pain was assessed on visual analogue scale and improved dramatically after surgery (before surgery; 8 for low back pain, 10 for leg pain : 1 week after surgery; 2 for low back pain, 2 for leg pain). The patient was discharged at postoperative 7 days and returned to daily living activities while wearing a corset.\nSeven weeks after surgery, he visited to our outpatient clinic with severe low back and left leg pain for 7 days without any neurological deficit. He denied any history of trauma. Plain radiographs showed anterior dislodgement of the fusion cage as well as a reduction loss of the spondylolisthesis at the L4-5 level (). Sagittal images on a CT scan demonstrated that the intervertebral space was not fused and the screws were loosened with halo change (). Physical signs and laboratory findings on admission did not support infection. Revision surgery using an anterior approach was performed to remove the displaced cage. A 5-cm-long midline incision was made and a retroperitoneal approach to the affected level was done using a robotic arm retractor. The anterior longitudinal ligament and annulus were not perforated. The cage had slipped down and was positioned anterior to the L5. After removal of the cage and previously grafted bones in the disc space, the endplates were carefully prepared. A wedge-shaped, lordotic titanium cage (WSH cage, WINNOVA CO., Ltd., Seoul, Korea) filled with allograft chips was inserted a little laterally to the left to avoid a collapsed portion of the inferior endplate of the L4 body. After the closure of the anterior surgical wound, the patient was positioned prone for pedicle screw replacement. The pedicle screws found unstable and in spite of being with thicker and longer ones, two L4 screws still remained loose. Therefore, cement augmentation was added to the L4 screws (). Postoperatively, however, the patient complained of persistent pain on the anterolateral side of the left leg and difficulty in walking. CT images showed a fracture on the pedicle and anterolateral lateral body wall of the L5 vertebra (). As a result, he had additional surgery for paraspinal decompression on the left side at the L4-5 level. Removal of the left L5 screw followed by bilateral extensions of the pedicle screw fixation to S1 was performed (). Because the L5-S1 level was congenitally fused due to the LSTV, we considered that extension of the screw fixation made no additional motion limitation of the lumbosacral spine but increased stability.\nAfter the second revision surgery, the patient showed significant improvement of his symptom except mild left leg discomfort. His gait was improved and the lumbar corset was applied for 3 months. At 6 months follow-up, his left leg discomfort was completely resolved. Radiographs and a 3-dimensional CT scan obtained at 6 months postoperatively revealed a solid fusion at the L4-5 level. | [[51.0, 'year']] | M | {'19011543': 1, '16816765': 1, '20505562': 1, '11317111': 1, '11242386': 1, '20634726': 1, '16540856': 1, '11891448': 1, '15855373': 1, '18675496': 1, '9546475': 1, '2533403': 1, '16284577': 1, '6495013': 1, '12221375': 1, '26180692': 2, '17023854': 1, '20203111': 1, '31435555': 1, '12897471': 1, '9361917': 1, '28407708': 2, '25588711': 1, '1523506': 1, '19475436': 1, '16572618': 1, '24175028': 2} | {'4494582-1': 1, '4494582-2': 1, '5402863-1': 1} |
163,875 | 3809440-1 | 24,175,029 | noncomm/PMC003xxxxxx/PMC3809440.xml | Differential Diagnosis and Management of a Pituitary Mass with Renal Cell Carcinoma | A 40-year-old woman presented with mild headache. Three years prior, she had undergone a left radical nephrectomy for renal cell carcinoma. Video-assisted thoracic surgery was performed for metastatic lymph node excision and left lower lobe superior segmentectomy. Additional procedures included the excision of a retroperitoneal lymph node metastasis and thoracotomy for lymph node dissection along the descending aorta. She received chemotherapy for multiple metastases, including the adrenal gland, psoas muscle and mediastinum. During the follow-up after chemotherapy, she complained of intermittent headache. Magnetic resonance (MR) imaging demonstrated a 13 mm sellar mass with suprasellar extension without optic nerve compression (). The pituitary stalk was deviated to the left side. An endocrinological evaluation revealed hyperprolactinemia as follows : serum prolactin, 89.5 ng/mL [reference range (RR) : 0-25 ng/mL]; free T4, 0.75 ng/dL (RR : 0.70-1.80 ng/dL); TSH, 1.73 uIU/mL (RR : 0.4-4.1 uIU/m); ACTH at 8 am, 52 pg/mL (RR : 0-60 pg/mL); Cortisol at 8 am, 7.2 ug/dL (RR : 5-25 ug/dL); LH, 6.7 mIU (RR : 1-12 mIU); and FSH, 11.5 mIU (RR : 2-13 mIU). 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) showed no uptake in the sellar area, and increased uptake in metastatic lesions in other sites (). She did not complain of the visual symptoms, and Goldmann perimetry revealed no visual field defects. A careful history revealed that she had experienced galactorrhea and amenorrhea, which continued for 5 months and resolved without management 9 years ago prior to her current presentation. With these clinical backgrounds, a presumptive diagnosis of pituitary adenoma was made and regular follow-up was recommended because of the relatively rare incidence of pituitary metastasis.\nSix months after the first visit, her vision worsened. Snellen visual acuity without correction at a 5 m distance in 200 lux of light showed a marked decrease in visual acuity from 1.0/1.0 to 1.0/0.4. Goldmann perimetry revealed superior temporal quadrantanopsia of the left eye. The follow-up MR imaging showed that the mass from 13 mm to 23 mm, and compression of the optic apparatus was observed (). The cocktail test showed hyperprolacinemia (prolactin, 74.4 ng/mL) and hypocortisolism (peak cortisol, 11.9 ug/dL). The other pituitary axes were intact, and there were no symptoms suggesting diabetes insipidus.\nThe patient underwent trans-sphenoid surgery to obtain a pathologic diagnosis and decompress the optic apparatus. The sellar floor was very thin and showed a mottled appearance. The tumor was gray and hypervascular (). Its hard consistency and the distinct demarcation helped to easily dissect it from the pituitary gland and cavernous sinus. However, we removed parts of the diaphragma sellae with the superior surface of the tumor because the tumor was strongly adhered to it. The tumor was completely removed in a piecemeal fashion, and the pathology was compatible with renal cell carcinoma (). The post-operative course was uneventful and her vision recovered to its previous original state within one month after surgery. The clinical and radiological follow-up has been continued without adjuvant therapy and hormone replacement. | [[40.0, 'year']] | F | {'28044054': 1, '7196526': 1, '14764764': 1, '21421711': 1, '20694412': 1, '8770309': 1, '17541748': 1, '1203849': 1, '30461658': 1, '22500201': 2, '22990000': 1, '34185289': 1, '32908722': 2, '24175029': 2} | {'7450332-1': 1, '3322215-1': 1} |
163,876 | 3809441-1 | 24,175,030 | noncomm/PMC003xxxxxx/PMC3809441.xml | Pulsed Radiofrequency Neuromodulation for the Treatment of Saphenous Neuralgia | A 65-year-old male presented with severe pain and a tingling sensation in the right medial knee, calf, and ankle. He walked with a limp due to pain but and not weakness. The patient had experienced severely disabling conditions for over 1 month. The pain and tingling sensation occurred every 5-10 minutes and lasted more than 5 minutes per episode. A neurological examination was normal, except for severe pain and tingling sensation in the right medial knee, calf, and ankle.\nLumbar magnetic resonance imaging (MRI) revealed no acute lesions except for distal degenerative changes at multiple levels. Knee MRI revealed no acute lesion except for mild degenerative osteoarthritis. A nerve conduction study revealed an absence of a right saphenous response in both the medial leg and the infrapatellar region, while normal findings were recorded from the left side. Electromyography was normal for all muscles tested. Before visiting our outpatient clinic, the patient had undergone a variety of treatments, including medication, an intra-articular injection for knee pain, and acupuncture around the right knee and medial calf. However, his symptoms did not improve but instead progressed. Saphenous nerve blocks using a local anesthetic and steroids were performed twice at 1-week intervals with fluoroscopy in our clinic. The target sites of nerve blocks were two point, the saphenous nerve around adductor's canal and the sartorial branch of the saphenous nerve around superficial saphenous vein. These blocks provided temporary pain relief that lasted about 3 days. After the positive results of the diagnostic nerve blocks, the patient was scheduled for PRF neuromodulation of the saphenous nerve.\nWe performed fluoroscopically guided selective saphenous nerve PRF using a model NT1000 radiofrequency generator (NeuroTherm, Middleton, MA, USA). In the operating room, the patient was supine, with the right leg positioned with hip external rotation, hip abduction, and knee flexion. We drew a hypothetical line for the saphenous nerve (complete nerve, infrapatellar branch, and sartorial branch) and the trajectory for the cannula on his leg (). The target site was prepped with betadine and aseptically draped, and the right knee joint and epicondyle were identified under C-arm fluoroscopy. Disposable 20-gauge, 10-cm radiofrequency cannulas (Model S-1505; NeuroTherm) with a 5-mm active tip were inserted at the level of the adductor's canal and below the epicondyle. The introducer needles were withdrawn, and a Model RFDE-15 disposable radiofrequency electrode (NeuroTherm) was advanced ().\nSelective stimulation of the sensory fibers (50 Hz) showed concordant pain between 0.3-0.5 V, which confirmed proper localization of the PRF electrode. Motor stimulation was negative. After stimulation, PRF neuromodulation was performed for 240 pulses. The maximal temperature was 42℃. After the procedure, the pain measured on a visual analog scale had decreased by 90% without medication. The pain relief was maintained for 6 months of follow-up without medication. | [[65.0, 'year']] | M | {'16336478': 1, '14410944': 1, '6864036': 1, '1997901': 1, '907036': 1, '11904038': 1, '2782531': 1, '14622704': 1, '1619412': 1, '15891719': 1, '11027764': 1, '3229266': 1, '10204759': 1, '1129703': 1, '6621837': 1, '28217060': 2, '8443553': 1, '2847334': 1, '507971': 1, '26896944': 1, '6703186': 1, '20205890': 2, '24175030': 2} | {'2827394-1': 1, '5292859-1': 1} |
163,877 | 3809442-1 | 24,175,031 | noncomm/PMC003xxxxxx/PMC3809442.xml | Hypertensive Encephalopathy with Reversible Brainstem Edema | A 36-year-old male with idiopathic hypertension (duration >6 yrs) was admitted to our hospital for abrupt-onset headache, right facial palsy, dysarthria, and right hemiparesis that had developed three hours earlier. Two weeks prior to admission, he stopped his antihypertensive medication. BP recorded at the time of presentation was 230/160 mm Hg.\nLaboratory studies were within normal range and ophthalmologic evaluation was unremarkable. Specifically, no papilledema was evident. Routine chest X-ray and echocardiogram suggested severe concentric left ventricular hypertrophy, later confirmed by transthoracic echocardiography. Emergency computed tomographic (CT) scan of the brain revealed small amount (7 cc) of intracranial hemorrhage involving the left basal ganglia, and there was relative hypodensity of the brainstem (). CT angiography demonstrated no cerebral vascular abnormalities, including vertebrobasilar circulation. Brain MRI showed diffuse high-signal intensities on T2-weighted images and fluid-attenuated inversion recovery images without gadolinium enhancement in the pons and midbrain. No high signal intensities in diffusion-weighted images (DWI) and high signal intensities in apparent diffusion coefficient (ADC) images, implying that the changes were not due to cerebral infarction (). There were also no abnormal findings other than the small amount of hemorrhage in basal ganglia, which was confirmed already in CT ().\nBased on these findings, a diagnosis of acute hypertensive encephalopathy with intracranial hemorrhage was made. We immediately initiated intravenous antihypertensive therapy. Ten days later, systolic and diastolic pressures were successfully stabilized. Follow-up MRI (including DWI) on Day 16 of hospitalization revealed complete resolution of prior imaging aberrations involving the brainstem (). | [[36.0, 'year']] | M | {'18854436': 1, '19198757': 1, '11123390': 1, '18403560': 1, '8559202': 1, '18676082': 1, '16498216': 1, '10449143': 1, '7976528': 1, '34904080': 1, '34925205': 1, '24175031': 2} | {} |
163,878 | 3809443-1 | 24,175,032 | noncomm/PMC003xxxxxx/PMC3809443.xml | Barotrauma-Induced Pneumocephalus Experienced by a High Risk Patient after Commercial Air Travel | A 49-year-old female presented to the emergency department with a severe headache, nausea, and vomiting after one hour flight on a domestic commercial airliner. Her mental status was alert without confusion. A cranial nerve examination revealed anosmia through both nostrils and a visual field defect of the left inferior homonymous quadranopsia. Additional cranial nerve function, motor and sensory function, the deep tendon reflex, and cerebellar function were normal.\nTen years ago, this patient was diagnosed with meningioma in the occipital lobe and underwent a suboccipital craniotomy to remove the tumor at another hospital. Further questioning revealed that the patient underwent four additional otolaryngologic operations (two operations involving the mastoid sinus and two involving the frontal skull base through the nose) to manage CSF rhinorrhea four years after initial the craniotomy. The patient did not know the precise cause of the CSF leak. Finally, a lumboperitoneal shunt was placed, and the patient did not experience further symptoms of a CSF leak. The revision surgery for a recurrent tumor was performed last year; at the time of the incident discussed here, the patient was returning home after gamma knife radiosurgery for the residual tumor.\nA computed tomography (CT) scan of the head () demonstrated extensive air within the subarachnoid space of the basal cistern, bilateral lateral and third ventricle, and extending to the intraparenchymal portion of the left frontal lobe.\nThe routine laboratory blood tests (leukocyte count, hemoglobin, hematocrit, glucose, blood urea nitrogen, creatinine, sodium, potassium, chloride, and C-reactive protein) were normal.\nNormal saline and analgesics were administered via an intravenous line, and a gradual resolution of the headache was achieved within several days. Seven days after presentation, the patient reported no complaints, and no evidence of meningoencephalitis was observed. The patient was warned not to fly before a definite diagnostic work up and sealing procedure for the CSF leak site was performed, and the patient was then discharged. | [[49.0, 'year']] | F | {'19306175': 1, '20464820': 1, '22195398': 1, '6032371': 1, '10985450': 1, '26500801': 2, '11486697': 1, '18053859': 1, '15277656': 1, '15309929': 1, '12602445': 1, '2026828': 1, '22931355': 1, '32926695': 2, '18225775': 1, '12817610': 1, '24175032': 2} | {'7434277-1': 1, '4596054-1': 1} |
163,879 | 3809444-1 | 24,175,033 | noncomm/PMC003xxxxxx/PMC3809444.xml | Acute Hydrocephalus Following Cervical Spinal Cord Injury | A 75-year-old male patient was referred to our emergency department with a tetraparesis after a trivial fall at home. He had been intermittently admitted to our spine center due to cervical OPLL and diffuse idiopathic skeletal hypertrophy. There was no evidence of head injury and his mental status was alert. On neurological examination, his sensation was off below the C5 dermatome, with right side motor weakness of 0/V and left side motor weakness of II/V. In addition, we detected decreased anal tone, loss of urinary sense, and hypotonia of deep tendon reflex. He also exhibited signs of spinal shock, including hypotension and bradycardia.\nExcept for brain cortical atrophy, no abnormal findings were observed on brain computed tomography (CT). Plain cervical radiographs and CT showed diffuse, thick OPLL from level C1 to C4, which was slightly thickened, compared to a previous imaging study performed six years ago. Cervical magnetic resonance imaging showed severe spinal cord compression with signal change of the spinal cord from C1 to C4 (). In particular, heterogeneous signal change of the C1-2 level suggested acute intramedullary hemorrhage of the spinal cord.\nWe performed emergency cervical spine surgery. Decompressive total laminectomy from C1 to C5, and occipitocervical fusion from occiput to C5 were performed (). In the operation field, cord edema was severe and pulsation of the cord was weak. After the operation, his motor weakness showed slight improvement.\nTwo days after surgery, his mental status had deteriorated to drowsiness, with dilation of the right pupil of 4 mm. Findings on brain CT revealed acute hydrocephalus and subarachnoid hemorrhage (SAH) in the cerebellomedullary cistern (). Brain and carotid CT angiography showed no vascular abnormality. To alleviate symptoms, we performed lumbar cerebrospinal fluid (CSF) drainage. The pressure of lumbar drainage was as high as 26 cmH2O, and CSF was mixed with fresh blood. Despite lumbar drainage, his symptoms did not show improvement, therefore, extraventricular drainage (EVD) was performed. Two weeks after EVD, ventriculo-peritoneal shunt was performed, however, neurologic deterioration was not fully recovered. Three months after trauma, he eventually died due to heart failure. | [[75.0, 'year']] | M | {'1994264': 1, '10598715': 1, '18661317': 1, '1986132': 1, '11305760': 1, '21928038': 1, '15303114': 1, '2588057': 1, '16010272': 1, '12037714': 1, '25110487': 2, '24175033': 2} | {'4124928-1': 1} |
163,880 | 3809445-1 | 24,175,034 | noncomm/PMC003xxxxxx/PMC3809445.xml | Intracranial Calcification Caused by a Brain Abscess : A Rare Cause of Intracranial Calcification | A previously healthy 40-year-old man presented with mental deterioration after a head injury. On neurological examination, he was stuporous with a Glasgow Coma Scale of 8. Routine hematological and serum chemistry testing, including erythrocyte sedimentation rate and C-reactive protein, revealed no abnormality. However, CT scan of the brain revealed severe brain swelling and hemorrhagic contusion in the right frontotemporoparietal (FTP) region. He underwent emergent decompressive craniectomy on the right FTP region (). Postoperatively, he became conscious and was able to obey commands without any neurologic deficit. However, three weeks later, he complained of a febrile sensation and had a temperature of 38.4℃. A CT scan of the brain with intravenous contrast showed a ring-enhanced brain abscess (). Third generation cephalosporin and sufficient hydration were continuously administered. However, despite this management, the fever continued and he complained of mild left hemiparesis (Grade IV+/Grade IV+). A CT scan and magnetic resonance imaging (MRI) with intravenous contrast on hospital day 35 revealed an increase in both the size and extent of the brain abscess (). Navigation-guided culture and biopsy following drainage of the brain abscess using a 5 L catheter were performed. A dark yellowish pus was drained from the abscess. Gram stain and acid-fast bacilli cultures were negative and revealed no organisms. No evidence of granulomas or larval cysts were seen. However, from cultures of the purulent drainage on blood agar, coagulase negative staphylococcus hominis was isolated. His antibiotics were changed to nafcillin and ciprofloxacin based on the results of culture test, and after 6 weeks on antibiotics, he achieved complete clinical recovery except for mild hemiparesis. However, follow-up CT performed 5 months after admission revealed that the brain abscess had developed into a large calcified mass (). Because of its deep-seated location and a lack of clinical symptoms, surgical removal was not performed. Instead, a series of CT scans were taken 3 monthly. No change in either the size or extent of the calcified region was observed over 2 year of follow-up. The patient remains symptom free with mild hemiparesis (). | [[40.0, 'year']] | M | {'6856080': 1, '2335625': 1, '3267286': 1, '6527142': 1, '12889171': 1, '4824739': 1, '10775955': 1, '30617192': 1, '15942285': 1, '12772710': 1, '16515234': 1, '24175034': 2} | {} |
163,881 | 3809446-1 | 24,175,035 | noncomm/PMC003xxxxxx/PMC3809446.xml | Multiple Myeloma and Epidural Spinal Cord Compression : Case Presentation and a Spine Surgeon's Perspective | A 62-year-old woman with no significant medical background, presented with upper back pain for one month and progressive lower extremity numbness and weakness. She was unable to walk unaided in the last several days and had developed urinary incontinence. A neurological examination revealed bilateral lower extremity weakness with grade IV strength, decreased deep and superficial sensation, a tingling sensation below the umbilicus and increased knee jerk. Initial laboratory tests revealed a hemoglobin of 14.0 g/dL, white cells of 8200/mm3, erythrocyte sedimentation rate of 120 mm/h, and elevated serum total protein of 10.1 g/dL (normal range, 6.6-8.3 g/dL), but she did not have renal or hepatic insufficiency. Additional laboratory tests including a bone marrow biopsy revealed κ chain immunoglobulin G (IgG) multiple myeloma. On magnetic resonance imaging (MRI) of the entire spine that was taken to evaluate the neurological condition, an epidural mass was found to compress the spinal cord posteriorly, extending from the C7 to T2 vertebra. The epidural mass was hypointense to the spinal cord on T1-weighted images and hyperintense on T2-weighted images, with moderate contrast enhancement. No pathological fracture of the adjacent vertebra was found. High-dose steroid therapy (dexamethasone, 40 mg/day) and emergent radiotherapy were performed under the diagnosis of MM and spinal cord compression. Before this medical treatment, her neurological status was Frankel B. MRI, checked after 3000 cGy fractioned radiotherapy for the C7-T2 lesion, revealed complete resolution of the epidural mass (). However, during 6 months of follow-up, the patient did not experience any neurological improvement (final neurological status, Frankel B). | [[62.0, 'year']] | F | {'19609421': 1, '1520997': 1, '9132825': 1, '21216573': 1, '8793437': 1, '33668980': 2, '11805699': 1, '6729378': 1, '21498133': 1, '466107': 1, '20189464': 1, '13717759': 1, '15522061': 1, '17194905': 1, '17905632': 1, '19827269': 1, '20191332': 1, '25552888': 1, '20606090': 1, '24175035': 2} | {'3809446-2': 2, '3809446-3': 2, '7930977-1': 1} |
163,882 | 3809446-2 | 24,175,035 | noncomm/PMC003xxxxxx/PMC3809446.xml | Multiple Myeloma and Epidural Spinal Cord Compression : Case Presentation and a Spine Surgeon's Perspective | A 39-year-old woman presented with both shoulder and upper back pain for 1 month. A bone marrow biopsy was performed due to findings of an A/G ratio reversal, anemia, hypercalcemia and azotemia on laboratory tests revealed multiple myeloma. The findings of multiple punched out lesion in the skull and multiple osteolytic lesions over the spine on the radiological examination were matched with MM (IgG, λ chain). Computed tomography (CT) scans for the upper back pain revealed an epidural mass compressing the spinal cord. The initial neurological examination revealed normal motor and sensory functions of Frankel E grade. High-dose steroid therapy and fractioned radiotherapy (C7-T2, 3000 cGy) were conducted for the spinal cord compression lesion. After the ninth fraction of radiotherapy, she suddenly developed both lower extremity weakness, sensory disturbance below the T4 level and urinary incontinence (Frankel B). A follow-up MRI revealed sustained compression of the spinal cord by an epidural mass without any additional pathological fractures. An emergent decompressive laminectomy was performed. No pathological fractures of the posterior element of the involved spine were observed intraoperatively. A friable bluish gray colored soft tissue mass was found at the epidural space compressing the spinal cord with mild adhesion to the underlying dura. Coincident microscopic findings of multiple myeloma with <10% necrosis rates were observed from the excised mass (). At the 6 month follow-up after surgery, her neurological status remained unchanged (Frankel B). | [[39.0, 'year']] | F | {'19609421': 1, '1520997': 1, '9132825': 1, '21216573': 1, '8793437': 1, '33668980': 2, '11805699': 1, '6729378': 1, '21498133': 1, '466107': 1, '20189464': 1, '13717759': 1, '15522061': 1, '17194905': 1, '17905632': 1, '19827269': 1, '20191332': 1, '25552888': 1, '20606090': 1, '24175035': 2} | {'3809446-1': 2, '3809446-3': 2, '7930977-1': 1} |
163,883 | 3809446-3 | 24,175,035 | noncomm/PMC003xxxxxx/PMC3809446.xml | Multiple Myeloma and Epidural Spinal Cord Compression : Case Presentation and a Spine Surgeon's Perspective | A 62-year-old woman was presented with upper back pain and progressive weakness for one month. On her history, she had undergone posterior spine surgery for a multiple compression fracture 6 months ago. She denied hearing about multiple myeloma at that surgery. Laboratory and radiological tests revealed multiple myeloma (IgG, κ chain). MRI showed multiple pathological fracture involving T4, 7, and 9 and an epidural mass was compressing the spinal cord at the T4 level. On neurological examination, her lower extremity motor power was over grade IV and she was able to walk unaided (Frankel D), even though she complained of lower extremity weakness. High-dose steroid and fractioned radiotherapy were performed. A radiological examination conducted 3 months post-radiotherapy revealed complete resolution of the cord compression and disappearance of the epidural mass (). No further pathological fracture were found. At the 18 month follow-up, her neurological status had improved with mild discomfort over the upper back region. | [[62.0, 'year']] | F | {'19609421': 1, '1520997': 1, '9132825': 1, '21216573': 1, '8793437': 1, '33668980': 2, '11805699': 1, '6729378': 1, '21498133': 1, '466107': 1, '20189464': 1, '13717759': 1, '15522061': 1, '17194905': 1, '17905632': 1, '19827269': 1, '20191332': 1, '25552888': 1, '20606090': 1, '24175035': 2} | {'3809446-1': 2, '3809446-2': 2, '7930977-1': 1} |
163,884 | 3809851-1 | 24,142,665 | noncomm/PMC003xxxxxx/PMC3809851.xml | Successful Azathioprine Treatment with Metabolite Monitoring in a Pediatric Inflammatory Bowel Disease Patient Homozygous for TPMT | An 18 year-old male was referred to our hospital for abdominal pain and loose stool. On physical examination, he had tenderness on the lower left quadrant of the abdomen. Routine laboratory tests, including complete blood cell counts (CBC) and liver function were all within normal limits except mild anemia and an elevated erythrocyte sediment rate of 82 mm/hr (reference interval, 0-22 mm/hr).\nThe patient was diagnosed with Crohn's disease according to standard clinical, endoscopic, and histologic criteria. Oral treatment with AZA (1.8 mg/kg/day) and mesalazine (55.6 mg/kg/day) was started. Two weeks later, the absolute neutrophil count (ANC) and white blood cell count (WBC) decreased from 5140/µL to 1010/µL, and 6270/µL to 2810/µL, respectively. The AZA dosage was reduced from 1.8 to 0.9 mg/kg/day. Three weeks later, ANC and WBC continued to decline further to 190/µL and 1910/µL, respectively. The AZA was discontinued. After leukopenia was recovered, the patient was restarted on AZA (0.8 mg/kg/day) with the discontinuation of mesalazine. The patient's daily dose of AZA was cautiously increased to 1.2 mg/kg while monitoring CBC levels.\nPeripheral blood samples were taken from the patient for TPMT genotyping. After obtaining written informed consent, sequence analysis of all coding exons with their flanking intron regions of TPMT gene were performed, and we identified a homozygous variant (c.719A>G; p.Tyr240Cys), TPMT.\nSimultaneously, 6-TGN and 6-MMPN concentrations were measured by the Waters 2795 Alliance HPLC system and a Quatro Micro API tandem mass spectrometer (Waters, Manchester, UK). The thresholds indicating increased likelihood efficacy (6-TGN >235 pmole/8×108 red blood cells, RBC), increased risk of leukopenia (6-TGN >450 pmole/8×108 RBC), and increased risk for hapatotoxicity (6-MMPN >5700 pmole/8×108 RBC) were suggested., The patient's 6-TGN concentration (7206 pmole/8×108 RBC) corresponded to a higher risk of leukopenia, although the daily dose had already been reduced from 1.2 mg/kg to 0.8 mg/kg because of neutropenia. The daily dosage was readily decreased to 0.2 mg/kg, and 6-TGN declined to therapeutic levels (437 pmole/8×108 RBC). Daily AZA dose was reduced further to 0.1 mg/kg as 6-TGN concentration increased again to 745 pmole/8×108 RBC (). 6-MMPN concentrations were detected at less than the limit of quantitation. The patient's laboratory parameters, including CBC and liver function, were within normal limits during the follow-up period of 24 months. | [[18.0, 'year']] | M | {'28839871': 1, '16166171': 1, '15118980': 1, '19214663': 1, '10734022': 1, '1960624': 1, '8873214': 1, '10833476': 1, '11683683': 1, '9177237': 1, '19682195': 1, '18516013': 1, '20308917': 1, '16842460': 1, '16431304': 1, '18266236': 1, '17026564': 1, '8644731': 1, '23407052': 1, '11337944': 1, '23422873': 1, '18250137': 1, '16543290': 1, '12477776': 1, '20629710': 1, '20393862': 1, '33824446': 1, '30927276': 1, '24142665': 2} | {} |
163,885 | 3809864-1 | 24,142,664 | noncomm/PMC003xxxxxx/PMC3809864.xml | A Proposal to Prevent the "Mephisto Sign" Side Effect of Botulinum Toxin Type A Injection in Chronic Migraine | A 25-year-old female patient visited the hospital due to frequent headaches, and was diagnosed with chronic migraine. There was no specific medical history. She did not effectively respond to various types of pharmacotherapy, and BoNT-A injection was indicated. BoNT-A injections were performed as described above, so that a total of 155 U was injected into 31 sites. At the follow-up appointment 2 weeks later, the patient reported a change in eyebrow morphology, showing the Mephisto sign. An additional BoNT-A dose of 2 U each was administered to the lateral-most point of the frontalis muscle bilaterally. However, the morphology of eyebrow became normalized within 2-3 weeks after this additional injection. | [[25.0, 'year']] | F | {'26507959': 1, '20647171': 1, '34401486': 1, '33603602': 1, '20958294': 1, '20647170': 1, '24142664': 2} | {} |
163,886 | 3809873-1 | 24,142,666 | noncomm/PMC003xxxxxx/PMC3809873.xml | Ceramic Head Fracture in Ceramic-on-Polyethylene Total Hip Arthroplasty | A 72-year-old woman underwent THA for idiopathic osteonecrosis of left femoral head in February, 2000. In 2012, she visited our emergency room for left hip pain with clunk sounds after squatting position 3 days ago. She had no problems in gait before the accident of squatting position. She has obese appearance; her height was 164 cm, weight was 90 kg, and bone mass index was 33.5 kg/m2. There was no evidence of infection including redness or heating sensation around left hip.\nPlain radiographs showed ceramic head fractures with multiple fragments around the joint. The former arthroplasties included the cementless cup (Trilogy® acetabular system, Zimmer, Warsaw, IN, USA), cementless stem (Versys® hip system, Zimmer, Warsaw, IN, USA), polyethylene liner (Trilogy® acetabular system, UHMWPE, Zimmer, Warsaw, IN, USA), and ceramic head (Versys® hip system, 28 mm diameter, short neck length, zirconium oxide ceramic). The inclination of acetabular cup was 43 degree, and anteversion was 10 degree, which were within acceptable range ().\nRevision operation was done. Posterolateral approach was used, similar to previous operation. After capsulectomy thorough posterolateral approach, various sizes of ceramic particles were observed. Intraoperatively, ceramic fragments were meticulously removed, and extensive capsulectomy was performed. Inner surface of polyethylene liner and metal neck taper junction of the femoral components were severely scratched to retain (). There were concerns about refracture of ceramic head and galvanic corrosion of metal head because of the scratched femoral neck. Thus, femoral stem was removed. In addition, the acetabular cup that was loosened because of osteolysis was also removed. After the removal of all components, massive irrigation and extensive synovectomy were done to remove microscopic ceramic fragments.\nFor revision, new cementless acetabular cup (Delta-PF Cup, Lima, Udine, Italy), full-coated modular cementless stem (Revision hip uncemented stem-Lima, Udine, Italy) were used. And, the 4th generation ceramic liner (Neutral liner, 36 mm I.D., Biolox Delta, CeramTec, Plochingen, Germany) was implanted for revision surgery. Full-coated modular cementless stem (Revision hip uncemented stem-diameter 16 mm, length 140 mm, Neck with screw-height 60 mm, Lima, Udine, Italy) was inserted with allogenic bone graft around proximal femur. Finally, the 4th generation ceramic head (Femoral head, 36 mm short taper 12/14, Biolox Delta, CeramTec, Plochingen, Germany) was applied. Intraoperative testing of the stability of the revised implants was advisable. The cup position was checked with 42 degree of abduction, and 31 degree of anteversion in postoperative plain radiographs ().\nAt her 6 months follow-up, she could return to her previous level of activity, and had Harris hip score of 82. In radiographs, the implant showed stable fixation without sign of osteolysis or loosening. | [[72.0, 'year']] | F | {'16810547': 1, '22258782': 1, '31198780': 2, '34401417': 1, '22219244': 1, '33842105': 2, '8749773': 1, '20660234': 1, '21680138': 1, '17272452': 1, '19202119': 1, '22434477': 1, '17179781': 1, '26183804': 1, '23008021': 1, '18196411': 1, '18245593': 1, '21119933': 1, '24142666': 2} | {'8020614-1': 1, '6546678-1': 1} |
163,887 | 3809874-1 | 24,142,667 | noncomm/PMC003xxxxxx/PMC3809874.xml | Extensive Tuberculous Lymphadenitis Mimicking Distant Lymph Node Metastasis on F-18FDG PET/CT in a Patient with a History of Malignant Melanoma | A 62-year-old woman was diagnosed with malignant melanoma on the left sole of the foot and underwent wide excision of the sole melanoma with inguinal lymphadenectomy. She was well without evidence of tumor recurrence 4 years after surgery.\nAfter 4 years, she complained of a palpable right neck mass. F-18FDG PET/CT was performed for the recurrent melanoma evaluation. A F-18FDG PET/CT showed markedly increased FDG uptakes (SUV max: 12.4) in the bilateral neck, mediastinum, hila, left parasternal, and abdominal lymph nodes, which were suspicious for metastases ().\nPlain chest X-ray and PET/CT of both lungs showed normal.\nUltrasonography (US) showed multiple enlarged cervical lymph nodes considered to be suspicious for metastasis (), and US guided fine needle aspiration was performed for diagnosing the cause of cervical lymphadenopathy.\nCytology result was negative for malignancy, and immunocytochemistry result for HMB45 that reacts against an antigen present in melanomas was also negative. Therefore, excisional lymph node biopsy was performed to discover the reason behind the image-pathologic discordance.\nExcisional lymph node biopsy for cervical lymph node showed chronic granulomatous lymphadenitis with caseous necrosis () and tuberculosis polymerase chain reaction was positive, compatible with tuberculosis lymphadenitis. Finally, tuberculosis lymphadenitis was diagnosed by excisional biopsy. | [[62.0, 'year']] | F | {'12971641': 1, '20139845': 1, '19145057': 1, '16652317': 1, '15221923': 1, '20194002': 1, '25550993': 1, '18716117': 1, '14734916': 1, '17460000': 1, '24142667': 2} | {} |
163,888 | 3809882-1 | 24,142,663 | noncomm/PMC003xxxxxx/PMC3809882.xml | A Case of Cerebellar Infarction Caused by Acute Subclavian Thrombus Following Minor Trauma | A 56-year-old woman was admitted to the emergency room for sudden onset vertigo and right sway on awakening. She had received an intense chiropractic manipulation of her shoulders the day before admission. Her medical history included diabetes mellitus, which had been managed for six years. On examination, blood pressure was 137/71 mmHg and 113/56 mmHg in the right and left arms, respectively. Her left hand was pale and cold with an absent radial pulse on the left (). An audible subclavian bruit was present on the left side. Downbeat nystagmus and a right falling tendency during tandem gait were observed. No motor and sensory deficits were shown. No musculoskeletal abnormalities that could have been implicated in compression of the subclavian artery were evident. Diffusion-weighted MRI revealed multiple acute infarctions in the left cerebellar hemisphere and vermis, compatible with the medial territory of the left posterior inferior cerebellar artery (). Doppler ultrasonography of the left vertebral artery showed bidirectional wave. Marked mid-systolic deceleration was seen with a sharp peak immediately before deceleration and return of forward direction during diastole. A provocative hyperemic cuff test (occlusive inflation of a blood pressure cuff for three minutes with subsequent release) of the left arm aggravated reverse flow. Therefore, these findings were compatible with a partial subclavian artery steal phenomenon (). Digital subtraction angiography (DSA) showed a large thrombus in the proximal left subclavian artery as well as retrograde flow through the left vertebral artery. No vertebral artery dissection was observed (). Neck CT showed a narrowed space between the anterior and lateral scalene muscles in the left side, more so than on the right. Blood tests for coagulation abnormalities, including protein C, S, lupus anticoagulant, and anti-cardiolipin antibody, were normal. After two days of treatment with heparin, warmth returned to her left arm. Follow-up Doppler ultrasonography showed improvement of the steal phenomenon. A systolic deceleration was still seen, but there was no retrograde flow and no augmented reversal flow was noted in the hyperemic cuff test, which was consistent with pre-steal phenomenon (). Follow-up DSA at 10 days after admission revealed markedly decreased thrombus size (). | [[56.0, 'year']] | F | {'16373786': 1, '3362359': 1, '10701631': 1, '21431969': 1, '2874328': 1, '4678043': 1, '15775708': 1, '17325282': 1, '21078767': 1, '29234493': 1, '22534720': 1, '24142663': 2} | {} |
163,889 | 3810345-1 | 24,187,502 | noncomm/PMC003xxxxxx/PMC3810345.xml | Endometrial carcinoma with yolk sac tumor-like differentiation and elevated serum β-hCG: a case report and literature review | A 28-year-old, nulligravid, married Chinese woman presented in December 2010 with a 14-month history of abnormal vaginal bleeding. The patient had been on barrier contraception, and to her knowledge had never been pregnant. Past medical history included epilepsy and hypothyroidism due to thyroidectomy. In October 2010, a diagnostic curettage specimen revealed endometrial adenocarcinoma with glandular squamous metaplasia, and an exploratory laparotomy was performed in a local hospital. A large omental mass and diffuse miliary nodules in the pelvic peritoneum made exposure of the surgical field difficult, so biopsy of the mass and peritoneum only was performed and histologic examination showed endometrial adenocarcinoma with yolk sac tumor-like differentiation. Chemotherapy, including intravenous paclitaxel 120 mg, adriamycin 60 mg, and intraperitoneal cisplatin 150 mg for one course, was administered at the local hospital. The patient was then referred to our hospital, where laboratory tests showed serum alfa-fetoprotein level of 1,522 ng/mL (normal value ≤20 ng/mL), β-hCG 518.9 mIU/mL (normal value ≤5 mIU/mL, chemiluminescent technology, Advia Centaur™ XP immunoassay system, Siemens, Erlangen, Germany), and CA 125 129 U/mL (normal value ≤35 U/mL). A chest computed tomography scan was negative.\nThe patient underwent cytoreductive surgery, including total abdominal hysterectomy, bilateral salpingo-oophorectomy with pelvic lymphadenectomy, omentectomy, appendectomy, partial sigmoidectomy with anastomosis, and resection of abdominal and pelvic metastases, without residual visible metastases. The uterus measured 10 × 8 × 5 cm and the cavity was filled with a cauliflower-like tumor measuring 6 × 3 × 2.5 cm and containing areas of ulceration (see ). This solid tumor had a grayish-white cut surface and moderate texture. Histopathologic examination of the uterine tumor revealed well to moderately differentiated endometrial adenocarcinoma with yolk sac tumor-like differentiation intraendometrially, with a close transition between the two components (). No trophoblastic component was found. The metastases were identical to the primary lesion on histology. The myometrium, cervix, appendix, bilateral adnexa, and iliac lymph nodes were negative for tumor. Periodic-acid Schiff stain was positive in yolk sac tumor cells. Immunohistochemical analysis revealed that both endometrial adenocarcinoma and yolk sac tumor components were positive for AE1/AE3. The yolk sac tumor component was strongly positive for alfa-fetoprotein, while the endometrial adenocarcinoma was relatively negative (). The endometrial adenocarcinoma component was positive for EMA, CA125, and CK7, suggesting epithelial neoplasms. There was focal positive staining for p53. Estrogen receptor and progesterone receptor status were both negative, as were hCG and β-hCG.\nTwo days after surgery, serum alfa-fetoprotein and β-hCG levels decreased dramatically to 166.4 ng/mL and 13.7 mIU/mL, respectively, and the CA125 level dropped into the normal range. Six courses of intravenous chemotherapy with paclitaxel 175 mg/m2 per day followed by carboplatin for an area under the concentration-time curve of 5 mg/mL per minute were administered every 21 days. Serum alfa-fetoprotein dropped to the normal range after three courses, while β-hCG fluctuated in the range of 5–20 mIU/mL despite two additional courses of chemotherapy with etoposide, methotrexate, actinomycin D, etoposide, and cisplatin followed by two courses with bleomycin, etoposide, and platinum. The persistent slightly elevated β-hCG was considered due to abnormal pituitary feedback, so chemotherapy was stopped. Unfortunately, β-hCG and alfa-fetoprotein rose again 2–3 months later. Despite salvage chemotherapy with two cycles of floxuridine, dactinomycin, etoposide, and vincristine, serum alfa-fetoprotein reached 311.1 ng/mL and β-hCG reached 2,716.5 mIU/mL. After the final course with oxaliplatin 200 mg and cyclophosphamide 800 mg, the patient abandoned further treatment and was lost to follow-up. | [[28.0, 'year']] | F | {'21239399': 1, '1688508': 1, '9890238': 1, '21696729': 1, '9571002': 1, '9863921': 1, '15767921': 1, '7507793': 1, '30985686': 2, '32064359': 2, '1717127': 1, '21293290': 1, '22211141': 1, '19967492': 1, '3292037': 1, '8600080': 1, '3026934': 1, '9740707': 1, '21355958': 1, '28776560': 1, '4334242': 1, '16810062': 1, '10701796': 1, '21345404': 1, '28494767': 2, '16814851': 1, '34262772': 2, '18066564': 1, '34211846': 2, '15151215': 1, '17701427': 1, '3169623': 1, '11136577': 1, '23235667': 1, '23115073': 1, '19232701': 1, '10849320': 1, '11104628': 1, '6158720': 1, '24187502': 2} | {'5427532-1': 1, '8243095-1': 1, '8240588-1': 1, '8240588-2': 1, '7005913-1': 1, '6485813-1': 1} |
163,890 | 3810492-1 | 24,187,513 | noncomm/PMC003xxxxxx/PMC3810492.xml | Assessing the long-term clinical benefit of prolonged-release fampridine tablets in a real-world setting: a review of 67 cases | Patient #2 was a 49-year-old white woman with a 27-year history of MS and secondary-progressive MS for the past 2 years. She had previously received intramuscular interferon β-1a, steroids, and rehabilitation therapy, but not compounded 4-AP. She was only receiving rehabilitation therapy once weekly at the time of the baseline visit. Patient #2 reported several MS-related symptoms (fatigue; imbalance; heat intolerance; and loss of sensation, weakness, muscle tightness, and spasticity in her lower limbs) and that her walking speed and distance had deteriorated over the past 2 years. She sometimes tripped and felt her walking was powerless and exhausting, which aggravated her existing fatigue. Her walking impairment made activities of daily living more difficult and exhausting to perform. Clinical examination at baseline revealed an EDSS score of 4.0; walking impairments that impacted distance, endurance, and balance; spastic paresis in her left leg, and slightly diminished left leg strength (LEMMT grade 4 out of 5); and a T25FW time of 7.1 seconds (walking speed, 1.07 m/second: see ).\nAfter 4 weeks of treatment with PR-fampridine, the patient reported that some days she noticed improvement in her walking speed and balance and experienced less exhaustion, but there were other days where she did not notice these improvements. She reported no change in fatigue. She wanted to continue treatment despite the lack of a consistent benefit. Clinical assessment at the 4-week follow-up visit found slight (7.5%) improvement in T25FW walking speed, a clinically meaningful 27-point improvement in MSWS-12 score ( and see ), and no changes in leg spasticity and strength. Based on physician assessment and patient report, this patient was considered to demonstrate modest clinical benefit with PR-fampridine treatment. It was agreed that the patient should continue treatment with PR-fampridine and be re-evaluated at the next visit.\nAt the 3-month visit, the patient showed a 15% improvement in T25FW walking speed versus baseline and sustained improvements in MSWS-12 score (). Furthermore, the patient reported that her walking endurance and balance had more clearly improved, her walking was smoother, and overall she felt more confident and powerful in her walking. She could now walk for 30 minutes without interruption, resting, or stopping. She reported that her fatigue had improved and she could participate more actively in daily tasks and leisure activities, which made her happy. Physician assessment showed no change in lower limb spasticity and strength from baseline, further improvement in T25FW walking speed versus baseline, and sustained improvement in MSWS-12 score (). Additionally, improvements in FSS score at 3 months compared with baseline reflected the patient’s verbal report of improvements in fatigue. The patient reported that mild dizziness, which she had initially reported at the 4-week visit, had resolved; however, she still experienced exacerbation of constipation that was an issue before starting PR-fampridine.\nAt the 6-month visit the patient reported that previous improvements in walking were sustained over the last 3 months of treatment and overall her walking was better with improved balance and self-confidence. Clinical assessments confirmed the patient report, which showed additional improvement in walking speed after 6 months of treatment (20.6% versus baseline), maintenance of benefits on patient-perceived walking ability, and fatigue (), and smoother walking as assessed by the treating physician versus baseline (see ). The patient also reported that her constipation was better and she was no longer experiencing dizziness. | [[49.0, 'year']] | F | {'20976768': 1, '27472992': 1, '31098882': 1, '26041616': 1, '19916707': 1, '22989365': 1, '21475081': 1, '20082242': 1, '6685237': 1, '10467383': 1, '28127507': 1, '30090638': 1, '2803071': 1, '27965804': 1, '21635193': 1, '20534650': 1, '21694807': 1, '23184313': 1, '29977342': 1, '12525714': 1, '23067032': 1, '31037211': 1, '11078767': 1, '21436388': 1, '25475652': 1, '18505775': 1, '22740603': 1, '19249634': 1, '31157008': 1, '18179687': 1, '24187513': 2} | {'3810492-2': 2} |
163,891 | 3810492-2 | 24,187,513 | noncomm/PMC003xxxxxx/PMC3810492.xml | Assessing the long-term clinical benefit of prolonged-release fampridine tablets in a real-world setting: a review of 67 cases | Patient #3 was a 39-year-old white woman with a 26-year history of MS and secondary-progressive MS for the past 9 years. She had previously received intramuscular interferon β-1a, intravenous immunoglobulin, baclofen for spasticity, steroids, and rehabilitation therapy, but had not been treated with compounded 4-AP. Patient #3 reported fatigue; heat intolerance; cerebellar symptoms; vertigo; imbalance; loss of vision associated with nystagmus; and pain, parathesias, loss of sensation, weakness, spasticity, and muscle tightness in her legs. The patient had sensory impairment, imbalance, limitations in leg muscle strength, and bilateral visual impairment that together contributed to a severe walking impairment and made it difficult for her to walk a great distance. She reported that she could walk a maximum of 20 m using two walking crutches. The patient was currently receiving rehabilitation therapy but not disease-modifying therapy for MS or drugs for spasticity. Clinical assessment revealed that she had severe walking impairment due to spastic paraparesis and ataxia (see ), an EDSS score of 6.5, severe spasticity in both legs, proximal and distal paraparesis (LEMMT grades 4 out of 5 and 2 out of 5, respectively), and a T25FW time of 29.4 seconds (walking speed, 0.26 m/second).\nAfter 4 weeks of treatment with PR-fampridine, patient #3 reported experiencing dizziness, confusion, and difficulties with short-term memory tasks after initiating PR-fampridine. She had a slower walking speed on the T25FW (decrease of 46.2%), no change on the MSWS-12, and worse fatigue and overall health status ( and see ). She continued to have severe spasticity in both legs, and her paraparesis remained unchanged proximally but worsened distally (LEMMT grade 1 out of 5). Interestingly, this patient did report an improvement in her vision and physician assessment at the 4-week visit found no detectable nystagmus. Based on physician assessment and patient report, this patient was considered to have no clinical benefit with PR-fampridine treatment and she reported potentially treatment-related side effects. Treatment with PR-fampridine was stopped and the patient was no longer followed-up on. | [[39.0, 'year']] | F | {'20976768': 1, '27472992': 1, '31098882': 1, '26041616': 1, '19916707': 1, '22989365': 1, '21475081': 1, '20082242': 1, '6685237': 1, '10467383': 1, '28127507': 1, '30090638': 1, '2803071': 1, '27965804': 1, '21635193': 1, '20534650': 1, '21694807': 1, '23184313': 1, '29977342': 1, '12525714': 1, '23067032': 1, '31037211': 1, '11078767': 1, '21436388': 1, '25475652': 1, '18505775': 1, '22740603': 1, '19249634': 1, '31157008': 1, '18179687': 1, '24187513': 2} | {'3810492-1': 2} |
163,892 | 3810550-1 | 24,179,690 | noncomm/PMC003xxxxxx/PMC3810550.xml | A Case of Sulfasalazine-Induced Hypersensitivity Syndrome Confirmed by Enzyme-Linked Immunospot Assay | A 24-year-old Thai male presented with high fever and abdominal pain for 4 days. The patient first noticed his fever accompanied with fatigue and a bitemporal throbbing pain without organ-specific symptoms, 2 weeks prior to admission when attending an outpatient clinic. Viral infection was the presumptive diagnosis. His low-grade fever remained for several weeks until 4 days prior to admission, when high fever and a progressive maculopapular rash developed. He also experienced epigastric pain, which brought him to our hospital again seeking medical attention.\nThe patient was diagnosed with bilateral chronic uveitis 2 years ago, when topical steroids had been prescribed. Low-dose oral prednisolone (15 mg/day) was subsequently added before tapering off within 11 months. Two months later, a diagnosis of spondyloarthropathy was suspected by the rheumatologist, when Achilles tenosynovitis, plantar fasciitis, and tenderness over the sacroiliac joints developed. Sulfasalazine was then prescribed starting at 1 g/day, gradually increasing to 2 g/day for 2 weeks prior to the development of fever.\nPhysical examination revealed high fever (38.5℃), cervical lymphadenopathy, pharyngitis with whitish patches on soft palate and buccal mucosa. The patient had a scattered maculopapular rash over his trunk and extremities and abdominal examination revealed mild epigastrium tenderness. A complete blood count revealed marked leukocytosis with a total white blood cell count of 23,740/µL, 50% neutrophils, 16% lymphocytes, 31% monocytes, and 3% eosinophils. Atypical lymphocytes were detected in peripheral blood smears. Blood culture and anti-viral antibody profiles were investigated; sulfasalazine was promptly discontinued.\nOn the third day of admission, the patient developed severe abdominal pain and mild icteric sclera was noted. Liver function tests showed direct hyperbilirubinemia with total bilirubin 3.34 mg/dL and direct bilirubin 2.94 mg/dL. ASL and ALT levels were 536 and 734 U/mL, respectively, and serum alkaline phosphatase was 301 IU/mL. Upper abdominal ultrasonography revealed gallbladder wall thickening with pericholecystic fluid collection and positive sonographic Murphy's sign. Intravenous ceftriaxone was then administered. On the ninth day of admission, he developed hypotension (blood pressure of 70/40 mmHg) before being rescued with 1,500-mL intravenous fluid. Abdominal computed tomography scans showed a collapsed gallbladder with a moderate amount of pericholecystic fluid, but no gallstones could be demonstrated (); hepatosplenomegaly and minimal ascites were also noticed. Dexamethasone (5 mg) was administered every 12 h intravenously for six doses, resulting in cessation of the fever and abdominal pain, after the third dose.\nThe viral studies yielded negative results for IgM and IgG against Epstein-Barr virus, cytomegalovirus, and Dengue virus. Blood culture results showed no bacterial growth. Anti-HIV and anti-human herpes virus 6 (HHV-6) IgM antibodies were also negative, but anti-HHV-6 IgG was positive (17.05 units with a cut-off value of 11 units). Two days after the initiation of steroids, the numbers of IFN-γ-releasing cells in the peripheral blood were measured by ELISPOT assay (Mabtech, Stockholm, Sweden) upon stimulation with four drugs as described previously. Significant numbers of IFN-γ-secreting cells were demonstrated (1,048 spots forming cells/106 PBMCs) upon incubation with 100 µg/mL sulfasalazine, but not with other drugs administered concurrently (ceftriaxone), previously (amoxicillin), or never (ceftazidime) (). Dexamethasone was then replaced with prednisolone 1 mg/kg/day before being tapered off over 3 weeks. His liver function tests returned to normal levels in 1 month; no complications were noted after 2 years of follow-up. His symptoms are now well controlled with NSAIDs and methotrexate. | [[24.0, 'year']] | M | {'10612272': 1, '27753687': 1, '22722755': 1, '17300272': 1, '28961208': 1, '33039012': 1, '12636244': 1, '26006718': 1, '17075280': 1, '21592453': 1, '19563993': 1, '17381452': 1, '29700201': 1, '11255328': 1, '16461148': 1, '15230812': 1, '19154548': 1, '24179690': 2} | {} |
163,893 | 3810557-1 | 24,175,270 | noncomm/PMC003xxxxxx/PMC3810557.xml | Florida Sleeve Repair for Aortic Root Aneurysm | A 74-year-old man was referred to our hospital for surgical management of aortic root aneurysm found by echocardiography during a preoperative work-up for spinal surgery. He presented with intermittent left-sided chest pain. His vital signs and laboratory data were unremarkable on admission. His past medical history revealed hypertension requiring drug therapy and herniated nucleus pulposus at the lumbar area. Trans-thoracic echocardiography revealed an enlarged sinus of Valsalva 58 mm in diameter with mild aortic regurgitation (). The left ventricular ejection fraction was 60% without regional wall motion abnormality. A computed tomography (CT) scan identified severe aortic sinus dilatation and a coaptation defect in the aortic valve (). The maximal diameter of the aortic sinus and aortic tubular portion were 60 and 36 mm, respectively. A coronary angiography showed 80% stenosis of the proximal left anterior descending artery (LAD), and total occlusion of the distal left circumflex artery. Thallium single-photon emission computed tomography showed fixed medium-sized moderately decreased perfusion in the basal anterolateral and basal inferolateral wall. Consequently, the patient was scheduled for concomitant aortic root surgery and coronary artery bypass grafting (CABG).\nAt the beginning, the patient underwent off-pump CABG (from the in situ left internal mammary artery to the LAD and the saphenous venous graft to the obtuse marginal branch). After establishing cardiopulmonary bypass (CPB) and aortic clamping (cardioplegic solution was delivered via the coronary sinus in a retrograde manner and concomitant antegrade infusion via saphenous vein graft to the obtuse marginal graft), the ascending aorta was transected above the sinotubular junction and the aortic root was mobilized to the aortic annular level, and the origins of the coronary arteries were mobilized. After measuring the aortic annular size, a 30-mm vascular graft (Gelweave Valsalva; Terumo Inc., Tokyo, Japan) was trimmed with two key holes (). Then, six anchoring sutures were made on the lowest level of the annulus, at the commissure and midpoint of each leaflet. After locating the graft to the patient's aortic root, a running suture was done together with the transected sinotubular junction and the graft. After confirming adequate coaptation of the aortic leaflets, distal anastomosis between the graft and distal ascending aorta was made. After CPB weaning, sternal closure was done. Aortic clamping and cardiopulmonary bypass times were 88 and 128 minutes, respectively.\nThe patient was extubated on postoperative day 1 and transferred to the general ward on day 2. CT and echocardiographic evaluations were performed on postoperative day 4, and they demonstrated a competent aortic valve with no regurgitation, and a stable aortic graft without any distortion or leakage. The diameter of the sinus portion of the aorta was measured at 37 mm with excellent coaptation of the aortic valve (). The patient was discharged on postoperative day 8 without any postoperative complications. Serial follow-up echocardiographic assessments were performed up to one year after surgery. There was no aortic insufficiency and the stability of the sinus portion of the aorta was maintained with its diameter at 38 mm. | [[74.0, 'year']] | M | {'1532219': 1, '16039256': 1, '19324144': 1, '22880164': 1, '24175270': 2} | {} |
163,894 | 3810559-1 | 24,175,272 | noncomm/PMC003xxxxxx/PMC3810559.xml | Left Atrial Myxoma Presenting with Unusual Cystic Form | A 65-year-old woman was referred to our department because of a recently diagnosed left atrial (LA) mass. She presented with a five-month history of fever, malaise, and myalgia and had been diagnosed with ventricular septal defect (VSD) two years earlier. On physical examination, a grade of 4/6 systolic murmur was heard at the left sternal border. Electrocardiography and a chest X-ray were unremarkable. Two-dimensional transthoracic echocardiography showed an LA cyst (24×23 mm) that was attached to the interatrial septum and detected the trace of blood flow at the margin of the cyst (). The VSD was a small perimembranous type and the pulmonary blood flow to systemic blood flow ratio (Qp/Qs) was 1.2.\nThe patient underwent surgical treatment. The cystic mass attached to the left side of the interatrial septum was white-pink-yellowish and oval in shape. It had a small opening on the surface and was 2.2×1.6 cm (). The cystic mass was widely excised with the atrial septum, leaving the defect in the atrial septum, and the small VSD was closed with two pledgeted sutures without a patch. The defect on the atrial septum was closed with an artificial patch (polytetraflouroethylene, Gore-Tex patch; WL Gore & Assoc, Flagstaff, AZ, USA). The mass was a single cyst and didn't have any content. The diagnosis of myxoma was confirmed by microscopic examination. Histologically, the mass consisted of myxoid cells in abundant loose and myxoid stroma, and the tumor cells were round or polygonal with eosinophilic cytoplasm (). Postoperative echocardiography revealed no VSD shunt and no mass in the left atrium. The patient was discharged 16 days after surgery without any problem. | [[65.0, 'year']] | F | {'11156679': 1, '17126161': 1, '10363879': 1, '28090362': 2, '18706121': 2, '29974293': 1, '19187653': 1, '16868856': 1, '24175272': 2} | {'5206423-1': 1, '2531170-1': 1} |
163,895 | 3810560-1 | 24,175,273 | noncomm/PMC003xxxxxx/PMC3810560.xml | Two-Stage Endovascular Repair for Concurrent Penetrating Atherosclerotic Ulcers of the Thoracic and Abdominal Aorta | A 66-year-old man was transferred to our hospital for the treatment of two asymptomatic saccular aneurysms caused by a penetrating atherosclerotic ulcer in the descending thoracic aorta and the infrarenal abdominal aorta. All of the laboratory data were within normal range except serum creatinine. The level of serum creatinine was slightly high at 1.5 mg/dL. A computerized tomography (CT) scan demonstrated that a saccular aneurysm measuring 60 mm in the longest diameter in the descending thoracic aorta was at the level of the 9th thoracic vertebra, and the other saccular aneurysm measuring 55 mm in the longest diameter in the infrarenal abdominal aorta was at the level of the 3rd lumbar vertebra (). We decided to perform staged endovascular repair on this patient in order to prevent contrast-induced nephropathy by reducing the total amount of contrast material administered, and to prevent paraplegia that could occur if the long segment of the aorta were covered with a stent graft in one session. In addition, we tried to avoid the risk of rupture while waiting for the second endovascular procedure by decreasing the interval time between the staged procedures.\nDuring the first stage, a 34×100 mm stent-graft, a self-expandable custom-made type (S&G Biotech Inc., Seongnam, Korea), was deployed along the thoracic saccular aneurysm and spinal fluid drainage was performed to prevent paraplegia. Additional 36×80 mm stent-graft was used because of a wind-sock effect (). During this procedure, 200 mL of nonionic and iso-osmolar contrast medium iodixanol (Visipaque; Nycomed Imaging AS, Oslo, Norway) was used. In the second stage, one month later, Zenith stent-grafts (Cook Inc., Minneapolis, MN, USA) were placed from the saccular abdominal aneurysm to both common iliac arteries, thereby excluding the aneurysm from circulation. During this second stage, 240 mL of iodixanol (Visipaque, Nycomed Imaging AS) was used. Perioperative cerebrospinal fluid drainage was performed to prevent spinal cord ischemia (SCI). The patient presented no perioperative deterioration of renal function or paraplegia. A ten-month follow-up CT angiogram showed both stent-grafts were patent with no evidence of thrombus, endoleak, aneurysm growth, or complications derived from the procedure (). Two-stage endovascular repair may therefore be used to successfully treat separate saccular thoracic and abdominal aortic aneurysms without any deterioration of renal function or paraplegia. | [[66.0, 'year']] | M | {'16763513': 1, '10931815': 1, '12151944': 1, '16012446': 1, '18723308': 1, '17353130': 1, '15760265': 1, '15996476': 1, '2729314': 1, '17327549': 1, '2296101': 1, '16392608': 1, '16242540': 1, '24175273': 2} | {} |
163,896 | 3810561-1 | 24,175,274 | noncomm/PMC003xxxxxx/PMC3810561.xml | A Giant Popliteal Artery Aneurysm Treated with Exclusion and Bypass Using a Saphenous Vein | A 67-year-old male, having a history of diabetes mellitus and classified as a heavy smoker (50 pack-years), presented with left thigh pain that had been aggravated in sitting or squatting positions for the previous four months. The patient felt tenderness on the mass-like lesion on the left thigh, which was large and pulsatile. A computerized tomography angiography image revealed a giant aneurysm of the left popliteal artery and mild atherosclerotic aneurysmal change of the right popliteal artery (). There were mild atherosclerotic calcifications in the lower abdominal aorta and iliofemoral arteries without significant aneurysmal changes.\nSurgery was performed separately from upper and lower medial approaches to allow for a direct view of the aneurysm under spinal anesthesia. The patient was placed supine with the knee flexed over a sandbag. The line of the incision ran from four fingerbreadths above the adductor, opening downwards and backwards to a little behind the medial femoral condyle and avoiding the greater saphenous vein. The deep fascia was incised, and the anterior border of the sartorius muscle was identified. The muscle was displaced backwards to reveal the thicker aponeurosis of the adductor canal running into the tendon of the adductor opening. A lower medial approach was made along the posterior tibial border from the lower aspect of the medial condyle, avoiding the greater saphenous vein. The deep fascia was incised and the medial head of the gastrocnemius muscle was displaced backwards. The loose popliteal fat was dissected free from the vascular bundle to reveal the vein with the popliteal artery. Since the aneurysm was too large and long (6×6 cm) to dissect between the adductor opening and the sartorius muscle, we could not clamp the distal and proximal end of the aneurysm (). We performed a bypass from the common femoral artery (end-to-side) to the distal popliteal artery (end-to-side) below the knee, using the autologous greater saphenous vein (). An exclusion of the aneurysm by double ligation back and forth using black silks was performed at the sites of anastomoses (the proximal superficial femoral artery and the distal popliteal artery) following the identification of the distal pulse.\nWhile the patient obtained good pulsation of the posterior tibial artery and the dorsalis pedis artery postoperatively, the popliteal artery aneurysm lost pulsatile movement immediately. The patient could walk five days after the operation because of severe postoperative wound pain. However, an immediate follow-up angiography showed a patent vein graft and a completely thrombosed aneurysm (). The patient was discharged 19 days after the operation, and was able to walk without ambulatory equipment at that time. In addition, scanty delayed bleeding from the dissected medial gastrocnemius muscle occurred two months after the operation, and we performed a hematoma evacuation and a primary closure. At three months' follow-up, the patient was ambulating without leg pain or claudication. The previously palpable aneurysm had reduced in size and the tenderness on the aneurysm had disappeared. | [[67.0, 'year']] | M | {'22516241': 1, '26900314': 1, '21885475': 1, '20036499': 1, '22263174': 2, '17398379': 1, '22321483': 1, '18774688': 1, '24175274': 2} | {'3249325-1': 1} |
163,897 | 3810562-1 | 24,175,275 | noncomm/PMC003xxxxxx/PMC3810562.xml | Surgical Treatment for an Invasive Leiomyosarcoma of the Inferior Vena Cava | A 49-year-old woman was admitted with right lumbar pain and edema of both legs. At admission, she was not very ill looking and had experienced no weight loss. Abdominal computed tomography (CT) showed a large low attenuated mass around and in the S7 segment of the liver: the mass measured 9×12 cm, and it involved the right kidney (). In addition, there were multiple enlarged mesenteric lymph nodes and multiple variably sized discrete nodules in both lungs (). Cavography showed subtotal occlusion of the inferior vena cava (). During cavography, intracaval biopsy was performed and spindle cell sarcoma was found.\nAn operation was performed via midline laparotomy with subcostal extension. Before beginning to resect the tumor, we checked the lymph nodes and the rectal shelf and omental seedings. All were negative on frozen biopsy. During dissection around the tumor, partial bypass (femoro-femoral) was inevitable due to massive bleeding of collateral vessels. Through the right femoral artery and vein, arterial and venous cannulation was done. The pump flow was 3 L/min and the total bypass time was 30 minutes. During en bloc resection of the mass from the hepatic vein to the iliac bifurcation, partial duodenal excision, partial liver resection, and right nephrectomy were performed due to tumor invasion.\nThe left renal vein was clamped for one hour because we had confirmed good drainage of the gonal vein. After resection, the IVC was replaced with a 12-mm vascular graft, and the left renal vein was re-implanted in the vascular graft. The gross findings are shown in . Histological analysis revealed a moderate grade malignant spindle cell tumor that arose in the IVC with intraluminal spread into the vena cava and the right renal vein. No lymph node involvement was found. The tumor border had infiltrated to the renal parenchyma, the adrenal gland, and the IVC, but the resection margins were clear. The patient's postoperative recovery was uneventful except for minor gastrointestinal troubles and the patient was discharged at the 24th day. The patient remained asymptomatic for 8 months when she was readmitted for radiation therapy and pulmonary metastasectomy. At this time, the vascular graft in the IVC was occluded on the CT angiography, but she did not complain of any symptoms such as leg edema or abdominal discomfort. Periodic follow-up is being conducted at the department of oncology. | [[49.0, 'year']] | F | {'26943403': 2, '27920691': 2, '8920790': 1, '14522326': 1, '31558957': 1, '16858193': 1, '20178598': 2, '9236931': 1, '9632161': 1, '20610268': 1, '10664496': 1, '3807376': 1, '16393338': 1, '1942380': 1, '9685133': 1, '24175275': 2} | {'5118828-1': 1, '4747934-1': 1, '2838855-1': 1} |
163,898 | 3810563-1 | 24,175,276 | noncomm/PMC003xxxxxx/PMC3810563.xml | Giant Cell Tumor Arising from Anterior Arc of the Rib | A 27-year-old man presented with a 9-month history of chest wall pain and a palpable growing mass in the anterior end of the left sixth rib. The mass was hard and fixed to the chest wall. There was mild tenderness. The overlying skin was normal. He had a history of contusion at the left anterior chest wall 9 months earlier. There were no specific pulmonary symptoms.\nA chest X-ray demonstrated an expansile bony mass in the distal end of the left 6th rib. Computed tomography revealed a large irregular contoured and heterogeneously enhancing soft tissue mass in the anterior arc of the left 6th rib. The tumor contained peripheral calcification and bony destruction (). No abnormality was found on laboratory examinations.\nA surgical resection was performed. The tumor was completely resected, including surrounding soft tissue. The tumor was adhered to the parietal pleura. There was no visceral pleural invasion. The distance of the margin from the tumor was 3 cm (medial) and 6 cm (lateral). The medial margin of the resected rib was the lateral border of the sternum. A frozen biopsy of the tumor was performed in the operating room, and the tumor was confirmed to be a giant cell tumor (GCT). Partial resection of the ribs above (5th) and below (7th) the GCT including the intercostal muscle and soft tissue was performed. The lengths of the resected ribs were 10.5 cm, 13.5 cm, and 13 cm (). The chest wall defect was covered with a 2-mmthick Gore-Tex Soft Tissue Patch (W. L. Gore & Associates Inc., Flagstaff, AZ, USA).\nThe tumor was 6×4.5×4.5 cm in size. There were focal hemorrhage and a yellowish mass-like lesion in gross findings. The tumor was composed of round, oval, or spindle-shaped stromal mononuclear cells and uniformly interspersed multinucleated giant cells (). The pathological diagnosis was a primary GCT of the left sixth rib.\nNo adjuvant treatment was performed. The patient has been receiving follow-up care for 3 months since the surgery with out evidence of recurrence. | [[27.0, 'year']] | M | {'28559944': 1, '19319545': 1, '29556745': 1, '23322837': 1, '20058142': 1, '3872579': 1, '34401267': 1, '12483015': 1, '22781387': 1, '24175276': 2} | {} |
163,899 | 3810584-1 | 24,174,955 | noncomm/PMC003xxxxxx/PMC3810584.xml | Severe gastrointestinal burn with hydrochloric acid | Herewith, we report the case of a 49-year-old male patient who had attempted suicide by drinking about 800 mL of 25% hydrochloric acid, and was in the Ankara Güven Hospital, Ankara, Turkey, in 2009. The patient was admitted to the Emergency Department within 30 minutes of ingestion of the corrosive liquid, with severe abdominal pain, agitation, and respiratory discomfort. Due to subsequent psychological problems, he had attempted to commit suicide. The patient, with a history of no previous systemic disorder, was evaluated by Gastroenterology, General Surgery, and Emergency Department practitioners, as also the İntensive Care Unit (ICU) team. On admission to the ICU, his consciousness was delirious in nature and he was confused. His blood pressure was 130/90 mmHg, heart rate 115/minute, oxygen saturation (SpO2) 90%, and respiratory rate 25 per minute. In the physical examination of the respiratory system, wheezing and prolonged expirium existed, together with fine rales. There were increased abdominal irritability and peritoneal irritation signs, but no pathological findings in the thoracoabdominal tomographic examination. There were ulcerative lesions, and bloody and dirty material in his mouth. His initial leucocyte count was 20.600 cell/uL, creatinine 1,68 mg/dL, aspartate aminotransferase 455 U/L, alanine aminotransferase 175 U/L, lactate dehydrogenase 701 U/L, gamaglutamyl transferase 110 U/L, sodium 152.1 mEq/L, potassium 3.21 mEq/L, pH 7.29, pO2 71 mmHg, pCO2 43 mHg, HCO3- 17.4 mmol/L, and SpO2 89%. Intravenous hydration, meperidine, antibiotics, nonsteroidal anti-inflamatory agents, methylprednisolone, and proton pump inhibitors were given for his symptoms. After admission to the Emergency Department, the patient was moved to the ICU and sedated with opioids and benzodiazepines, because of his agitative state. With nasal oxygen delivery his SpO2 was 98%. Nine hours after ingestion, due to gradually increasing metabolic ascidosis and respiratory deterioration, the patient was intubated and connected to the mechanical ventilator. Arterial, central venous, and urinary catheterization were performed. His Acute Physiology and Chronic Health Evaluation II (APACHE II) score was 27 and estimated mortality rate was 61%. At the forty-eighth hour, because of extensive abdominal pain and serious respiratory discomfort, the thoracoabdominal computerized tomography (CT) was repeated []. An urgent surgical intervention was made because free abdominal fluid was detected on CT. During the operation, six liters of intra-abdominal fluid with infected material was aspirated. Total gastrectomy, duodenal resection, partial jejunectomy, and partial pancreatectomy were performed. Due to splenic hemorrhage, splenectomy was also applied [Figures - show pictures of the resected material]. Histopathological analysis of the surgical material revealed stage IIIb necrosis, which was also called ‘black necrosis’. Hemogram and electrolyte levels were closely followed up during the perioperative period. The blood components were given and fluid replacements were administered when needed.\nThe patient was extubated eight days after the operation, without deterioration of oxygenation. However, he had abdominal infections and / or serious metabolic problems in common, such as, lactic ascidosis or low serum sodium bicarbonate levels, due to abdominal low perfusion andrenal insufficiency. After surgery, antibiotherapy, parenteral nutrition, and palliative care were applied to the patient for 140 days, 105 of which passed in the ICU. Nine complemantary or intra-abdominal debridement and clean-up surgeries were performed during this period. Oral nutrition was started on the one hundred and twenty-fifth day of hospitalization. Parenteral nutrition was gradually stopped and he was discharged with recommendations for Psychiatry, Gastroenterology, General Surgery, and Physical Therapy Departments on the one hundred and fortieth day. After six months, he came for a follow-up without any further complication. | [[49.0, 'year']] | M | {'33327320': 2, '19543088': 1, '15735282': 1, '15362762': 1, '8283919': 1, '12869880': 1, '8086095': 1, '21991535': 1, '21858575': 1, '21554849': 1, '16891276': 1, '11191021': 1, '16937538': 1, '19111425': 1, '24174955': 2} | {'7738082-1': 1} |
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