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162,600 |
3738344-1
| 23,986,835 |
noncomm/PMC003xxxxxx/PMC3738344.xml
|
FDG-PET/CT finding of benign metastasizing leiomyoma of the lung
|
A 50-year-old woman with a history of hysterectomy for uterine leiomyoma 12 years ago was examined for multiple small lung nodules, including the largest one (30 × 25 mm in size) which were incidentally discovered on chest radiographs at a private hospital (Fig. ). Unenhanced CT images showed multiple peripheral parenchymal nodules of variable sizes with smooth margins (Fig. ).\nFDG-PET was performed using a PET/CT system (GE Discovery STE, GE Healthcare, Milwaukee, WI, USA) to identify primary malignancy and metastatic lesions. A whole-body imaging from the head to the thigh and chest imaging were performed 1 hour (early) and 2 hours (delayed), respectively, after intravenous injection of FDG (3.7 MBq/kg body weight). At PET/CT, her blood glucose level was 93 mg/dl. Faint FDG uptake was noted in the largest nodule (Fig. a and b), and its early and delayed maximum standardized uptake values (SUVmaxs) were 1.3 and 1.2, respectively. In this connection, early and delayed SUVmaxs were 0.5 and 0.5 in the lung field, 1.5 and 1.4 in the thoracic muscle, and 2.4 and 1.6 in the mediastinum at the Fig. a tomographic level, respectively. The remaining smaller nodules ≤ 8 × 8 mm in diameter showed no visible uptake (early SUVmax 0.5–0.8; delayed SUVmax 0.4–0.6) (Fig. c and d). There was no other pathologic FDG uptake to suspect primary malignancy and metastatic lesions in the whole body.\nCT-guided needle lung biopsy was performed for the largest nodule to obtain a pathological diagnosis of the lung nodules. Microscopic examinations showed an interlacing pattern by spindle cells having elongated nuclei without cellular atypia (Fig. a). The Ki67 proliferative index was less than 1%. Tumor cells were positive for alpha-smooth muscle actin (Fig. b) and both estrogen and progesterone receptors and negative for CD31, CD34, AE1/AE3, EMA, HMB45, and S-100 protein on immunohistochemical stains. The pathological findings of the tumor confirmed the diagnosis of benign metastasizing leiomyoma. The patient selected careful observation as a management and the chest radiographs showed no change to date, 1 year after the biopsy.
|
[[50.0, 'year']]
|
F
|
{'28426767': 1, '11948260': 1, '21498277': 1, '27790528': 1, '19001649': 1, '29951323': 2, '8929320': 1, '18848459': 1, '16549957': 1, '17017672': 2, '20435308': 1, '19161793': 1, '19242303': 1, '21070909': 1, '19333516': 1, '28927125': 1, '19559496': 1, '23986835': 2}
|
{'3890726-1': 1, '5987332-1': 1}
|
162,601 |
3738345-1
| 23,986,836 |
noncomm/PMC003xxxxxx/PMC3738345.xml
|
A case of lymphatic malformation/lymphangioma of the scrotum
|
A 12-year-old boy presented to our hospital with a swollen right scrotum without tenderness. He had a surgical history of bilateral inguinal hernia, uncal hernia, and scrotal hydrocele at 2 years old. Ultrasonographic examination revealed a well-defined multicystic mass in the right scrotum. Color Doppler examination showed no blood flow in the septum of the cysts (Fig. ). Bilateral testes were normal. Magnetic resonance imaging revealed a multicystic mass (6.5 × 6.5 × 9.0 cm) with multiple thin septae and locules located in the right scrotal sac. The mass showed high intensity on T2-weighted imaging and low intensity on T1-weighted imaging. On diffusion-weighted imaging, the mass showed no restriction of diffusion. The mass had displaced the right testis to the left. No evidence of any extrascrotal extension into the abdomen was noted (Fig. ). The radiological diagnosis was multiple scrotal hyadrocele or lymphatic malformation/lymphangioma. Since right scrotal swelling was progressing, surgery was performed.\nSurgical findings showed that the mass existing in the right scrotum had probably originated from the internal spermatic fascia. Microscopic examination revealed membranous tissue with some hemorrhage. Tissue thought to represent a thin wall of the cystic mass was identified as fibrous tissue with hemorrhage. Infiltration of lymphocytes around the small vessels was detected. Pathological findings were consistent with lymphatic malformation/lymphangioma.
|
[[12.0, 'year']]
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M
|
{'11742043': 1, '7063565': 1, '2911671': 1, '21060188': 1, '12750933': 1, '20548330': 1, '21470038': 1, '12888864': 1, '23986836': 2}
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{}
|
162,602 |
3738346-1
| 23,986,837 |
noncomm/PMC003xxxxxx/PMC3738346.xml
|
Hydrocele of the canal of Nuck: imaging findings
|
A 5-year-old girl presented with a palpable mass in the right inguinal region with occasional pain. Physical examination revealed smooth swelling in the right inguinal region which was tense but not tender. No thrill or bruit was seen over the swelling. Ultrasound examination of the right inguinal region was done using 7–12 MHz linear array transducer. There was well-defined sausage-shaped hypoechoic lesion with small internal septations (Fig. ) and the tail of the lesion was directed cranially and posteriorly. On color Doppler or power Doppler imaging no internal or peripheral vascularity was seen. On Valsalva maneuver the lesion did not change size or position.\nMRI was performed using 1.5-T system (Magnetom Avanto, Siemens, Erlangen, Germany) with a body coil. Axial and coronal T1 spin echo and T2 fast spin echo images of the inguinal region were obtained. Axial and coronal T2-weighted MR images showed a well-defined fluid intensity lesion in the right inguinal region with thin internal septa (Fig. ). The lesion did not communicate with the peritoneal cavity. The signal intensity of the lesion was similar to the urinary bladder. The imaging features were consistent with hydrocele of canal of Nuck. The lesion was removed surgically and histopathology revealed the diagnosis of hydrocele of canal of Nuck.
|
[[5.0, 'year']]
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F
|
{'17453186': 1, '32801942': 2, '11598262': 1, '31885966': 1, '7724148': 1, '27689059': 1, '20806583': 1, '1168323': 1, '7486426': 1, '26989112': 1, '27042529': 1, '31918159': 1, '15020367': 1, '17279318': 1, '28444423': 1, '24761084': 2, '23986837': 2}
|
{'7410395-1': 1, '3996740-1': 1}
|
162,603 |
3738347-1
| 23,986,838 |
noncomm/PMC003xxxxxx/PMC3738347.xml
|
Chronic post-traumatic high-flow priapism treated with temporary gelatin sponge embolization
|
A 26-year-old man presented with a non-painful priapism in the urology ambulatory care unit. The patient reported having a permanent full erection for more than 3 months following a perineal trauma by falling from a ladder and hitting his pelvic floor on the window board. The physical examination 3 months after the trauma revealed stiff corpora cavernosa and a well-perfused corpus spongiosum. There was no visible or palpable perineal trauma. He had no history of sickle cell disease and denied any use of cocaine. The ability to perform sexual intercourse was not impaired. A penile color Doppler sonography was performed and demonstrated an arteriocorporal fistula with turbulent flow between the right cavernosal artery and the corpus cavernosum, conclusive for a high-flow priapism.\nThe patient was admitted to our hospital and a selective angiography was performed. The internal pudendal artery was catheterized bilaterally with a 4 F RIM Tempo4 open-ended catheter (Cordis, Miami, FL, USA) by a right transfemoral approach and a selective angiography was performed. The diagnostic angiography revealed the presence of a bilateral contrast leak from the cavernosal artery to the corpus cavernosum which was most prominent via the right cavernosal artery (Figs. and ). Thereafter a microcatheter (2.7 F; Microferrit; Cook, Bloomington, IN, USA) was placed into the cavernosal artery with its catheter tip positioned right into the leak to the corpus cavernosum (Fig. ). The fistula was then embolized with gelatin sponge. The gelatin sponge was prior to the procedure fragmented into small pieces with a scalpel and eluted in contrast media resulting in a viscous thick fluid. Approximately 2 mL of the gelatin contrast media elution was injected via the microcatheter until stasis of the leakage was obtained. A superselective embolization via the right cavernosal artery was performed. The ACF disappeared completely (Fig. ). The patient described a complete penile detumescence 48 h after the procedure.\nFollow-up consisted of a color Doppler sonography 6 weeks after embolization. No ACF was detectable. The cavernosal arteries and the corpora cavernosa were bilaterally intact and well perfused. The priapism resolved completely and the patient reported a normal erectile function (Fig. ).
|
[[26.0, 'year']]
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M
|
{'19728271': 1, '16481268': 1, '17430268': 1, '14501756': 1, '16328682': 1, '15229624': 1, '17911511': 1, '17453510': 1, '17644141': 1, '18619653': 1, '17983902': 1, '22033848': 1, '8755084': 1, '16151866': 1, '16422992': 1, '18173765': 1, '12324819': 1, '11781746': 1, '12425873': 1, '23986838': 2}
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{}
|
162,604 |
3738348-1
| 23,986,839 |
noncomm/PMC003xxxxxx/PMC3738348.xml
|
Uterine cervical melanoma presenting with rapid progression detected by PET/CT
|
The patient was a 66-year-old woman who had been menopausal for 13 years, complaining of recent vaginal bleeding. Gynecologic examination found a small cervical polyp. The polypoid tumor was excised, measuring 1.7 × 1.7 × 1.5 cm in size. Microscopic examination revealed sheets or solid nests of epithelioid tumor cells with pleomorphic nuclei and scattered mitotic figures. The tumor cells were diffusely positive in staining for vimentin and S-100 protein. Some of the cells were also positive for HMB-45 (Fig. ). A diagnosis of malignant melanoma was made. Initial staging with magnetic resonance imaging (MRI) showed a vaginal tumor and an enlarged lymph node in the right part of the pelvis (Fig. a). Whole-body PET/CT was then performed, and revealed metabolic active lesions in the areas corresponding to those seen on the MRI (Fig. b). The patient thus received radical hysterectomy, a total vaginectomy, and pelvic lymphadenectomy. The final diagnosis was malignant melanoma of the uterine cervix with metastases to pelvic lymph nodes and vagina. Two months after the operation, without any further treatment, PET/CT identified a recurrence of metabolic active lesions in one of the abdominal para-aortic lymph node (Fig. a). Debulking surgery to remove the lymph node was performed and the lesion was proven to be metastatic. The patient then received radiotherapy targeting the para-aortic region. Three months after completion of radiotherapy, a pelvic MRI examination was negative. However, whole-body PET/CT demonstrated unsuspected multiple metastases that extensively involved the brain, right breast, both lungs, and lymph nodes of the right side of the neck, supraclavicular region, and abdominal cavity (Fig. b). Histological analysis found the massive tumor in her right breast to be a metastatic melanoma. The patient refused further management except for palliative radiotherapy targeting the brain.
|
[[66.0, 'year']]
|
F
|
{'20386135': 1, '18502488': 1, '9576286': 1, '21515070': 1, '19132380': 1, '21654876': 1, '18362381': 1, '17349716': 1, '14745871': 1, '18980825': 1, '21941976': 1, '12640157': 1, '23986839': 2}
|
{}
|
162,605 |
3738349-1
| 23,986,840 |
noncomm/PMC003xxxxxx/PMC3738349.xml
|
Crouzon syndrome associated with acanthosis nigricans: prenatal 2D and 3D ultrasound findings and postnatal 3D CT findings
|
A healthy 31-year-old woman had infertility treatment with ovulation induction and intrauterine homolog insemination at a private fertility clinic. In early pregnancy she experienced acute abdominal pain. At laparoscopy a ruptured tubal pregnancy was found, indicating a heterotopic pregnancy, and a salpingectomy was performed.\nShe had a first trimester scan which produced a combined risk for Down syndrome of 1:507. She chose to have a chorionic villus sample (CVS) taken, which showed a normal karyotype. At 19 + 6 weeks she had a normal anomaly scan. At 27 + 3 weeks she was referred to the fetal medicine unit (FMU) for a growth scan. This ultrasound showed intrauterine growth restriction (estimated fetal weight 24.8% compared to the normative mean value) and a small head circumference (227.8 mm). The anomaly scan was repeated and found to be normal. Fetal biometry was performed every second week showing normal growth, although the head circumference remained below the 5th centile.\nAt 35 + 5 weeks the woman was referred for an expert scan at the FMU because of an abnormally-shaped cranium (Fig. ). 2D and 3D scans were performed showing brachycephaly, hypertelorism, ocular proptosis, and a beaked nose (Fig. ). No hand or foot anomalies were seen. These findings gave rise to the suspicion of Crouzon syndrome. The fetal DNA saved from the CVS was analyzed for mutations in the FGFR2 gene (Crouzon, Apert, and Pfeiffer syndrome) and reflex tested for Muenke syndrome in the FGFR3 gene. No mutations were found.\nAt 39 + 6 weeks a Cesarean section was performed on maternal request and a boy was delivered (weight, 3.156 g; length, 51 cm; Apgar, 10/1 and 10/5; and normal cord blood gas values). Craniofacial abnormalities were evident, but choanal atresia was not suspected. At 7 days of age he developed intermittent obstructed nasal airways with compromised breastfeeding. Acceptable weight gain was obtained after introduction of formula milk. The boy was referred to the Copenhagen Craniofacial Unit at Rigshospitalet, University of Copenhagen.\nAt clinical examination at 5 weeks of age, he had pronounced oxycephaly (Kleeblatt-Schädel) and ocular proptosis. In addition he had pronounced maxillary hypoplasia and severe breathing difficulties with clinical suspicion of apnea. No skin changes such as hyperkeratotic papules or pigmentations were noted. He gradually developed hydrocephalus and at age 9 weeks a 3D craniofacial CT scan was done. The CT scan was performed using a Toshiba Aquillion helical CT-scanner (Toshiba, Zoetermeer, The Netherlands) (slice thickness, 0.5 mm; pixel spacing, 0.39/0.39; KVp, 120; X-ray tube current, 60mA; exposure, 24 mAs).\nThe 3D CT scan (Figs. and ) revealed a brachycephalic skull shape (the cephalic index, which describes the relationship between the long and short axis of the cranium was 85, normal values are 75–83) with protrusion of the forehead and flattened occiput. The skull was wide and the temporal regions were bulging. Both coronal and lambdoid sutures were prematurely fused. A wide midline defect of the skull extended from the nasal root to the occiput. The skull was paper thin with extremely increased digital markings, especially in the posterior portion of the skull. Markedly increased digital markings on CT may suggest that intracranial pressure (ICP) is increased or that ICP has been increased at an earlier stage. The synchondroses of the cranial base were patent and the cranial base angle was flat (platybasia). The nasal root was depressed; the orbital roofs were short and the distance between the orbits was increased (hypertelorism); the maxilla was hypoplastic, especially in the sagittal and vertical dimensions. Choanal height was decreased and the nasopharyngeal airway was constricted. The mandible was unremarkable.\nSince the child developed signs of increased intracranial pressure a ventriculoperitoneal shunt was placed.\nDue to the patient's physical findings consistent with the diagnosis of Crouzon syndrome, a full mutation screening for the more uncommon Crouzon mutations in the FGFR2 and FGFR3 gene was performed. It identified the heterozygous c.1172C > A; p.Ala391Glu mutation in the FGFR3 gene, which is responsible for Crouzon syndrome with acanthosis nigricans.\nFurther treatment involves multidisciplinary control and coordination by the Copenhagen Craniofacial Unit. Midface distraction will be performed at 7–10 years of age.
|
[[31.0, 'year']]
|
F
|
{'17935505': 1, '10903683': 1, '11426459': 1, '26914936': 1, '10670894': 1, '7493034': 1, '10213050': 1, '30202723': 1, '32517430': 1, '23986840': 2}
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{}
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162,606 |
3738351-1
| 23,986,842 |
noncomm/PMC003xxxxxx/PMC3738351.xml
|
A case of postoperative pyopneumothorax following CT-guided radiofrequency ablation for lung cancer with interstitial pneumonia
|
The patient was a 67-year-old man with cT1bN0M0 non-small-cell lung cancer complicated with mild interstitial pneumonia. Prior to referral to our hospital, he had been under observation at the referring hospital for idiopathic pulmonary fibrosis/usual interstitial pneumonia for 1 year, during which a nodule of 2 cm was detected in the superior segment of the right lower lobe (S6) by chest computer tomography (CT) in May 2010 but remained undiagnosed even after additional bronchoscopy. At our center, pulmonary rehabilitation and oxygen inhalation at 3 l/min on exertion were started on an inpatient basis. Despite another diagnostic bronchoscopy, diagnosis was not made until September 2010 when CT-guided biopsy was performed. Non-small-cell lung carcinoma was diagnosed based on the biopsy results and staged as cT1bN0M0, as no metastasis was detected by contrast-enhanced CT and fluorodeoxyglucose positron emission tomography. Because the patient was considered at high risk for surgery, chemotherapy, and radiotherapy due to the complication with usual interstitial pneumonia and did not wish to undergo high-risk treatment, RFA was considered as an option.\nAfter review and approval by the institutional review board of Osaka City University Graduate School of Medicine and obtaining informed consent from the patient and his family, CT-guided lung RFA was performed in October 2010 (). Arterial blood gas measurements were: pH 7.41; PCO2 44; PO2 59.7; HCO3\n− 27.9; and SaO2 90.7 in room air. Pulmonary function test results were as follows: total lung capacity 6.15 l (percentage predicted total lung capacity 89.6%), total vital capacity 5.37 l (percentage predicted total vital capacity 87.3%); vital capacity 2.99 l (percentage predicted vital capacity 89.5%); forced expiratory volume in 1 s (FEV1.0) 2.71 l (percentage predicted FEV1.0 90.6%) and diffusion capacity for carbon monoxide 7.09 mL/min/mmHg (percentage predicted diffusion capacity for carbon monoxide; 43.8%). After subcutaneous and subpleural local anesthesia, the 2-cm lesion in the right S6 was punctured with a 17-gauge LeVeen Needle Electrode (array diameter of 3 cm, Boston Scientific, Natick, MA, USA) under CT guidance. 0.2 mg of fentanyl and 7 mg of midazolam were used in combination for analgesia and sedation, respectively. Electric current was applied to the tumor four times, starting at 30 W and then increasing by 5 W every 2 min. When the maximum resistance was reached, the current automatically stopped (“roll off”) indicating the completion of treatment. Ablation was applied for a total of 59 min and 37 s. The tumor was contained within the ablation range of the electrode, and a safety margin was considered achieved. Postoperatively, a prophylactic antibiotic was administered intravenously (Cefamezin, 1 g BID for 3 days). Only a small amount of hemoptysis was observed, and postoperative fever did not develop. Minor pneumothorax was indicated by CT after 2 days, but the patient did not exhibit dyspnea nor require oxygen administration at rest. The patient was discharged 3 days after RFA.\nChest X-ray and clinical follow-up after discharge, 2 weeks after RFA, revealed no pneumothorax requiring evacuation, dyspnea on exertion or other respiratory symptoms. Pulmonary rehabilitation was restarted as an outpatient basis. Progression of pneumothorax was evident on CT performed at 4 weeks after RFA. The patient was rehospitalized for aspiration via a 4 Fr chest tube. Pneumothorax improved, but the patient complained of back pain, and the tube was removed 5 weeks after RFA and continued administration of the antibiotic. Symptoms improved for 4 weeks, but the fever and back pain reappeared and elevated C-reactive protein and white blood cell count were observed. CT showed pleural effusion with an air-fluid level 12 weeks after RFA. Therefore, video-assisted thoracoscopic debridement of empyema and drainage were performed 13 weeks after RFA (). Necrosis of the S6 tumor was confirmed during the procedure. 24Fr conventional double lumen drain and 19Fr silastic flexible drain (BLAKE silicone drain; Ethicon, Somerville, NJ, USA) were inserted. Exudative pleural effusion cytology and cell culture tests were both negative. Because the control of air leak was poor even with debridement and drainage, 4 mL of a tissue adhesive (Bolheal, Kaketsuken, Kumamoto, Japan) and two times of autologous blood were administered. The air leak and fever finally subsided 24 weeks after RFA, and the drain was removed. Even though evidence of pleural effusion and pneumothorax was still detectable on CT, the patient did not present associated symptoms and was discharged 7 months after RFA. Follow-up CT at 11 months after RFA showed no signs of pleural effusion, though pneumothorax was still detected. No local recurrence or metastasis of the RFA-treated tumor was seen.
|
[[67.0, 'year']]
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M
|
{'21701013': 1, '19231433': 1, '16368397': 1, '20032160': 1, '27974695': 1, '17392258': 1, '19017870': 1, '16908680': 1, '12830051': 1, '17296716': 1, '15678967': 1, '21940529': 1, '23986842': 2}
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{}
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162,607 |
3738352-1
| 23,986,843 |
noncomm/PMC003xxxxxx/PMC3738352.xml
|
Solitary fibrous tumor of filum terminale
|
A 50-year-old woman suffered from intermittent pain in the lumbosacral area for about 10 years. Her back pain became aggravated progressively and radiated to the bilateral lower extremities 1 year before she arrived at our hospital. A general physical examination was normal. Neurological examination, which included mental status, cranial nerves, cerebellar testing, and motor and sensory tests of the extremities, was also negative. Routine blood tests were within normal limits.\nMagnetic resonance imaging was performed with a commercially available 3.0 Tesla MR scanner (Signa EXCITE HD, GE Healthcare, Milwaukee, WI, USA) and demonstrated a well-defined mass measuring 18×20 mm in transverse diameter located at the level of L2. The irregular intraspinal mass showed isointensity on T1-weighted images and hypointensity on T2-weighted images, and was avidly and homogeneously enhanced after intravenous injection of Gd-DTPA (Magnevist; Bayer Schering Pharma AG, Berlin, Germany) at a dose of 0.1 mmol/kg (Fig. ).\nA L2-L3 laminectomy was performed and an obvious tumor surrounded by nerve bundles was found. The dura mater was opened, as was the overlying arachnoid. Also, the nerve roots of the cauda equina were retracted. A well-defined tumor arising from the filum terminale was exposed. There was a dilated feeding artery and a draining vein running to and from the tumor. The tumor was completely removed. The microscopic appearance showed that the tumor was composed of cytologically scattered spindle cells arranged randomly. Immunohistochemically, the tumor cells had strong and diffuse positivity for vimentin, but were negative for S-100 and EMA antigen. With these findings, SFT of the filum terminale was considered to be the final diagnosis based on the World Health Organization's classification of soft tissue tumors (2002).\nPostoperatively, the patient became free of pain in the lumbosacral area, however, she had numbness of the buttocks and sacral region.
|
[[50.0, 'year']]
|
F
|
{'1536613': 1, '7260861': 1, '2665534': 1, '8712177': 1, '7573687': 1, '16145288': 1, '11920476': 1, '16702568': 1, '8509708': 1, '32181204': 1, '8116796': 1, '8160648': 1, '6193863': 1, '19751244': 1, '7705826': 1, '18306486': 2, '23986843': 2}
|
{'2615256-1': 1}
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162,608 |
3738353-1
| 23,986,844 |
noncomm/PMC003xxxxxx/PMC3738353.xml
|
Macronodular hepatosplenic tuberculosis
|
A 7-year-old Chinese girl presented to our department with a 3-week history of low-grade fever and cough. Her previous history was unremarkable. Physical examination revealed a soft abdomen with a tender liver edge 3 cm below the right costal margin and a palpable spleen tip; the chest was found to be normal. Routine laboratory tests were normal except for hemoglobin 9.9 gr/dL (nv 11.5–14.5) and erythrocyte sedimentation rate (ESR) of 79 mm/h (nv < 38). Tuberculin skin test was positive with 20 mm induration. Quantiferon-TB Gold test was 59 IU/mL (nv < 0.34). HIV test was negative. Chest X-ray showed mild thickening along the right major fissure and bilateral hilar enlargement. Abdominal ultrasound (US) performed using a 3.5 mHz convex transducer (Acuson Sequoia 512, Siemens, Mountain View, CA, USA) revealed mild hepatomegaly, multiple hypoechoic nodules up to 13 mm in diameter scattered throughout the liver and spleen (Fig. ); slight wall thickening of the last ileal loop and ascending colon, and multiple enlarged mesenteric lymph nodes were also shown. Multidetector computed tomography (CT) of the abdomen was performed using 16-slice CT scan (LightSpeed, GE Healthcare, Milwaukee, WI, USA) with 5-mm slice thickness (reconstructed 2.5 mm) and low dose technique (80 kv, 50–90 mAs) after i.v. contrast medium administration. CT revealed multiple rounded, low-density lesions in the liver and spleen, ranging in size from 2 to 18 mm (Fig. ); peripancreatic, periportal, para-aortic, and paracaval lymph nodes up to 15 mm in diameter with no calcification, and diffuse small bowel wall thickening were also shown. CT of the chest demonstrated small opacities in the right lower lobe and multiple enlarged lymph nodes in the hilar, paraesophageal, and paratracheal regions (Fig. ). Direct smear microscopy for acid-fast bacilli in the sputum and gastric lavage was negative, but the culture for Mycobacterium tuberculosis was positive. Colonoscopy showed a nodular, ulcerated mass that partially obstructed the cecum. Intestinal biopsy and image-guided needle biopsy of the liver revealed granulomatous tissue with caseous necrosis. Both direct smear microscopy for acid-fast bacilli and culture for Mycobacterium tuberculosis of intestinal and liver biopsy specimens were negative.\nDiagnosis of macronodular hepatosplenic TB with concomitant intestinal and lung involvement was made, and a three-drug anti-TB therapy consisting of isoniazid, rifampicin, and pyrazinamide was planned. After 9-month therapy, there was a marked improvement in the general condition, and the liver and spleen were no longer palpable. Abdominal US revealed reduction in size and peripheral calcification of the hepatosplenic lesions (Fig. ); abdominal lymph nodal groups were normal.
|
[[7.0, 'year']]
|
F
|
{'15908155': 1, '10341698': 1, '7610239': 1, '9168707': 1, '12717865': 1, '20674801': 1, '14677893': 1, '9817044': 1, '11819069': 1, '7560154': 1, '20386326': 1, '23986844': 2}
|
{}
|
162,609 |
3738354-1
| 23,986,845 |
noncomm/PMC003xxxxxx/PMC3738354.xml
|
Migration to the pulmonary artery of nine metallic coils placed in the internal iliac vein for treatment of giant rectal varices
|
A 64-year-old man with liver cirrhosis, advanced hepatocellular carcinoma (HCC) that invaded the main portal vein, and adrenal metastasis was admitted for the treatment of giant rectal varices due to portal hypertension. During the preceding 6 years he had undergone partial hepatectomy, six sessions of transcatheter arterial chemoembolization, and radiation therapy (39 Gy) for his HCC. He had no history of melena.\nOn admission, his functional reserve of the liver was Child-Pugh grade B. Colonoscopy showed huge tortuous rectal varices. Contrast-enhanced computed tomography (CT) revealed giant varices with tori inside the rectal lumen (Fig. a). Flow from the dilated inferior mesenteric vein was into the rectal varices that drained primarily into the left internal iliac vein. On inspiratory CT the diameter of the inferior mesenteric vein and left internal iliac vein was 10 mm.\nAfter obtaining informed consent from the patient and his family we attempted interventional therapy to prevent rupture of the varices. The plan was to fill the varices with a sclerotic agent via the IVM using balloon assistance. As tumor thrombosis into a main portal vein ruled out the percutaneous transhepatic approach we chose an ileocolic vein approach after laparotomy under general anesthesia. Portal venography via the superior mesenteric vein (SMV) confirmed that the rectal varices were supplied by the inferior mesenteric vein and mainly drained into the left internal iliac vein (Fig. b–d). Inflation of a 6-Fr balloon catheter (Selecon MP Catheter, Terumo Clinical Supply, Gifu, Japan) with a 2-cm diameter balloon in the inferior mesenteric vein failed to produce congestion in the varices. Consequently, we inflated a 6-Fr balloon catheter placed in the main trunk of the left internal iliac vein via the right common iliac vein (CIV) to block the in- and outflow of the rectal varices. However, we could not obtain congestion in the varices and contrast material in the varices drained into the collateral circulation of the left and right internal iliac vein. Thinking that flow in the rectal varices could be reduced by balloon occlusion of the left common iliac vein after coil embolization of the left internal iliac vein, we embolized the main trunk of the left internal iliac vein with nine microcoils. A 3-Fr microcatheter (Renegade, Boston Scientific, Natick, MA, USA) was advanced through the inflated 6-Fr balloon catheter placed into the orifice of the left internal iliac vein to prevent coil migration. First, one interlocking detachable microcoil (diameter 12 mm, length 30 mm) (InterlockTM, Boston Scientific, Cork, Ireland) was introduced as an anchor coil. Then we intertwined six pushable microcoils (diameter 8 mm, length 14 cm) (Micronester, Cook, Bloomington, IN, USA) with the anchor coil. Lastly two InterlockTM coils (diameter 10 mm and 12 mm, length 30 cm) was placed to hold the other seven coils and to obtain embolization.\nPostprocedure portal venography obtained under double balloon inflation in the inferior mesenteric vein and left common iliac vein revealed flow reduction in the rectal varices. However, as drainage via collateral vessels in the pelvis persisted 5 mL of absolute ethanol and 40 mL of a glucose solution were injected via the inflated balloon catheter in the IMV to embolize these drainers. This also failed to obtain complete congestion in the varices. As filling the rectal varices with a sclerotic agent was difficult under the existing conditions we attempted to embolize the varices with liquid glue. A 3-Fr microcatheter was advanced through the inflated balloon catheter in the internal mesenteric vein into the left superior rectal vein as close as possible to the rectal varices. Then 5.5 mL of a 1:10 mixture of N-butyl cyanoacrylate (NBCA) (Histoacryl, Aesculap, Tuttlingen, Germany) – lipiodol (André Guerbet, Aulnay-sous-Bois, France) was injected via the microcatheter under inflation of the balloons in the IMV and left CIV. As portal venography revealed that the right superior rectal vein flowed into residual rectal varices we injected 40 mL of 50% glucose and 12.5 mL of 5% ethanolamine oleate (Oldamin, Takeda Pharmaceutical, Osaka, Japan) with iopamidol (Iopamiron 300, Bayer HealthCare, Osaka, Japan) as a sclerotic agent through the microcatheter in the right superior rectal vein. Then eight pushable microcoils (diameter 8 mm) (Micronester) were placed in the internal mesenteric vein under double balloon inflation. As portal venography confirmed the complete obliteration of the rectal varices we removed the catheters (Fig. e, f). A plain radiograph obtained 30 min later confirmed that the coils remained in the left internal iliac vein. Throughout these procedures the patient's condition was stable and he was under continuous observation by anesthesiologists.\nDuring extubation the patient suffered a paroxysm of coughing and immediately after extubation he developed dyspnea and shivering. His partial pressure of arterial oxygen and percutaneous oxygen saturation slightly fell to 87 mmHg and 95% under oxygen inhalation of 5 L/min. Under continuous oxygen inhalation his symptoms abated somewhat and he was placed under observation with oxygen inhalation.\nOn the first postoperative day his dyspnea disappeared and the percutaneous oxygen saturation was 98% in room air. There were no respiratory symptoms. Although the liver function deteriorated transiently he developed no acute complications. A CT study performed on the fifth postoperative day confirmed complete obliteration of the rectal varices (Fig. a). However, all nine metallic coils placed in the left internal iliac vein had migrated into a lower branch of the right pulmonary artery (Fig. b and c). As this elicited no respiratory symptoms and as we considered the removal of the coils by interventional procedures inadvisable at that time, he was discharged 10 days after undergoing the procedures.\nHe subsequently received hepatic arterial infusion chemotherapy for HCC and endoscopic treatment for aggravated esophageal varices. Although colonoscopy showed shrinkage of the rectal varices, CT obtained 3 months later revealed progression of his intrahepatic HCC, enlargement of the adrenal metastasis, and newly developed lung metastasis. He died of HCC 5 months after the obliteration of the rectal varices.
|
[[64.0, 'year']]
|
M
|
{'23452779': 2, '18756371': 1, '32926706': 2, '18540710': 1, '1490441': 1, '31762775': 1, '11830623': 1, '10382051': 1, '8479025': 1, '23986845': 2}
|
{'7434267-1': 1, '3599389-1': 1}
|
162,610 |
3738355-1
| 23,986,846 |
noncomm/PMC003xxxxxx/PMC3738355.xml
|
Littoral cell angioma mimicking hepatic tumor
|
A 53-year-old woman presented with a 10-year history of intermittent abdominal pain, swelling and continuous vomiting. The patient denied presence of fever, nausea, and weight loss. There were no significant findings at physical examination. An abdominal ultrasound exam revealed a 10.4 × 10.0 cm mass of heterogeneous echogenicity in the left upper abdomen. Axial unenhanced CT scan (Fig. a) confirmed an ill-defined heterogeneous mass 9.1 cm in diameter that filled the left abdominal quadrant, located between the left lobe of the liver and the spleen. The CT attenuation of the mass was around 26–53 HU on non-enhanced scan. After intravenous contrast medium injection the mass enhanced gradually and heterogeneously (Fig. b–e), but was still hypodense relative to the spleen. There was no accompanying lymphadenopathy or evidence of malignant process elsewhere in the abdomen. Because the origin of the mass was unknown and a primary malignancy could not be excluded, the patient underwent an explorative laparotomy. During the operation, a well-encapsulated mass was found under the left hepatic lobe and the pedicle arising from the spleen. Resection of the mass and the spleen was performed.\nGross examination of the spleen showed splenomegaly (580 g, 15 × 10 × 9 cm) with an ill-defined brownish nodule (5 × 8 × 8 cm). Histologic examination (Fig. ) revealed that the lesion was composed of variably sized vascular channels lined with flat and tall endothelial cells, with papillary fronds extending into the vascular channels. No atypical cells or mitosis were present. The endothelial lining cells of the vascular channels were positive for CD31 and CD68, factor VIII and negative for CD34, CD21, and CD8. These findings were considered diagnostic of benign splenic littoral cell angioma.
|
[[53.0, 'year']]
|
F
|
{'20409532': 1, '11737304': 1, '20349061': 1, '16971207': 1, '1928554': 1, '18208795': 1, '15909068': 1, '18830109': 1, '10663622': 1, '14752189': 1, '9862523': 1, '23986846': 2}
|
{}
|
162,611 |
3738356-1
| 23,986,847 |
noncomm/PMC003xxxxxx/PMC3738356.xml
|
Osteochondritis dissecans of the humeral capitellum in identical twins
|
17-year-old identical male twins had been actively playing ice-hockey for 7 years at a national level. During the last 18 months both patients had pain and occasional locking of the right elbow. The clinical history was unremarkable, as there were neither medical records nor history of previous major trauma to the elbow. Both were right-handed players, so more valgus stress on the right capitellum was created. On clinical examination, a slight extension deficit up to 5° of the affected elbow was present in both. There were no other clinical abnormalities.\nRadiographs (Figs. and ) showed some flattening and subchondral lucencies of the articular surface of the capitellum in both patients. Also, multiple loose bodies in the joint space were seen. Twin B had a small osteochondral lesion at the anterior part of distal capitellar surface, and osteophytes at the medial aspect of the elbow as an early sign of arthrosis was seen as well. Joint effusion was present in both patients.\nMRI was performed 3 months later using a 1.5T scanner (Siemens Symphony, Siemens Medical Solutions, Erlangen, Germany) with a standard flexible surface coil. Imaging was performed with the elbow in maximal extension. Coronal, axial, and sagittal T2 (TR 3000–5690/TE 107–110) and proton density (PD) (TR 3000–5690/TE 21–37) weighted spin-echo (SE) sequences with fat saturation were obtained with additional coronal T2 and PD SE sequences without fat saturation. Imaging matrix was 320 × 192–245, field of view ranged from 12 × 9 cm to 14 × 12.6 cm.\nTwin A (Fig. ) had cartilage defects, bone marrow edema, and osseous changes in the capitellum. Joint effusion and intra-articular loose bodies were also present. This twin had also osteophytes at the medial aspect of the elbow as an early sign of arthrosis.\nTwin B (Fig. ) had joint effusion and intra-articular loose bodies. There were cartilage and osseous defects with surrounding edema in the capitellum. On the cartilage surface there was a small loose cartilaginous particle, as a hyperintense rim extending to the articular space on T2-w images surrounded it.\nThe right elbow arthroscopy was performed in lateral decubitus position with the forearm hanging freely over a bar. The anterior compartment was first examined through anterolateral and anteromedial portals, followed by posterior compartment viewing through posterolateral and posterior portals.\nAt arthroscopy, Twin A had a mild synovitis, and loose bodies were detected (Fig. ). The articular surface of capitellum was soft without unstable cartilage or visible subchondral bone. There was fraying of the articular cartilage of the radial head but it was otherwise normal. Superficial damage was also seen on the articular cartilage of trochlea.\nTwin B also had mild synovitis and loose bodies (Fig. ). There was softening of the cartilage on the articular surface of capitellum. Articular cartilage of the radial head was normal.
|
[[17.0, 'year']]
|
M
|
{'14399666': 1, '12772874': 1, '2736009': 1, '2009106': 1, '4468320': 1, '10887249': 1, '7057469': 1, '1815188': 1, '16303997': 1, '19662464': 1, '7709246': 1, '14353962': 1, '2791462': 1, '23986847': 2}
|
{}
|
162,612 |
3738357-1
| 23,986,848 |
noncomm/PMC003xxxxxx/PMC3738357.xml
|
Selective embolization of the splenic vein for shunt-preserving disconnection of the portal and systemic circulation: report of two cases
|
This 50-year-old man with chronic hepatitis due to hepatitis C virus infection suffered from recurrent episodes of hepatic encephalopathy since undergoing transcatheter arterial chemoembolization for hepatocellular carcinoma 1 year earlier. He had repeated episodes of acute encephalopathy despite protein restriction and administration of lactulose and branched-chain amino acids and was admitted with hepatic encephalopathy (West Haven Criteria stage 4). His liver function was Child-Pugh B (total bilirubin, 1.9 mg/dl; albumin, 2.9 g/dl; prothrombin time, 94%; no ascites). The blood ammonia level was 333 µg/dl (normal range, 15–65 µg/dl). Contrast-enhanced computed tomography (CT) scans were acquired with a 64-row multidetector scanner (Brilliance-64, Philips Medical Systems, Best, The Netherlands) and 3D images revealed portosystemic shunts.
|
[[50.0, 'year']]
|
M
|
{'7872302': 1, '11283531': 1, '11464006': 1, '7258542': 1, '16250033': 1, '15387347': 1, '10227544': 1, '18036102': 1, '9177524': 1, '15590808': 1, '8865749': 1, '3685350': 1, '12818832': 1, '6724263': 1, '18038351': 1, '10720827': 1, '1468606': 1, '23986848': 2}
|
{'3738357-2': 2}
|
162,613 |
3738357-2
| 23,986,848 |
noncomm/PMC003xxxxxx/PMC3738357.xml
|
Selective embolization of the splenic vein for shunt-preserving disconnection of the portal and systemic circulation: report of two cases
|
This 70-year-old woman with chronic hepatitis due to hepatitis C virus infection had had recurrent episodes of hepatic encephalopathy despite protein restriction and the administration of lactulose and branched-chain amino acids. She was admitted with hepatic encephalopathy (West Haven Criteria stage 4). The liver function was Child-Pugh A (total bilirubin, 0.7 mg/dl; albumin, 3.2 g/dl; prothrombin time, 96%; no ascites) and the blood ammonia level 214 µg/dl. Contrast-enhanced CT scans were acquired with a 64-row multidetector scanner (Brilliance-64); 3D images revealed portosystemic shunts and a portal-hepatic vein shunt in the left lobe.\nThree-phase contrast-enhanced CT scans of the liver were acquired in the arterial, portal venous, and equilibrium phases in both patients. An automatic bolus-tracking program was used to time the start of scanning for each phase after contrast injection. Hepatic arterial, portal venous, and equilibrium phase scanning was started 18, 55, and 180 s after triggering. We used a bolus injection of 100 mL iopromide (Iopamiron 300; Nihon Beyer, Osaka, Japan) delivered at a rate of 3 mL/s. All images were obtained through the abdomen in a craniocaudal direction.\nFirst, under local anesthesia, superior mesenteric and celiac arteriography was performed to develop a treatment plan and to assess collateral circulations in both patients. DSA of the superior mesenteric artery and the celiac trunk was performed after the administration of 2.5 μg prostaglandin E1 (Liple; Mitsubishi Pharma Corp., Osaka, Japan), using a 4-Fr RC2 catheter (Medikit Co. Ltd., Tokyo, Japan) after injection of iomeprol (Iopamiron 300; Bayer, Osaka Japan) at a flow rate of 6 mL/s and 5 mL/s, respectively. In both cases, the venous phase of superior mesenteric arteriography demonstrated a spleno-renal and a spleno- retroperitoneal shunt, and an undetected portal vein trunk (Fig. ). There was enough distance to allow disconnecting the mesenteric-portal blood flow from the systemic circulation while preserving the shunt.\nStandard anesthesia consisted of 10 mL of 1% lidocaine injected locally; conscious sedation was with a continuous intravenous infusion of fentanyl (Phentanest, Sankyo, Tokyo, Japan) delivered at 100 μg/h during the procedure. Using a percutaneous transhepatic approach we performed ultrasonography-guided puncture of the portal vein, introduced a 6-Fr C-curved sheath (Medikit), and inserted a 5-Fr cobra catheter (Medikit) into the portal system to measure the pressure in the portal vein sequentially (23 mmHg). Splenic venography revealed a spleno-renal and a spleno-retroperitoneal shunt (Fig. ). We also inserted a 5-Fr catheter into the inferior mesenteric vein and identified the junction of the inferior mesenteric and the portal vein.\nBecause we use a balloon catheter as a flow control to prevent coil deviation, we used two 6-F balloon catheters with a 25-mm diameter balloon (Moiyan, Miyano, Osaka, Japan). One was inserted from the percutaneous transhepatic approach and wedged into the splenic vein during embolization, and the other from the right femoral vein wedged into the left adrenal vein.\nIn case 1, two coil anchors (Medikit) were placed in the proximal part of the splenic vein to prevent coil deviation. Embolization was performed with nine metallic coils (Vortex; Boston Scientific, Watertown, MA, USA) and 10 microcoils (interlocking detachable coils (IDC), Boston Scientific) using a 2.5-Fr microcatheter (Target, Boston Scientific) to prevent obstruction of the inferior mesenteric vein by coil migration. In case 2, one coil anchor (Medikit) was placed on the proximal part of the splenic vein to prevent coil deviation. Embolization was with one 3-dimensional Guglielmi detachable coil (GDC; Boston Scientific) and 11 IDCs (Boston Scientific) using a 2.5-Fr microcatheter (Target, Boston Scientific) to prevent inferior mesenteric vein obstruction by coil migration. In sequence, we then embolized the portal-hepatic vein shunt in the left lobe by introducing five IDCs (Boston Scientific) using a 2.5-Fr microcatheter (Target, Boston Scientific). This disconnected the mesenteric-portal blood flow from the systemic circulation while preserving the shunt.\nAfter successful embolization, the venous phase of superior mesenteric arteriography demonstrated a portal vein trunk toward the liver (Fig. ). There was enough distance to allow disconnection of the mesenteric-portal blood flow from the systemic circulation while preserving the shunt (Fig. a). The patients' encephalopathy resolved immediately and permanently and in the course of 30-month follow-up there was no evidence of ascites or esophageal varices. The pre- and postprocedure difference in portal pressure was 5 mmHg (from 18 to 23 mmHg, case 1) and 5 mmHg (from 11 to 16 mmHg, case 2). The blood ammonia level fell by 49 µg/dl from 333 µg/dl (case 1) and by 25 µg/dl from 214 µg/dl (case 2). Neither patient experienced episodes of hepatic coma during the follow-up period.
|
[[70.0, 'year']]
|
F
|
{'7872302': 1, '11283531': 1, '11464006': 1, '7258542': 1, '16250033': 1, '15387347': 1, '10227544': 1, '18036102': 1, '9177524': 1, '15590808': 1, '8865749': 1, '3685350': 1, '12818832': 1, '6724263': 1, '18038351': 1, '10720827': 1, '1468606': 1, '23986848': 2}
|
{'3738357-1': 2}
|
162,614 |
3738359-1
| 23,986,850 |
noncomm/PMC003xxxxxx/PMC3738359.xml
|
Unusual imaging profile of a solitary splenic lymphangioma
|
The patient was a 67-year-old Caucasian man who was found to have two colorectal masses on colonoscopy; which were diagnosed as a well-differentiated adenocarcinoma and a moderate-to-poorly differentiated adenocarcinoma. His CEA level was 15.1 ng/mL at presentation (normal healthy smoker <5.5 ng/mL). CT scan of the abdomen demonstrated a 1.0-cm left adrenal nodule and a 6-cm heterogeneous, ill-defined mass in the spleen (Fig. ). The attenuation of the splenic mass measured 42 Hounsfield units (HU) on the portal venous phase. This was unchanged on the 4 min delayed images. The left adrenal nodule was found to be adenoma on follow-up exams. Assuming metastatic disease, chemotherapy was initiated. The CEA level dropped to 0.9 ng/mL (within normal range) suggestive of a biochemical response to therapy. Meanwhile, a follow-up CT scan of abdomen and pelvis demonstrated stable size of the splenic lesions, suggestive of benign etiology.\nTo confirm if the splenic lesion was benign, a PET scan was performed, which did not show FDG uptake in the splenic mass (Fig. ).\nGiven that the most common benign lesion of the spleen is a hemangioma, a radiolabeled red blood cell (RBC) scan was performed to further characterize this lesion (Fig. ). During the dynamic and delayed images, the RBC scan demonstrated a photopenic region in the spleen that corresponded to the mass. This made the diagnosis of hemangioma unlikely.\nBecause the tagged RBC scan did not confirm the diagnosis of hemangioma, an MRI of the abdomen was performed with and without Gadovist IV contrast (Fig. ). The MRI showed a rounded, well-defined heterogeneously high T2 and low T1 signal lesion in the spleen with centripetal fill-in of contrast on delayed images. However, the lesion did not demonstrate homogeneous fill-in on the most delayed sequences. Nevertheless, MRI findings were reported to be suggestive of hemangioma or hemangioendothelioma. This was in some opposition to the tagged RBC scan. To further delineate the nature of the lesion, a contrast-enhanced ultrasound was recommended.\nDoppler and gray scale ultrasound studies were performed followed by intravenous contrast injection of a total of four doses of 0.2 mL, Definity (Lantheus Medical Imaging, N Billerica, MA, USA). A Philips iU 22 ultrasound machine (Philips Medical Systems, Bothell, WA, USA) with C5-1 and X6-1 transducers were used for contrast study with contrast specific mode (Fig. ). Pre-contrast images demonstrated a mildly hyperechoic mass in the spleen with peripheral vascular flow on Doppler images. Post-contrast ultrasound images immediately after contrast injection demonstrated straight vessels feeding the mass in the spleen. The lesion showed heterogeneous early enhancement and early wash-out. Again, the ultrasound findings were not typical for either a hemangioma or a lymphangioma.\nFinally, a core biopsy of the splenic lesion was done in the operating room at the time of colectomy. At the time of operation, the patient was noted to have a large palpable mass centered in the superior pole of the spleen but adjacent to several splenic hilar vessels. Upon palpation of the splenic hilum, there was no evidence of regional lymphadenopathy. A suitable core needle biopsy window was identified on ultrasound in order to avoid vascular injury. Using an 18-gauge core needle, two passes were made in the splenic mass under ultrasound guidance without complication.\nHistological sections showed the proliferation of variably sized thin-walled vascular channels filled with thin eosinophilic fluid and was reported as benign spleen with dilated lymphatics (Fig. ).
|
[[67.0, 'year']]
|
M
|
{'15286314': 1, '9630280': 1, '29656712': 2, '11318134': 1, '989835': 1, '15149994': 1, '32557234': 2, '15256634': 1, '20205289': 1, '9497231': 1, '11471610': 1, '32518789': 2, '12828616': 1, '19701979': 1, '12620551': 1, '26703174': 1, '3257108': 1, '17526609': 1, '16154823': 1, '17267469': 1, '25805954': 1, '21273021': 1, '16714641': 1, '23986850': 2}
|
{'7262707-1': 1, '7303252-1': 1, '5901864-1': 1}
|
162,615 |
3738360-1
| 23,986,851 |
noncomm/PMC003xxxxxx/PMC3738360.xml
|
Leiomyoma of the nipple diagnosed by MRI
|
A 32-year-old woman visited the surgery outpatient clinic in our hospital with a recently enlarged left nipple with discharge and erosion. The patient has been aware of the asymmetrically prominent left nipple for 6 years.\nShe did not have fever at the time of the visit, and no history of breast trauma. Additionally, there was no family history of breast cancer. On physical examination, she had a 2-cm pinkish superficial nodule in the left nipple-areolar complex. The nodule was firm and quite tender. The remainder of the breast examination revealed no abnormalities. The laboratory findings were normal.\nThe left mediolateral oblique mammogram revealed an enlarged nipple (Fig. ). Ultrasonography of the left breast showed a 2-cm sized well-circumscribed oval hypoechoic mass with posterior acoustic enhancement in the nipple (Fig. a). A Doppler sonogram of the left nipple mass demonstrated increased peripheral blood flow in the mass (Fig. b). No other abnormal findings were seen neither by mammography nor ultrasonography.\nTo exclude abnormalities in the subareolar region since the parenchyma in this patient was extremely dense, breast MRI was performed.\nMRI revealed an oval mass with circumscribed margins in the left nipple-areolar complex. This mass showed intermediate signal intensity on both T2-weighted images (Fig. a) and T1-weighted images (Fig. b). A dynamic MRI study showed a peripheral rim enhancement (Fig. c). The mass in the left nipple-areolar complex had a higher diffusion-weighted imaging (DWI) signal intensity and lower apparent diffusion coefficient (ADC) value than the right nipple (Fig. d). A kinetic curve demonstrated delayed persistent enhancement (Fig. e). No other abnormal findings were observed.\nAn ultrasound-guided core needle biopsy was performed using a 14-gauge needle. The core needle biopsy demonstrated spindle cell proliferation consistent with leiomyoma of the nipple (Fig. ).\nFinally, on the basis of the histopathological and radiological findings, this case was diagnosed as leiomyoma of the nipple.
|
[[32.0, 'year']]
|
F
|
{'9843313': 1, '8618404': 1, '10336188': 1, '21498361': 1, '21416339': 1, '18180236': 1, '16848853': 1, '7840010': 1, '21352311': 1, '23986851': 2}
|
{}
|
162,616 |
3738361-1
| 23,986,852 |
noncomm/PMC003xxxxxx/PMC3738361.xml
|
Primary signet ring cell carcinoma of the appendix mimicking acute appendicitis
|
An 80-year-old man presented to the Emergency Department in May 2009 with persistent right lower quadrant abdominal pain. Baseline blood tests showed neutrophilic leukocytosis. Preoperative contrast-enhanced CT scan (Figs. and ) showed a wide and severe thickening of the appendiceal walls with extensive soft-tissue stranding and inflammation of the peri-appendicular fat. Loculated fluid and lymphadenopathy adjacent to the appendix were also detected on the CT examination.\nThe patient underwent an appendectomy. At laparotomy the appendix appeared severely inflamed with an associated abscess at its apex. The inflammatory process also involved the first part of the cecum, making it difficult for the identification of the ceco-appendiceal junction. The final histological diagnosis was consistent with well-differentiated infiltrating adenocarcinoma of the appendix with mucinous and “signet ring cells” appearance, with signs of infiltration of peri-appendicular fat and a peritoneal abscess (Fig. ).\nThe patient underwent colonoscopy for the evaluation of synchronous disease, which was negative. Neoplastic markers were negative as well.\nThe patient subsequently underwent right hemicolectomy and no residual carcinoma with negative lymph nodes was found. The patient was discharged from the hospital 10 days later and had an uneventful postoperative course.
|
[[80.0, 'year']]
|
M
|
{'32670686': 1, '12202713': 1, '34729168': 2, '29043541': 1, '25717258': 1, '11931535': 1, '30022916': 2, '15856001': 1, '1609724': 1, '14616200': 1, '32699593': 2, '29915638': 2, '30065515': 1, '29348959': 2, '14572318': 1, '12115365': 1, '30182291': 2, '26753605': 2, '16919190': 1, '18837098': 1, '16258711': 1, '32606501': 1, '23986852': 2}
|
{'5733899-1': 1, '5733899-2': 1, '6047566-1': 1, '6123337-1': 1, '7365044-1': 1, '4825206-1': 1, '8557668-1': 1, '5997481-1': 1}
|
162,617 |
3738366-1
| 24,175,074 |
noncomm/PMC003xxxxxx/PMC3738366.xml
|
Metastatic paraganglioma: management of orthostatic hypotension – a case report
|
A 40 year old lady with malignant metastatic paraganglioma was admitted electively to a medical ward for management of severe and incapacitating orthostatic hypotension.\nShe had been diagnosed at the age of 10 following unsuccessful treatment of suspected migraines. She had had symptoms of severe headaches and visual disturbances associated with sweating and vomiting, and had been treated with clonidine therapy. During a visit to her general practitioner, her blood pressure was noted to be unreadably high, and she was therefore immediately sent to hospital. In hospital, chest x-ray demonstrated a right-sided paravertebral opacity, and 24 hour urine collection revealed increased catecholamine levels. She underwent thoracotomy and tumour excision, and a diagnosis of extra-adrenal phaeochromocytoma was made. She was discharged from follow-up 3 years later.\nAt the age of 23, she became pregnant and had debilitating morning sickness and regular urinary tract infections. At 32 weeks' gestation, a 24 hour urine collection was performed and revealed increased catecholamines once again, at which point she was admitted to hospital. Investigations, including MIBG scanning, revealed recurrence of the paravertebral mass in her chest, and a deposit in the left scapula was also noted. She was started on oral labetalol at this point. She remained in hospital until the onset of labour at 38 weeks, at which point she underwent elective Caesarean section under general anaesthesia. 3 months post-partum, she commenced the first of five cycles of intravenous MIBG therapy, the duration of treatment lasting 2 ½ years in total.\nFollowing this treatment she remained well for the next 8 years, during which time she underwent premature menopause at age 25. At age 29, with the assistance of in-vitro fertilization, she gave birth to twins, this pregnancy being eventful only by the need for Caesarean section due to breech position and hysterectomy being necessary intra-operatively due to intra-partum haemorrhage. She was subsequently commenced on hormone replacement therapy.\nShe remained under regular follow-up, and another 24 hour urine collection 5 years following her second pregnancy revealed increased catecholamines once again. MIBG imaging demonstrated the known lesions in the shoulder and chest, and she underwent 2 cycles of MIBG therapy, which was complicated by thrombocytopenia. Following this she underwent repeat resection of the right thoracic mass which was adherent to the lung.\nAfter this she remained under regular follow-up and was well, with normal urinary catecholamine secretion, until three years later when 24 hour urinary cathecholamines increased again. She underwent four further cycles of MIBG therapy, however on this occasion the catecholamine response was poor and she had also developed pain in the thoracic spine, which on further investigation (including MIBG and magnetic resonance imaging) proved to be caused by spread into the vertebral column at T3. She underwent debulking surgery including vertebral reconstruction, which led to a reduction in urinary catecholamine level; however, over the course of several months her pain increased, and further investigation revealed re-growth of the debulked tumour along with multiple new lesions throughout the spine. She underwent radiotherapy to the spinal lesions and was commenced on CVD chemotherapy.\nManagement of blood pressure in this patient has been extremely complex, with the need to control severe blood pressure surges whilst at the same time to avoid postural drops both from the anti-hypertensive medications used and from the disease process itself.\nFollowing the completion of her first cycle of CVD she developed profoundly symptomatic orthostatic hypotension requiring admission, with postural drops of 40–90mmHg in systolic BP, leaving the patient virtually bed-bound and causing severe distress. Her BP prior to this had been managed successfully with labetalol 200mg twice daily and amlodipine 5mg once daily. In hospital, she was found to be clinically dehydrated and management was initially with aggressive intravenous fluid replacement, which caused a transient improvement in both symptoms and postural BP drop. Relief of symptoms with intravenous hydration was very short-lived however, and although clinically euvolaemic following this, her orthostatic symptoms persisted. The amlodipine dosage was reduced to 2.5mg daily and sertraline (which she had been taking for depression) was stopped. Her BP having stabilized to some degree, she was discharged, but then readmitted for recurrence of severe orthostatic hypotension associated with paroxysms of severe hypertension; on this occasion, she was liberally intravenously hydrated, amlodipine was stopped and phenoxybenzamine was commenced, titrating up to a final dose of 20mg twice daily whilst continuing labetalol 200 mg twice daily. On this regimen she improved. Although her BP surges settled, she continued to have symptomatic orthostatic hypotension. Therefore labetalol was reduced to 50mg twice daily and phenoxybenzamine to 10mg twice daily. This resulted in an improvement both in symptoms and in BP profile, with only occasional (and short-lived) paroxysms of hypertension and, although she continues to have orthostatic hypotension, this is reduced in severity and causing very little in the way of symptoms.
|
[[40.0, 'year']]
|
F
|
{'18071700': 1, '8628505': 1, '12788870': 1, '13805323': 1, '10371366': 1, '10363888': 1, '18607252': 1, '26236513': 2, '1729490': 1, '17156452': 1, '18780317': 1, '24175074': 2}
|
{'4508462-1': 1}
|
162,618 |
3739470-1
| 23,936,627 |
noncomm/PMC003xxxxxx/PMC3739470.xml
|
Fungal granulomatous interstitial nephritis presenting as acute kidney injury diagnosed by renal histology including PCR assay
|
A 73-year-old Japanese man was admitted to the otolaryngology department for the treatment of pharyngeal cancer. Laboratory tests revealed a serum creatinine level of 0.8 mg/dL (71 µmol/L) and an estimated glomerular filtration rate of 72 mL/min/1.73 m2 (1.2 mL/s/1.73 m2) with no abnormality in urinalysis.\nSix courses of a chemotherapy regimen including docetaxel (28 mg/day) and cisplatin (7 mg/day) were given over 5 days, and, concomitantly, a total of 68 Gy of radiation was administered during 2 months. Patient's serum creatinine was 0.9 mg/dL (80 µmol/L) at the end of chemotherapy. One month after the completion of chemotherapy and radiation therapy, the patient's body temperature rose to 40°C. Although chest X-ray showed no consolidation in the lungs, antibiotics (piperacillin sodium and teicoplanin) were started because sputum cultures were found to be positive for Pseudomonas aeruginosa and methicillin-resistant Staphylococcus aureus. Two days later, the patient was referred to our nephrology department because of elevated serum creatinine and oliguria. Laboratory results were: creatinine, 8.1 mg/dL (716 µmol/L); serum albumin, 2.1 g/dL (21 g/L); and C-reactive protein (CRP), 11.1 mg/dL. The white blood cell count was 14.3 × 103/µL (14.3 × 109/L) with 70% neutrophils. The hemoglobin level was 8.2 g/dL (82 g/L). The serum level of β-d-glucan was high (>600 pg/mL); however, antigen titers for Cryptococcus (the Eiken latex agglutination test; Eiken, Tokyo, Japan), Aspergillus (Platelia ELISA kit; Fujirebio, Tokyo, Japan) and Candida (Platelia ELISA kit; Fujirebio, Tokyo, Japan) were negative.\nUrinalysis showed no proteinuria, 5–9 red blood cells/high-power field and 5–9 white blood cells/high-power field. Abdominal computed tomography (CT) showed markedly enlarged kidneys bilaterally. The central venous line via the internal jugular vein was removed because catheter infection was suspected. Blood and urine cultures were negative; however, culture of the tip of the central venous catheter was positive for C. albicans. Piperacillin and teicoplanin were continued and fluconazole was added for C. albicans. Hemodialysis was started 1 week later, and a biopsy of the patient's left kidney was performed 10 days later after consultation.\nMicroscopic findings showed severe interstitial cell infiltration and fibrosis with granulomatous formation. Inflammatory cells included mononuclear, epithelioid and giant cells. Most of the glomeruli were highly collapsed. Grocott's methenamine silver (GMS) stain showed multiple small, rounded, yeast-like features in the interstitium ().
|
[[73.0, 'year']]
|
M
|
{'17699417': 1, '19644480': 1, '16549149': 1, '4075600': 1, '17122000': 1, '10074611': 1, '20605281': 1, '11007702': 1, '18524711': 1, '30127380': 1, '12612999': 1, '17900469': 1, '33652638': 1, '19525518': 1, '26413275': 2, '16501836': 1, '27799926': 1, '29276711': 2, '31435719': 1, '16254108': 1, '27799331': 1, '12407659': 1, '8522308': 1, '11340531': 1, '6433667': 1, '21974966': 1, '23936627': 2}
|
{'3739470-2': 2, '5734493-1': 1, '4581373-1': 1}
|
162,619 |
3739470-2
| 23,936,627 |
noncomm/PMC003xxxxxx/PMC3739470.xml
|
Fungal granulomatous interstitial nephritis presenting as acute kidney injury diagnosed by renal histology including PCR assay
|
A 23-year-old Japanese man was admitted to another hospital for a severe bronchial asthma attack. The patient had a medical history of asthma for more than 10 years; however, no medication had been prescribed. On the day of admission, as his respiratory status worsened, he was intubated and mechanical ventilation was started. Methylprednisolone pulse therapy (1 g/day for 3 days) was administered. Two weeks after admission, the patient's renal function deteriorated and hemodialysis was initiated. Abdominal CT demonstrated enlargement of both kidneys. At the same time, the patient's body temperature rose to 37.5°C. Antifungal therapy (fluconazole, 400 mg on alternate days) was started because C. albicans was detected by blood culture. One month after admission, the patient was transferred to our hospital.\nPhysical examination showed a body temperature of 38.0°C and blood pressure of 133/66 mmHg. Coarse crackles were auscultated in both lungs. Eye examination showed no endophthalmitis and no abnormalities of fundus. Laboratory results were: creatinine, 3.0 mg/dL (265 µmol/L); serum albumin, 1.3 g/dL (13 g/L); and CRP, 13.8 mg/dL. The white blood cell count was 17.7 × 103/µL (17.7 × 109/L) with 72% neutrophils. The hemoglobin level was 7.1 g/dL (71 g/L). The serum level of β-d-glucan was high (>1200 pg/mL), and a titer of Candida antigen was positive. Urinalysis showed 3 (+) proteinuria, too many red blood cells/high-power field and 50–99 white blood cells/high-power field. Abdominal CT showed markedly enlarged kidneys bilaterally. Chest X-ray demonstrated diffuse consolidations and pleural effusions in both lungs. Echocardiography revealed no valvular abnormalities, including vegetation. Sputum and blood cultures were positive for P. aeruginosa. Antibiotics (imipenem/cilastatin, 0.25 g/day) were started. The antifungal medication was changed from fluconazole to amphotericin B because of prolonged elevation of β-d-glucan (>1200 pg/mL). One month after admission, the patient was withdrawn from mechanical ventilation. Despite improvement of the pulmonary infection, the decline in renal function and elevation of β-d-glucan continued. Two months after admission, CT showed multiple low-density areas in both kidneys. Scintigraphy with gallium citrate Ga67 showed strong radionuclide uptake in both kidneys. These findings were considered multiple renal abscesses. Three months after admission, we decided to perform bilateral nephrectomy because eradication of organisms was regarded impossible without the removal of the whole tissue.\nMacroscopic inspection of the patient's removed kidneys found multiple abscesses, mainly in the subcapsular cortical area. Microscopic examination revealed severe interstitial cell infiltration and fibrosis with granulomatous formation. Inflammatory cells included lymphocytes, plasma cells and multinucleated histiocytes. Most of the glomeruli were highly collapsed. The GMS stain showed multiple small, rounded, yeast-like features and branching filamentous features in the interstitium, including at the center of the abscess formation ().\nAn appropriate area of formalin-fixed, paraffin-embedded tissue (FFPE) blocks was selected aligned with GMS stain and a 2 mg of segment was excised and minced using a clean disposable scalpel. DNA was extracted using Genomic DNA purification Kit (Qiagen GmbH, Hilden, Germany). The internal transcribed spacer (ITS) region was amplified with the PCR assay using the universal primer set of the ITS region of the fungi []. Nucleotide sequence analysis and a BLAST (Basic Local Alignment Search Tool) search of the European Molecular Biology Laboratory (EMBL) and GenBank® databases revealed 100% homology with T. laibachii in Patient 1 and C. albicans in Patient 2.
|
[[23.0, 'year']]
|
M
|
{'17699417': 1, '19644480': 1, '16549149': 1, '4075600': 1, '17122000': 1, '10074611': 1, '20605281': 1, '11007702': 1, '18524711': 1, '30127380': 1, '12612999': 1, '17900469': 1, '33652638': 1, '19525518': 1, '26413275': 2, '16501836': 1, '27799926': 1, '29276711': 2, '31435719': 1, '16254108': 1, '27799331': 1, '12407659': 1, '8522308': 1, '11340531': 1, '6433667': 1, '21974966': 1, '23936627': 2}
|
{'3739470-1': 2, '5734493-1': 1, '4581373-1': 1}
|
162,620 |
3740108-1
| 23,967,034 |
noncomm/PMC003xxxxxx/PMC3740108.xml
|
Radiofrequency Ablation of Accessory Pathways in Children with Complex Congenital Cardiac Lesions: A Report of Three Cases
|
A 7-year-old girl, weighing 21 kg, presented with frequent palpitations and documented narrow complex tachycardia. Her electrocardiogram during sinus rhythm showed a manifest left lateral AP (). In the past, she had been diagnosed to have tricuspid atresia (type IIb) with D-transposition of the great arteries, a large ventricular septal defect, and pulmonary hypertension (). She had undergone pulmonary artery banding, followed by Glenn shunt, and was awaiting total cavopulmonary connection. She had associated severe scoliosis. We conducted an electrophysiological study and documented both an orthodromic atrioventricular reentrant tachycardia and atrial tachycardia with a rapid conduction over the AP. There was no direct access to the right ventricle, and the ventricular catheter was placed via the right atrium into the left atrium and through the atrial septal defect before it was positioned in the left ventricle. Endocardial ablation on the mitral annulus had previously failed at another center. We mapped the mitral annulus again during sinus rhythm: no good signals could be recorded and, thus, no energy was delivered there. We successfully carried out the ablation of the sub-epicardial AP in the coronary sinus near the origin of the middle cardiac vein (). Interestingly, atrial tachycardia was easily inducible before ablation, but it could not be induced after the elimination of the AP (). The P-wave morphology during atrial tachycardia was in favor of a left atrial origin. The procedure time was 120 minutes, and the fluoroscopy time was 35 minutes.
|
[[7.0, 'year']]
|
F
|
{'15999040': 1, '9358496': 1, '3964800': 1, '11733398': 1, '24728424': 1, '25372472': 1, '30546690': 1, '8249846': 1, '34144149': 1, '12137336': 1, '7211677': 1, '11050280': 1, '33262322': 1, '23967034': 2}
|
{'3740108-2': 2, '3740108-3': 2}
|
162,621 |
3740108-2
| 23,967,034 |
noncomm/PMC003xxxxxx/PMC3740108.xml
|
Radiofrequency Ablation of Accessory Pathways in Children with Complex Congenital Cardiac Lesions: A Report of Three Cases
|
A 9-year-old girl, weighing 30 kg, presented with recurrent palpitations. Electrocardiography during sinus rhythm revealed a manifest posteroseptal AP (). In the past, she had been diagnosed to have tricuspid atresia (type Ib) with normally-related great arteries, a small ventricular septal defect, and pulmonary stenosis. She had previously undergone extracardiac total cavopulmonary connection and was awaiting fenestration closure with device (because of cyanosis). We conducted an electrophysiological study and documented orthodromic atrioventricular reentrant tachycardia. There were two approaches to the ventricle: 1) from the inferior vena cava into the intracardiac tunnel, fenestration, atria, and left ventricle, respectively; and 2) via the retrograde aortic approach. We opted to ablate the AP via the retrograde approach on account of its less complexity but failed to obtain appropriate signals, containing atrial electrogram. We were, therefore, obliged to resort to the antegrade approach and pass the ablation catheter through the fenestration ( and ). We subsequently ablated the left posteroseptal AP from the atrial aspect of the annulus (). The procedure time was 90 minutes, and the fluoroscopy time was 22 minutes.
|
[[9.0, 'year']]
|
F
|
{'15999040': 1, '9358496': 1, '3964800': 1, '11733398': 1, '24728424': 1, '25372472': 1, '30546690': 1, '8249846': 1, '34144149': 1, '12137336': 1, '7211677': 1, '11050280': 1, '33262322': 1, '23967034': 2}
|
{'3740108-1': 2, '3740108-3': 2}
|
162,622 |
3740108-3
| 23,967,034 |
noncomm/PMC003xxxxxx/PMC3740108.xml
|
Radiofrequency Ablation of Accessory Pathways in Children with Complex Congenital Cardiac Lesions: A Report of Three Cases
|
A 14-year-old boy, weighing 42 kg, presented with recurrent drug (Propranolol and later Amiodarone) refractory tachycardia. Resting electrocardiogram was normal. In the past, he had been diagnosed to have situs inversus totalis with dextrocardia, common atrioventricular canal, and pulmonary stenosis, for which extracardiac total cavopulmonary connection was performed (). Orthodromic atrioventricular reentrant tachycardia was documented (), and the retrograde aortic approach was selected (). The AP was localized to the right posterior region of the common atrioventricular valve. Ablation was successfully performed under ventricular pacing (). The procedure lasted for 60 minutes, and the fluoroscopy time was 12 minutes.\nIn all the cases, the AP was ablated on the atrial aspect of the annulus, using Stinger M, curve D, 7F, 4-mm tip catheters (C.R. Bard, Inc., MA, USA) with a power of 20– 30 Watts in the first case and 40 Watts in the others, and a temperature of 55– 60 °C. The patients were observed for 15 minutes after ablation, and electrophysiological studies were repeated to confirm the abolition of the recurrence of the substrate. Amiodarone was discontinued in the third patient.
|
[[14.0, 'year']]
|
M
|
{'15999040': 1, '9358496': 1, '3964800': 1, '11733398': 1, '24728424': 1, '25372472': 1, '30546690': 1, '8249846': 1, '34144149': 1, '12137336': 1, '7211677': 1, '11050280': 1, '33262322': 1, '23967034': 2}
|
{'3740108-1': 2, '3740108-2': 2}
|
162,623 |
3740109-1
| 23,967,035 |
noncomm/PMC003xxxxxx/PMC3740109.xml
|
Endovascular Treatment of Isolated Bilateral Internal Iliac Artery Aneurysms with a Branched Endograft: A Case Report
|
A 68-year-old male presented with severe pelvic pains. The patient had stable coronary artery disease (with a history of coronary artery bypass), severe left ventricular dysfunction (ejection fraction = 20%), hypertension, and hyperlipidemia. A computed tomography scan revealed a right IIA with a 46-mm aneurysm, a left IIA with a 27-mm aneurysm, and an ectatic right common iliac artery (CIA) (31 mm in diameter). The abdominal aorta (24 mm in diameter) and external iliac arteries (8.5 mm in diameter) were all healthy ().\nThe patient was considered high risk for open surgical repair, and an endovascular solution was developed.\nThe following was implemented via the femoral access. The right IIA aneurysm was embolized using three Cook Tornado embolization coils with a 10-mm tapering diameter (Cook Medical Inc., Bloomington, Indiana). A Zenith Iliac Branch endograft (ZBIS-12-45-41; Cook Medical Inc.) was deployed at the level of the left iliac bifurcation, and a Fluency Plus (Bard Peripheral Vascular, Inc., Tempe, Arizona) peripheral covered stent (9 × 80mm) was deployed in the left IIA (). Finally, a Zenith Flex main body endograft (TFFB-26-96-ZT; Cook Medical Inc.) was inserted from the right CIA; the main body graft was extended into the Zenith Iliac Branch endograft by an iliac leg extension (TFLE-16-56- ZT; Cook Medical, Inc.) and also extended into the right external iliac artery by another iliac leg extension (TFLE-12-107-ZT; Cook Medical, Inc). The procedure lasted for one hour forty-five minutes, and 300 cc of contrast dye was used. The patient was discharged 72 hours post-procedure.\nTwo years after the procedure, computed tomography angiography showed complete exclusion of the bilateral isolated IIA aneurysms, patency of the pelvic arteries, and no signs of endoleaks or device migration ().
|
[[68.0, 'year']]
|
M
|
{'3294450': 1, '11331829': 1, '8632032': 1, '7130268': 1, '28207510': 1, '2795762': 1, '1914397': 1, '8605752': 1, '3130996': 1, '23967035': 2}
|
{}
|
162,624 |
3740469-1
| 23,943,692 |
noncomm/PMC003xxxxxx/PMC3740469.xml
|
Acute Corneal Hydrops following Post-keratoplasty Suture Removal in Pellucid Marginal Degeneration
|
A 31-year-old female patient presented with blurred vision in both eyes which was more severe in her left eye. The problem had started 3 years prior to presentation. The condition had been slowly progressive 6 months prior to her first visit. The patient did not use glasses or any optical aids.\nFamily and past history were unremarkable. Best corrected visual acuity (BCVA) was 2/10 and counting fingers at 2 meters with -18.0-5.0 × 70 and -19.0 in her right and left eyes respectively.\nSlit lamp biomicroscopy showed inferior corneal thinning bilaterally about 2 mm above the limbus with a stromal scar involving the central cornea, extending to the inferior area of thinning in her left eye. The remainder of the ocular examination was unremarkable bilaterally. Corneal topography, showed a crab- claw pattern in the right eye and a very irregular pattern in the left one ().\nPK was performed in the left eye and a 7.50 mm sized recipient bed received a 7.75 mm donor with small inferior graft decentration.\nOn the first postoperative day, the patient was found to have a positive Seidel test and mildly shallow anterior chamber (AC); the microleakage was from a suture tract located at the 6 o’clock position of the host-graft junction. There was no apparent wound gap but a small host-graft mismatch was present. The patient was followed while receiving steroid and antibiotic drops; a few days later the leakage ceased and the AC was fully formed.\nThe rest of her postoperative course was uneventful up to 8 months when her last sutures including the one at 6 o’clock were removed. Several days later, the patient developed acute hydrops at the inferior host-graft area mostly involving the recipient cornea (). Seidel test was positive but the AC was formed. Antibiotic drops were started and the eye was patched; 2 days later the leakage stopped and edema in the inferior recipient cornea decreased. One week later there was no leakage and the hydrops disappeared with final uncorrected BCVA of 2/10 ().
|
[[31.0, 'year']]
|
F
|
{'2643881': 1, '6966644': 1, '6269865': 1, '16462877': 1, '10703124': 1, '16925716': 1, '12686250': 1, '15177959': 1, '23198069': 1, '23943692': 2}
|
{}
|
162,625 |
3740606-1
| 23,956,933 |
noncomm/PMC003xxxxxx/PMC3740606.xml
|
Occipital-posterior cerebral artery bypass via the occipital interhemispheric approach
|
A 70-year-old male with a previous history of bilateral MCA occlusion treated with STA-MCA bypass 20 years ago presented to the emergency room with 3 days of vertigo and nausea. Significant neurological examination findings on admission included horizontal nystagmus and right extremity ataxia. Magnetic resonance imaging (MRI) revealed infarction on the right middle cerebellar peduncle on diffusion-weighted imaging (DWI) as well as poor visualization of the basilar artery. Angiography revealed right VA occlusion and a left VA terminating in a PICA []. Collateral circulation was identified in the distal basilar artery via the diminutive posterior communicating artery of the stenotic right internal carotid artery []. The patient’s level of consciousness decreased to semicoma, and the area of infarction in the cerebellar peduncle and left occipital lobe was noted to have increased. There was a reduction in regional cerebral blood flow (rCBF) in the posterior fossa on N-isopropyl-123I-p-iodoamphetamine (IMP) and single photon emission computed tomography (SPECT). The patient underwent right OA-PCA bypass at 26 days after hospital admission []. His consciousness improved postoperatively, and no further deterioration was observed either in clinical status or on imaging studies. Postoperative angiography revealed patency of the bypass []. He was transferred to a rehabilitation hospital 2 months later with a modified Rankin Scale (mRS) score of 3.
|
[[70.0, 'year']]
|
M
|
{'11189888': 1, '660243': 1, '20559088': 1, '8545776': 1, '23101451': 1, '22068990': 1, '9657206': 1, '18275303': 1, '7057977': 1, '2319313': 1, '3380284': 1, '20106358': 1, '10917358': 1, '21960571': 1, '11213977': 1, '33432972': 1, '1265632': 1, '7155360': 1, '10193628': 1, '23956933': 2}
|
{'3740606-2': 2, '3740606-3': 2}
|
162,626 |
3740606-2
| 23,956,933 |
noncomm/PMC003xxxxxx/PMC3740606.xml
|
Occipital-posterior cerebral artery bypass via the occipital interhemispheric approach
|
A 65-year-old male was admitted to our hospital due to a decreased level of consciousness, nausea, and cerebellar ataxia. Symptoms progressed along with an increase in the size of ischemic lesions in the pons, cerebellum, thalamus, and occipital lobe on DWI, despite intensive medical treatment. Angiography revealed severe stenosis of the left VA, occlusion of the mid-basilar artery, and leptomeningeal anastomosis from the MCA to the PCA []. IMP and SPECT revealed reduced rCBF in the bilateral cerebellar hemispheres and bilateral PCA territory. The patient underwent successful left OA-PICA bypass and right OA-SVG-PCA bypass []. Postoperative angiography revealed opacification of the left distal VA through the OA-PICA bypass and opacification of the upper basilar artery via the OA-PCA bypass []. No neurological deterioration was observed postoperatively. Angiography obtained 1 month postoperatively and MRA obtained 2 months postoperatively both revealed bypass patency.
|
[[65.0, 'year']]
|
M
|
{'11189888': 1, '660243': 1, '20559088': 1, '8545776': 1, '23101451': 1, '22068990': 1, '9657206': 1, '18275303': 1, '7057977': 1, '2319313': 1, '3380284': 1, '20106358': 1, '10917358': 1, '21960571': 1, '11213977': 1, '33432972': 1, '1265632': 1, '7155360': 1, '10193628': 1, '23956933': 2}
|
{'3740606-1': 2, '3740606-3': 2}
|
162,627 |
3740606-3
| 23,956,933 |
noncomm/PMC003xxxxxx/PMC3740606.xml
|
Occipital-posterior cerebral artery bypass via the occipital interhemispheric approach
|
A 51-year-old male presented with subarachnoid hemorrhage due to rupture of a PCA aneurysm. The lesion was treated by endovascular coil embolization twice because of coil compaction. Follow-up examination by cerebral angiography at 1 month demonstrated recurrence of coil compaction []. We therefore performed OA-RA-PCA bypass using an occipital interhemispheric approach. The patient subsequently underwent endovascular embolization of the parent artery. The patient experienced upper quadrant hemianopsia due to infarction in the posterior temporal region after the endovascular procedure, which was associated with occlusion of the posterior temporal artery branching at the base of the aneurysm. Three-dimensional CT revealed bypass patency [].
|
[[51.0, 'year']]
|
M
|
{'11189888': 1, '660243': 1, '20559088': 1, '8545776': 1, '23101451': 1, '22068990': 1, '9657206': 1, '18275303': 1, '7057977': 1, '2319313': 1, '3380284': 1, '20106358': 1, '10917358': 1, '21960571': 1, '11213977': 1, '33432972': 1, '1265632': 1, '7155360': 1, '10193628': 1, '23956933': 2}
|
{'3740606-1': 2, '3740606-2': 2}
|
162,628 |
3740615-1
| 23,956,930 |
noncomm/PMC003xxxxxx/PMC3740615.xml
|
Parasellar arachnoid cyst presenting with a nonpupil sparing third nerve palsy mimicking a posterior communicating artery aneurysm in an adult
|
The patient is a 45-year-old male with a past medical history significant for multiple hereditary cavernous hemangiomas and Hodgkin’s lymphoma in remission following treatment with chemotherapy and radiation. He presented to his primary care physician with acute onset double vision, frontal headaches, and lid lag of the right eye. On computed tomography (CT) imaging [], he was found to have a left occipital hemorrhage and was transferred to this facility for further work-up and management. On examination in the emergency room, he was found to have right eye ptosis, papillary dilation as well as restriction of leftward and upgaze consistent with a right third nerve palsy. There was no evidence of subarachnoid blood on the CT scan. A lumbar puncture was performed, which was unremarkable. MRI of the brain [] demonstrated a 2 cm left occipital pole hemorrhage and a 1 cm nonenhancing right parasellar mass with a fluid-hematocrit level that was hyperintense on T2 flair imaging without diffusion restriction that appeared to compress the right third cranial nerve []. These findings were concerning for a thrombosed PCommA aneurysm. Subsequent CT angiography of the head/neck and conventional cerebral angiography revealed normal intracranial and extracranial vessels without filling of the right parasellar mass.\nThe patient was taken to the operating room and underwent a right frontotemporal craniotomy. Intraoperatively, a right parasellar cystic lesion resembling an arachnoid cyst was identified, medial to the third nerve, which was pushed laterally []. The cyst was fenestrated and clear fluid was expressed, which appeared grossly similar to CSF. The fluid was easily aspirated, and there was no evidence of hemosiderin deposition in the cyst wall or of blood products within the cyst. This is in contrast to the suggestion of MRI, which raised the possibility of the content being hemorrhagic. The wall of the cyst was then carefully dissected and sent for permanent section analysis, which confirmed the diagnosis of an arachnoid cyst [].\nImmediately following surgery, the third nerve deficit improved but was still present. At his routine 2-week postoperative visit, he had subjective complaints of intermittent diplopia without evidence of a third nerve palsy on neurologic examination. When he presented for his three-month postoperative visit, he was symptom free and neurologically intact. MRI at that time revealed no evidence of a residual or recurrent arachnoid cyst [].
|
[[45.0, 'year']]
|
M
|
{'6651257': 1, '7701419': 1, '7205328': 1, '16302620': 1, '18057687': 1, '19541275': 1, '18769282': 1, '7279177': 1, '5026541': 1, '3762897': 1, '23956930': 2}
|
{}
|
162,629 |
3740616-1
| 23,956,939 |
noncomm/PMC003xxxxxx/PMC3740616.xml
|
Dural metastasis of Ewing’s sarcoma
|
A 24-year-old right-handed female was admitted to our hospital complaining of a 2-week history of moderate headache and weakness in her left leg for the past 2 days. She did not present with nausea, vomiting, dizziness, or seizures but reported an underestimated weight loss in the last 3 months.\nHer medical history was significant for a Pelvis Ewing’s sarcoma, operated with complete surgical removal and stabilization one and a half year ago [], and was recently diagnosed as having small lung metastases.\nOn admission, the patient’s neurological examination revealed no cognitive deficits but a left sided leg monoparesis with motor strength of 3/5. The deep tendon reflexes in her left leg were hyperreactive and the gait and standing position were impossible. Fundoscopic examination showed a grade II papilledema. The physical examination disclosed neither local signs of relapse at the primary site nor other clinical signs of metastatic spread.\nThe computed tomography (CT) scan showed an extra-axial, dural based, heterogeneously hyperdense, and enhancing lesion in the right frontoparietal parasagittal region, with moderate circumferential edema and mass effect []. No abnormalities in the skull abutting to the tumor were noted [] and imaging features were strongly suggestive of a meningioma.\nMagnetic resonance imaging (MRI) delineated better the tumor with its marked surrounding edema. The tumor appeared hypointense on T1-weighted MRI scans, hyperintense on T2-weighted MRI scans and displayed important enhancement with gadolinium. The tumor was attached to the dura of the convexity with present dural tail sign and invaded partially the superior sagittal sinus increasing evidence of a meningeal tumor [].\nThe patient underwent a right frontoparietal craniotomy with an amazing discovery: The tumor was associated with a small lobulated epidural extension tightly attached to the skull []. Macroscopic examination showed a reddish gray, rubbery in consistency and vascular tumor of dural origin. The tumor invaded the superior sagittal sinus but has clear delineation with cerebral parenchyma allowing near total excision; only a small portion involving the superior sagittal sinus was left and the remaining dural edges were coagulated.\nThe definitive histological diagnosis was metastatic Ewing’s sarcoma. The tumor was composed of densely packed, small round, dark staining cells with scanty cytoplasm on light microscopy []. A strong MIC-2 antigen expression was noted on immunohistochemical study.\nThe patient’s immediate postoperative course was uneventful, and she recovered quickly. Her neurological condition improved continuously, and follow-up examinations showed that the monoparesis had disappeared completely. A postoperative CT scan confirmed the extent of tumor resection with a postoperative craniotomy defect [].\nThe patient was administered a 55 Gy radiation therapy along with an adjunctive high dose chemotherapy associating alkylating agents and doxorubicin. Clinical status remained unchanged till the most recent follow-up examination, 8 months after surgery.
|
[[24.0, 'year']]
|
F
|
{'12452913': 1, '19190443': 1, '1262921': 1, '16202829': 1, '22174504': 2, '1745510': 1, '4189632': 1, '17337936': 1, '23345116': 1, '10626936': 1, '23292309': 1, '19533369': 1, '20547982': 1, '18525458': 1, '6367949': 1, '18235353': 1, '6722828': 1, '10658458': 1, '11419971': 1, '17316802': 1, '15815902': 1, '10472562': 1, '21856094': 1, '20039192': 1, '21516517': 1, '23717792': 1, '19841565': 1, '16131451': 1, '9818856': 1, '8840962': 1, '9698007': 1, '16551995': 1, '9286296': 1, '18253079': 2, '1995522': 1, '15939194': 1, '26266142': 1, '22024233': 1, '12972518': 1, '22587874': 1, '19148905': 1, '15929128': 1, '23956939': 2}
|
{'3237178-1': 1, '2627171-1': 1}
|
162,630 |
3740618-1
| 23,956,938 |
noncomm/PMC003xxxxxx/PMC3740618.xml
|
Facial necrosis after endovascular Onyx-18 embolization for epistaxis
|
A 52-year-old African-American woman with a history of aortic valve replacement, mitral valve repair, and deep venous thrombosis on chronic anticoagulation therapy with warfarin and aspirin presented after developing epistaxis from her right naris. She received blood products, underwent packing, ligation of the sphenopalatine artery, and silver nitrate cauterization with no resolution of her epistaxis.\nThe bleeding persisted and the patient underwent endovascular embolization. Under general anesthesia, transarterial embolization was carried out through a right femoral artery approach. A 6-Fr guiding catheter (Envoy; Cordis Endovascular Systems, Miami Lakes, FL) over a hydrophilic guidewire was placed into the left and right external carotid arteries (ECAs). A MarathonTMMicro Catheter (Covidien, Irvine, CA) was advanced over a X-pedionTM0.010" Guidewire (Covidien, Irvine, CA) into the left and right internal maxillary arteries and the left and right facial arteries. After confirmation that no opacification of the orbital contents was seen after injection of contrast, the catheter was slowly flushed with 0.5 cc of DMSO. Onyx-18 was injected until a cap formed over the catheter tip that allowed a small amount of reflux. After allowing the cap to solidify, the vessels were embolized with 0.8 cc of Onyx-18 over a period of minutes []. Repeat runs showed that there was adequate occlusion.\nOn postembolization day 3, the patient noticed a hyperpigmented patch on her left cheek that appeared, prompting dermatologic evaluation []. The plaque exhibited hyperpigmentation with surrounding erythema and was tender to palpation. A punch biopsy was performed at the left melonasal junction. Examination of the biopsy revealed full-thickness epidermal necrosis, as well as necrosis of the upper and mid-dermis, follicles, sebaceous glands, and eccrine glands []. Topical ointment and dressing changes were recommended, and no further treatment was required with eventual resolution of her skin necrosis months later.
|
[[52.0, 'year']]
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F
|
{'28508924': 1, '10556410': 1, '6410333': 1, '21472510': 1, '23350775': 1, '4818964': 1, '9917032': 1, '19372207': 1, '17698554': 1, '16491390': 1, '19949825': 1, '22537130': 1, '21476804': 1, '9927959': 1, '23350776': 1, '15966700': 1, '23956938': 2}
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{}
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162,631 |
3740655-1
| 23,956,546 |
noncomm/PMC003xxxxxx/PMC3740655.xml
|
Endodontic management of a mandibular second premolar with perforating internal resorption by using MTA and cone beam computed tomography as a diagnostic aid
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A 54-year-old woman reported to the dental office with pain and swelling in the right mandibular posterior region. The medical history was non-contributory. She had no history of traumatic injury or orthodontic treatment. Clinical examination showed small intraoral swelling with relation to 45. The tooth was slightly tender to percussion and served as an abutment to a long span bridge extending upto 48. The probing depths were within normal limits.\nIntraoral periapical radiographic examination revealed a well-circumscribed, fairly round radiolucency in the cervical third of the root with diffuse periapical rarefaction []. Clinical symptoms and radiographic examination suggested a diagnosis of internal resorption and pulp necrosis. The Bridge was cut and removed to preserve the integrity of tooth with resorption and endodontic treatment was scheduled. It was decided not to include 44 as the patient was reluctant to sacrifice a healthy tooth and was ready to wear a partial denture in case of future loss of tooth. Implant was not considered due to financial constraint of the patient. As the conventional intraoral radiographs do not indicate the true size and spread of the lesion, the patient was sent for CBCT to evaluate the true size and nature of the lesion. Informed consent was obtained from the patient and a CBCT imaging of the mandible was performed by using the CBCT scanner (CS 9300 3D Digital Imaging System, Hatfield, PA). The involved tooth was focused, and the morphology was obtained in axial sections of 90 μm thickness with 300 μm spacing. The CBCT images revealed well-circumscribed radiolucent area with relation to 45 below the level of cemento-enamel junction, involving the distal wall of the root and extend apically upto the middle of the root length suggestive of perforating internal resorption [].\nBased on above finding, root canal therapy was initiated. The tooth was isolated under rubber dam (Hygienic Dental Dam, Coltene Whaledent, Germany) and accessed without anesthesia. The necrosed pulp tissue was removed. Presence of hemorrhagic fluid in the canal suggested of a small communication between the resorptive defect and the lateral periodontium. Working length determination was established using apex locator (Root ZX II; Morita, Tokyo, Japan) and radiography []. The canal was prepared using crown down technique with ProTaper files (Dentsply, Tulsa dental specialities, Ballaigues, Swizterland) accompanied by copious irrigation with 2.5% sodium hypochlorite (Dentpro, Chandigarh, India). A calcium hydroxide paste dressing (Metapex; Meta Biomed Ltd, Choenju city, Chungbuk, Korea) was placed to alkalinize the environment and control bleeding at the perforation. The calcium hydroxide dressing was changed twice every 15 days. Master cone radiograph was taken [] and the canal below the resorptive defect was obturated with gutta percha (Dentsply, Maillefer) and AH Plus sealer (Dentsply, Maillefer, Konstanz, Germany) using a combination of cold lateral condensation and vertical compaction with heated pluggers and condensers. The resorptive defect and the remaining canal were then condensed with MTA (Proroot MTA, Maillefer, Dentsply, Swizterland), using MTA carrier and root canal pluggers [] (Dentsply, Maillefer). Since the perforation was very small it was decided not to place a matrix. A wet cotton pellet was placed on this and the access was temporarily sealed with MD Temp (Meta Biomed Ltd, Choenju city, Chungbuk, Korea). An immediate postoperative radiograph was taken to confirm a satisfactory filling of the resorptive defect []. Fourty-eight hrs later after checking the set of MTA the access cavity was finally sealed with light cure composite resin (Tetric Ceram, Ivoclare, and Vivadent). Finally, porcelain fused to metal fixed partial denture was placed after 4 weeks.\nThe patient was recalled after 3 months and 6 months and the tooth was found to be symptom-free with healthy gingiva. The periapical radiographs also showed satisfactory healing of the apical rarefaction and also formation of a calcific barrier between the perforation and lateral periodontium []. This was further confirmed with 6 month follow up CBCT scan [].
|
[[54.0, 'year']]
|
F
|
{'15347295': 1, '15709102': 1, '11504000': 1, '31641540': 2, '11202867': 1, '24944458': 2, '9759017': 1, '24944447': 1, '23349568': 2, '1778624': 1, '17580820': 1, '12929703': 1, '17442017': 1, '19840636': 1, '19627378': 1, '9477824': 1, '23112490': 2, '8151240': 1, '7595152': 1, '28512497': 2, '22144822': 2, '10323155': 1, '18215687': 1, '20630282': 1, '9550034': 1, '10321187': 1, '23956546': 2}
|
{'3482756-1': 1, '5431715-1': 1, '3548344-1': 1, '3548344-2': 1, '3548344-3': 1, '3227300-1': 1, '6770450-1': 1, '4056406-1': 1}
|
162,632 |
3740656-1
| 23,956,547 |
noncomm/PMC003xxxxxx/PMC3740656.xml
|
Type I canal configuration in a single rooted maxillary first molar diagnosed with an aid of cone beam computed tomographic technique: A rare case report
|
A 25-year-old male patient reported to the Department of Conservative Dentistry and Endodontics with the chief complaint of severe pain in the left upper back region of the mouth since 3 days. Pain was continuous and aggravated with the intake of hot and cold beverages. Clinical examination revealed deep mesial caries approximating pulp with respect to tooth # 26. The tooth was not tender to percussion and palpation. Pulp vitality testing using an electric pulp tester (Parkell, Farmingdale, NY, USA) showed exaggerated response lasting for several minutes. Further, the maxillary lateral incisors were missing and the deciduous right maxillary first molar was overretained. Intraoral periapical radiograph of tooth # 26 revealed deep caries involving the pulp space []. Also, a single root with single canal was seen in relation to 26 and 27. Based on the clinical and radiographic findings, the diagnosis of acute irreversible pulpitis was made and patient was advised root canal treatment in relation to tooth # 26. After obtaining patient's consent, an emergency pulpotomy was performed at the same visit under local anesthesia. In order to confirm the apparent finding of the IOPA radiograph, the patient was referred for CBCT imaging of tooth 26 with 3D reconstruction. The results of the CBCT showed the presence of a single root with the Vertucci's type I canal configuration,[] and the same was observed for tooth 27 []. Thereafter, the root canal treatment was initiated. The tooth was isolated using rubber dam and access preparation was modified to completely de-roof the pulp chamber, which showed the presence of a single wide root canal orifice. Working length was calculated using an electronic apex locator (Root ZX II™, Morrita, Tokyo, Japan) as well as the radiographic method. Working length radiograph also suggested positioning of endodontic files in a single canal []. The coronal shaping was carried out using Gates Glidden burs (Dentsply, New Delhi, India) in crown down manner followed by step back technique with an apical enlargement up to size 55 K file (Dentsply) along with copious irrigation with 5% sodium hypochlorite solution. The canal was finally rinsed with 17% EDTA solution and dried with absorbent paper points (Dentsply, New Delhi, India). The root canal was obturated using a resin-based endodontic sealer (AH PLUS™; Dentsply) and laterally condensed gutta percha followed by restoration of access preparation with silver amalgam. Posttreatment radiograph showed the adequate sealing of the root canal system and the patient was asymptomatic []. The patient was advised complete coverage restoration and referred to the Department of Prosthodontics for the same.
|
[[25.0, 'year']]
|
M
|
{'26858500': 1, '20660981': 1, '18926738': 1, '22794206': 1, '18329571': 1, '26023655': 1, '21444221': 1, '17931947': 1, '20850665': 1, '24944458': 2, '25125860': 2, '29075424': 2, '6595621': 1, '16793482': 1, '22842260': 1, '17942346': 1, '24944447': 1, '23956547': 2}
|
{'4127706-1': 1, '4056406-1': 1, '5650224-1': 1}
|
162,633 |
3740659-1
| 23,956,590 |
noncomm/PMC003xxxxxx/PMC3740659.xml
|
Apexification with calcium hydroxide and mineral trioxide aggregate: Report of two cases
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A 9-year-old female patient reported complaining of pain in the upper front tooth since 3 days. There was a history of trauma to the same tooth due to fall about 4 days back. On clinical examination, Elli's Class III fracture in permanent maxillary right central incisor was evident. Periapical radiograph showed incomplete root formation with wide open apices for the same tooth []. Apexification with calcium hydroxide dressing was planned. In the first visit, an access cavity was prepared with a straight line entry into the root canal. The working length was established within one mm of the radiographic apex by using size 30 Hedstrom file. Next, pulp extirpation and complete debridement of the canal was done using H file number 40 followed by copious irrigation with normal saline. After drying of the canal using paper points, calcium hydroxide powder was mixed with normal saline and this mixture was placed into the canal and pushed to the short of apex using plugger. Access opening was restored with glass ionomer cement []. Patient was called after 3 months. After 3 months when patient came back, a periapical radiograph was taken, which showed complete formation of the root apex in maxillary right central incisor, without any signs and symptoms and periapical radiolucency. Clinically, apical barrier formation was confirmed by using a size 30 Gutta-percha (GP) point to check for the presence of a resistant “stop” and absence of hemorrhage, exudates or sensitivity []. In the next visit, complete obturation was carried out with GP using lateral condensation technique [] followed by composite restoration.
|
[[9.0, 'year']]
|
F
|
{'9078646': 1, '29619378': 1, '29659350': 1, '29670732': 1, '15660748': 1, '30364277': 1, '3214629': 1, '5221182': 1, '9364090': 1, '296242': 1, '23956590': 2}
|
{'3740659-2': 2}
|
162,634 |
3740659-2
| 23,956,590 |
noncomm/PMC003xxxxxx/PMC3740659.xml
|
Apexification with calcium hydroxide and mineral trioxide aggregate: Report of two cases
|
An 11-year-old male patient reported with a chief complaint of discolored right maxillary central incisor with a history of trauma 1 year back. The concerned tooth did not respond to both electric and heat test. The periapical radiograph revealed a large blunderbuss canal of the same tooth []. On clinical examination, Ellis Class IV fracture in permanent right maxillary central incisor was evident. Apexification with MTA was planned. Access opening was prepared under rubber dam isolation and working length was determined. Pus was extruded from the root canal immediately after the access preparation; irrigation was done with saline. Biomechanical preparation was carried out using 80 size k file with circumferential filing motion. Root canal debridement was done using alternative irrigation with 2.5% NaoCl and saline. Calcium hydroxide was placed in the root canal and patient recalled after 5 days. At subsequent appointment, canal was irrigated with 2.5% NaoCl and 2% chlorhexidine. The canal was dried with paper points and MTA placed with pluggers until thickness of 6 mm []. A wet cotton pellet was placed in the canal and access cavity was sealed with temporary cement. In next appointment, root canal was obturated with GP using lateral condensation technique. Access cavity sealed with glass ionomer cement [].
|
[[11.0, 'year']]
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M
|
{'9078646': 1, '29619378': 1, '29659350': 1, '29670732': 1, '15660748': 1, '30364277': 1, '3214629': 1, '5221182': 1, '9364090': 1, '296242': 1, '23956590': 2}
|
{'3740659-1': 2}
|
162,635 |
3740661-1
| 23,956,592 |
noncomm/PMC003xxxxxx/PMC3740661.xml
|
Hyperplasia of the mandibular body: An anomaly in a developmental anomaly
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A 30-year-old male reported to dental O.P. with the complaint of asymmetric appearance of the face. The swelling had been present from childhood and had become evident after puberty. Patient had no history of significant medical problems, trauma or family history of any hereditary disease.\nClinical examination revealed a diffuse enlargement of the lower one-third of the right side of the face. The enlargement was also seen to involve the lower border of the right mandible []. Intra oral examination revealed a swelling involving both the buccal and lingual aspect of the right mandible. The enlargement was more prominent on the buccal side, extending from the distal aspect of 45 to the distal aspect of 47 obliterating the vestibule. On palpation, the enlargement was bony hard in consistency. No sign of inflammation of the overlying mucosa was seen. Intra oral examination revealed an impacted 38 and missing 48 []. Furthermore, observed was that the lesion had not caused any malocclusion [].\nOrthopantamogram (OPG) revealed an increase in vertical height of the body of the right mandible of normal bone density. The ramus and condyle of the affected side were normal. An OPG taken at the age of 25 years (5 years back) and the current OPG showed the lesion was stable [].\nComputed tomography (CT) axial image revealed a solitary well-defined homogenous mass seen on the right body of the mandible measuring around 2 cm × 3 cm with uniform radiopacity. Bony enlargement was seen on both buccal and lingual side, buccal aspect being more prominent than the contralateral side. The bony enlargement can be well-appreciated in three dimensional (3D) CT. Furthermore observed in the radiographs, the enlargement was restricted to the body and did not extend to the condyle, which later aided in the diagnosis [].\nThe histopathology showed compact bone and numerous, small marrow spaces. The compact bone exhibited reversal and resting lines with osteoblastic rimming. Osteocytes could also be seen entrapped within the bone [].\nBased on the clinical, radiographic and histopathologic findings the diagnosis of hyperplasia of the right mandible was given.
|
[[30.0, 'year']]
|
M
|
{'12387615': 1, '1066978': 1, '17465670': 1, '3461097': 1, '27140175': 1, '23956592': 2}
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{}
|
162,636 |
3740662-1
| 23,956,593 |
noncomm/PMC003xxxxxx/PMC3740662.xml
|
Rare form of cherubism: Case report with review of literature
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A 9-year-old male child reported to the Oral Medicine Department with the chief complaint of swelling over the right side of face for the past 3 years. Swelling started initially as smaller in size at 6 years of age, which gradually increases in size to attain the present size. There was no associated pain. Family history revealed second degree consanguineous marriage of his parents. On extra-oral examination, facial asymmetry was detected. Diffuse swelling was noticed over right side of the face measuring about 5 cm × 4 cm []. Skin over the swelling was smooth. Inspectory findings such as site, size, shape, surface, extent secondary changes were confirmed. There was no local rise in temperature, no tenderness, hard in consistency. Skin over the swelling was freely movable. Two right submandibular lymph each measuring about 1.5 cm × 1 cm in dimension, smooth, freely movable, non-tender and oval in shape was noticed. A single left submandibular lymph each measuring about 1.5 cm × 1 cm in dimension, smooth, freely movable, non-tender and oval in shape was noticed. No submental, upper deep cervical, lower deep cervical and supraclavicular nodes were detected. On intraoral examination, there were displacement of 21, 31 and lingually erupted 41, Retained 81, Erupting 12 and 22 []. Clinically, missing 16, 46. On palpation of right posterior mandibular region it was nontender and hard. Expansion of cortical plates and right ramus region was felt.\nConsidering all these features with missing 46, associated painless expansion of buccal and lingual cortical plate in molar and ramus region we provisionally diagnosed as dentigerous cyst.\nThe other provisional diagnosis considered is ameloblastoma, fibrous dysplasia and cherubism.\nSerum alkaline phosphatase – 236 IU/L (151-471 IU/L) Serum calcium – 8.0 mg /dl (8.5-10.5 mg /dl) Serum phosphorus – 6.8 mg /dl (2.1-5.6 mg /dl)\nOrthopantamogram (OPG) revealed multilocular radiolucency on the right side mandible with well-defined sclerotic borders extending from molar area to coronoid process involving the entire ramus with sigmoid notch sparing the condyle. A well-defined unilocular radiolucency with sclerotic border was noted in relation to tooth bud of 47. On the left side also similar multilocular radiolucency with well-defined sclerotic border extending from mandibular molar area to coronoid process. There was an unerupted 16, 12, 22.46 impacted [].\nPosteroanterior (PA) view of skull showed greater cortical expansion of right ramus when compared to left side of mandible. These radiographic features are suggestive of Cherubism Computed tomography (CT) showed replacement of mandibular bone by soft-tissue density involving right ramus region and also showed buccolingual bone expansion [].\nMultilocular cyst Central giant cell granuloma Hyperparathyroidism Odontogenic myxoma Aneurysmal bone cyst Metastatic tumors of jaws Central hemangioma of bone\nIncisional biopsy was done in relation to 85 under local anesthesia.\nA tissue section stained with H and E, showed a cellular lesion composed of loose fibrous stroma with interspersed with many multinucleated giant cells, small thin walled blood vessels and scattered sparse mononuclear inflammatory infiltrate []. Fragments of bone are seen in between the lesion. No atypia or evidence of malignancy.\nFinal impression was intraosseous fibrous lesion of jaw consistent with cherubism of mandible.\nBy correlating clinical feature, radiographic feature, histopathological examination a final diagnosis of cherubism of mandible was made.\nA molecular pathogenesis of cherubism has been proposed, with the detection of a mutation in the gene encoding SH3BP2[] and possible degradation of the Msx-1 gene, which is involved in the regulation of mesenchymal interaction during craniofacial morphogenesis.[] The most accepted theory regarding the pathogenesis of cherubism is its association with an autosomal dominant gene, i.e., family inheritance.[] However, there are reports of the cases in which no criteria of heredity could be established, or in which an autosomal recessive pattern of inheritance was suggested.[] In addition to genetic factors, Caballero and Vinals indicated other possible causes of cherubism such as mesenchymal alterations during jaw development, an odontogenic origin or even hormonal and traumatic factors.[] There are indications that the gene SH3BP2 plays a role in regulating the increased osteoblast and osteoclast activities that are seen in normal tooth eruption and point mutations in the gene could cause pathologic activation of osteoclasts.[] Mutation of the gene encoding for fibroblast growth factor receptor III has also been found in some cases of cherubism.\nAs the lesion tends to become static and show regression as the patient approaches puberty. No specific treatment was given. Patient was advised to report every 6 months for review. Patient was followed-up after 6 months. Showed a progressive increase in facial swelling both on the right and left side. Intraoral examination revealed an increase in buccal and palatal cortical expansion in relation to 55 region. OPG and PA view of skull did not show any significant change when compared to first visit []. However, CT scan showed large extensive lytic lesion with soft-tissue density present on both right and left ramus of mandible []. Patient was assured that the disease will regress after puberty and was asked to report after 6 months.\nFirst described by Jones in 1933 as “familial miltilocular cystic disease of jaws.” Renamed as cherubism in 1938 because of classical characteristics of full round cheeks and upward cast of the eyes to the angelic look of the cherubs immortalized by renaissance art. It usually occurs between 2 years and 5 years of age followed by a phase of rapid growth until 7-8 years of age, a phase of slow growth until 12 or puberty, a phase of stabilization of lesions at or after puberty and finally a phase of remission at about 25-30 years. According to recent literature 150 cases reported. Cherubism is typically limited to the craniofacial region. However, there are three reports in the literature that refer to involvement of the ribs. Symptomless non-expansile lesions at the anterior ends of ribs.[] The characteristic upward gaze of patients with cherubism provides the basis for the naming of the disease.[]\nAlthough rare, cherubism has a significant impact on affected children and their families. This is especially true in those cases where aggressive growth leads to facial deformity and functional problems. In majority of cases, cherubism is self-limiting and no surgical treatment is necessary apart from longitudinal clinical and radiographic observation, which should continue into adulthood. In cases of rapidly proliferating cherubism with significant functional consequences, resection may be indicated. Operative intervention does not change the disease progression, but may improve function and appearance.
|
[[9.0, 'year']]
|
M
|
{'11507493': 1, '17307601': 1, '17147794': 1, '17456964': 1, '280370': 1, '18336269': 1, '11355438': 1, '26064398': 1, '26656340': 1, '12907058': 1, '16053841': 1, '23956593': 2}
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{}
|
162,637 |
3740663-1
| 23,956,594 |
noncomm/PMC003xxxxxx/PMC3740663.xml
|
Immediate placement of dental implants in the mandible
|
A 50-year-old male patient presented with a history of moderate periodontitis with Grade 2 mobility of most of the mandibular [] teeth and his profession dictated for an immediate solution. Clinical and radiological evaluation revealed adequate alveolar bone support. Atraumatic extraction of 41 42 43 44 45 51 52 53 54 55 56 57 58 was carried out under local anesthesia [] using lignocaine with adrenalin. Atraumatic extraction using periotomes without excessive enlargement of the socket was done in order to preserve the alveolar bone which is very important to the success of immediate implant placement. The implant size is determined by the help of the root length and diameter also with conventional methods [Figures and ]. The sockets were debrided and 3i Biomet implants 4 mm × 11.5 mm were placed in the extracted sockets of 45 55 12 22 [Figures and ]. Stability was checked by osstell []. Patient was administered appropriate antibiotic and analgesic. A pre-fabricated mandibular provisional denture with a soft reline was placed [].
|
[[50.0, 'year']]
|
M
|
{'16122143': 1, '23858286': 1, '18412575': 1, '11913267': 1, '10874810': 1, '23956594': 2}
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{}
|
162,638 |
3740664-1
| 23,956,595 |
noncomm/PMC003xxxxxx/PMC3740664.xml
|
Ectodermal dysplasia in identical twins
|
A 23-year-old boy presented with a complaint of missing teeth with difficulty in speaking and eating to Farooqia Dental College and Hospital. He was moderately built, poorly nourished and had the typical face of EDA with features like: Frontal bossing, prominent supraorbital ridges, perioral pigmentation, dry skin, depressed nasal bridge, protuberant lips, low-set ears, recession of hair line all along with fine, sparse scanty scalp hair, scanty eyebrow and eye lashes. The left eye was slightly smaller than the right eye and the nails were not very brittle [Figures -]. Informed consent was procured from patients before any findings were reported. He was accompanied by his mother who gave a history of a total of six children born of a non-consanguineous marriage, with the boy and his younger male identical twin also suffering from the same condition since birth []. No other members of the family suffered from this trait. The mother also gave a history of the twins, presenting with partial anodontia in the upper jaw, complete anodontia of the lower jaw, progressive hyper pigmentation around eyes and mouth, complete absence of sweating since birth, repeated episodes of unexplained hyperpyrexia and thirst, which necessitated consistent drinking of cold water. They were of normal intelligence.\nMedical history revealed that the boy complained of frequent headache, dry eyes and poor vision in the left eye. Other systems were within normal limits. Intraoral examination revealed partial anodontia of the maxillary arch with the presence of four teeth suggestive of maxillary central incisors and canines on either side of the midline. The mandibular arch was completely edentulous with poorly developed alveolus. Moderate dryness of the mouth, with inflamed mucosa was evident []. A panoramic radiograph showed the presence of four cone-shaped crowns with roots in the maxilla consistent with central incisors and canines on either side of the midline. The mandibular alveolar ridge was narrow with complete anodontia and with evidence of right impacted canine like tooth [].\nThe younger twin brother also presented with almost the same identical physical and medical findings. He demonstrated good vision with no marked asymmetry of the eyes and a slight increase in scalp hair. Intraoral examination was identical. Examination of the panoramic radiographs of the younger twin showed the presence of four cone-shaped crowns with roots in maxilla consistent with central incisors and canines on either side of the midline. The mandibular teeth were missing with a narrow alveolar ridge. Cephalogram revealed normal growth pattern in both the twins []. Examination of impression and working model [] confirmed it. Since hypohidrosis, hypotrichosis and hypodontia were very evident on physical examination, the twins were diagnosed with hereditary hypohidrotic ectodermal dysplasia (HED) with partial anodontia. Treatment plan consisted of fixed partial dentures (FPD) for the conical shaped maxillary anterior teeth followed by construction of removable dentures.
|
[[23.0, 'year']]
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M
|
{'19008629': 1, '19061621': 1, '19029074': 1, '19189682': 1, '11522173': 1, '19551394': 1, '23956595': 2}
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{}
|
162,639 |
3740665-1
| 23,956,596 |
noncomm/PMC003xxxxxx/PMC3740665.xml
|
Scalpel versus electrosurgery: Comparison of gingival perfusion status using ultrasound Doppler flowmetry
|
A 22-year-old female patient reported, with a chief complaint of small teeth and black gums. On examination, gingiva appeared hyperpigmented (blackish purple in color) and the marginal gingiva was enlarged thick and fibrotic []. Complete medical history and blood investigation was carried out to rule out any systemic condition. A diagnosis of delayed apical migration of the gingiva with hyperpigmentation was made. Treatment plan included gingivoplasty and depigmentation under local anesthesia. The surgical procedure was explained to patient and informed consent was obtained.\nThe procedure was planned to be performed using a scalpel in lower anterior and electrosurgery (surgical techniques performed using controlled, high frequency electrical currents i.e., 1.5-7.5 million cycles/s) in upper anterior to determine the healing pattern with these two different techniques. Gingival vascularity was determined using soft-tissue USG with spectral Doppler study.\nUSG studies were performed using a high definition USG unit with 2D, 3D and color Doppler facilities []. For gingival study, intracavitary convex transducer with 9-5 MHz capacity was used since this probe facilitated adequate and satisfactory intra-oral accessibility. For the study of anterior segment gingiva, a cheek retractor was used and a water filled glove finger was placed over the gingiva. The transducer was applied over the water filled glove finger in a coronal plane with interspersed ultrasonic gel for proper contact. The water filled glove finger served as a water path for the sound waves and provided better clarity and detail. USG settings were adjusted for 4.5 cm depth, which would be adequate for covering the depth of the water path and the gingiva.\nIn Doppler settings, sound waves pass through blood vessels and get scattered (reflected) by moving red blood cells. Color Doppler settings delineate the color coded blood vessels as rounded or oval dots or linear or cylindrical structures. The number of color coded structures will indicate the number of blood vessels in the region under study. Thus, color Doppler gives information about the amount of vascularity in the region of interest. For spectral Doppler studies, pulse wave Doppler cursor is focused over the blood vessels, which are depicted as color coded blood vessels and the update key is pressed. This enables delineation of flow pattern in the gingival graphically. Recording the flow pattern in the form of a graph (spectral Doppler) allows measurement of velocity of flow both in peak systolic velocity (PSV) and end diastolic velocity phases. These values are displayed on the monitor once the tracing over the graph is marked by auto or manual mode. This helps to measure the velocity of flow.\nBy the placement of the transducer in a sagittal plane over both upper (13-23 region) and lower (33-43 region) segments, study of the gingiva in both arches is possible in the same field.\nPre-operatively the spectral Doppler study was performed in both upper [] and lower anterior gingival segment []. The PSV was determined.\nAfter administration of local anesthesia, gingivoplasty and depigmentation (the entire pigmented epithelium along with a thin layer of connective tissue was removed) was performed using No. 15 blade (scalpel) in lower anterior segment [Figures and ]. Hemostasis was obtained using sterile gauze and applying direct pressure on the surgical wound.\nIn relation to upper anterior segment, the procedure was performed using the electrosurgery. Using a loop electrode, the entire pigmented epithelium along with a thin layer of connective tissue was removed by a planning motion from the mucogingival junction to the marginal gingiva [Figures and ]. The region was irrigated with saline frequently to dissipate the heat generated by the electrode. Care was taken that the electrode did not touch the bone. Compared with the surgical technique carried out by using a scalpel, the electrosurgery procedure produced less bleeding, which offered better visibility. Patient was placed on analgesics and 0.2% chlorhexidine digluconate mouth rinse twice daily for 2 weeks.\nPatient was recalled on 7th, 15th and 30th day following surgery. Both clinical examination [Figure -] and spectral Doppler studies [Figure -] were performed in upper and lower anterior region to compare the perfusion state.
|
[[22.0, 'year']]
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F
|
{'4529261': 1, '16327140': 1, '17625623': 1, '4164520': 1, '9922763': 1, '1113878': 1, '25624625': 1, '1053800': 1, '1069751': 1, '30344388': 1, '13629825': 1, '6935992': 1, '25738096': 1, '5252096': 1, '12420570': 1, '4272072': 1, '3856796': 1, '15733147': 1, '23956596': 2}
|
{}
|
162,640 |
3740666-1
| 23,956,597 |
noncomm/PMC003xxxxxx/PMC3740666.xml
|
Early rehabilitation of facial defects using interim removable prostheses: A clinical case report
|
A 58-year-old woman presented to the dental hospital for prosthetic evaluation after a rhinectomy. The examination revealed a partial nasal resection leaving the bridge of the nose intact []. Healing was noted to be progressing well, though residual swelling and tenderness persisted. Patient expressed dissatisfaction with her appearance and was especially concerned about attending an upcoming social event because of her facial disfigurement. The patient elected to proceed with the fabrication of an interim nasal prosthesis.\nA facial moulage was made using standard dental impression material to permit the fabrication of a stone cast [] of the face. A model of the planned nasal prosthesis was sculpted in wax on this resultant cast using the remaining normal anatomic landmarks for reference []. An interim nasal prosthesis was processed from the wax model using self-cure acrylic resin with extrinsic coloring incorporated to match the surrounding skin tones. The bridge of the nose provided enhanced support for the prosthesis and eyeglass frames. At the subsequent 4-week follow-up appointment, the prosthesis was noted to be functioning well. Patient stated that she was satisfied with the cosmetic resulting [] and had felt very comfortable attending the social event while wearing the prosthesis. Definitive surgical reconstruction was scheduled to be performed at a later date.\nWhite surgical tape was used to permit easy masking, to anticipate discrepancies in marginal fit as healing progressed and to create the illusion of a less extensive surgical procedure having been performed. Retention of the prosthesis was obtained through the use of a medical-grade adhesive augmented by surgical tape, eyeglasses and the use of an eye patch over the prosthetic eye and tied behind the head. Patient accommodated the prosthesis well and was discharged to return to his out-of-state home with plans to return for reconstructive surgery after an adequate disease-free period had elapsed.
|
[[58.0, 'year']]
|
F
|
{'10512955': 1, '25587390': 2, '2079679': 1, '10384160': 1, '23956597': 2}
|
{'4288918-1': 1}
|
162,641 |
3740667-1
| 23,956,598 |
noncomm/PMC003xxxxxx/PMC3740667.xml
|
Mucormycosis in maxilla: Rehabilitation of facial defects using interim removable prostheses: A clinical case report
|
A 65-year-old male patient came to our hospital with the complaint of pain and difficulty in taking food of 6 months duration. Patient was apparently normal 1 year before this, he developed pain and swelling in the upper jaw region which gradually increased in size to present size. Pain was continuous and radiating to the temporal region had aggravated with movement of the head, patient was febrile. He gave a history having undergone extraction of mobile maxillary teeth 6 months before. He reported to our clinic with present symptoms. Apparently following the extraction, the socket never healed completely.\nPatient was a known diabetic on irregular treatment with oral hypoglycemics for the last 10 years. On general examination, middle aged man conscious and co-operative, febrile, no signs of anemia and jaundice. Intraoral oral examination showed [] exposure of black bare bone with the loss of mucoperiosteum over the entire maxillary alveolar process of palate up to the soft palate region with palatal fistula in the soft palate region.\nOn radiological examination [], computed tomography scan revealed erosion of the anterolateral wall of right maxillary antrum with thickening of the sinus lining with moth eaten appearance of the maxillary bone seen.
|
[[65.0, 'year']]
|
M
|
{'1521890': 1, '12684969': 1, '15583532': 1, '8464609': 1, '8762321': 1, '30805232': 2, '33152595': 1, '6489224': 1, '14613095': 1, '29721234': 2, '27162751': 1, '23956598': 2}
|
{'6362471-1': 1, '5923886-1': 1, '5923886-2': 1}
|
162,642 |
3740668-1
| 23,956,599 |
noncomm/PMC003xxxxxx/PMC3740668.xml
|
Benign fibroushistiocytoma of the gingiva
|
A 23-year-old male patient reported with a chief complaint of a growth on the gums of the lower front teeth region for past 1 month. The growth was small when he noticed it and gradually increased in size. Clinical examination revealed two small growths, on both the buccal and lingual aspect of the interdental papillae of 32 and 33. The surface of these growths appeared reddish pink in color measuring around 1 cm × 1 cm in size. On palpation, the growth was firm in consistency and non-tender [Figures and ].\nAn excisional biopsy was carried out and both the buccal and lingual growth were submitted separately for histopathological investigations. The section made from the buccal growth showed a connective tissue mass devoid of epithelium. The connective tissue showed budding capillaries toward the center with dense infiltrate of chronic inflammatory cells. The periphery of the mass appeared to be covered by a pseudomembranous layer.\nThe lingual growth showed a highly cellular connective tissue mass covered by a proliferating epithelium. The lesional cells were plump spindle shaped cells, which in certain areas showed the crisscross pattern or storiform arrangement. The connective tissue had also shown numerous round histiocytic cells and blood vessels.\nThe sections were sent for immunohistochemistry to detect the expression of Vimentin, smooth muscle actin (SMA), desmin, S-100 protein and CD34. The sections showed strong positivity for vimentin and negative expression for vascular, muscular or neural markers [].\nBased on the histopathological features and immunohistochemistry findings, a diagnosis of benign fibroushistiocytoma was given.
|
[[23.0, 'year']]
|
M
|
{'17561319': 1, '21566695': 2, '15329492': 1, '19108402': 1, '27047935': 1, '23956599': 2}
|
{'3091292-1': 1}
|
162,643 |
3740669-1
| 23,956,600 |
noncomm/PMC003xxxxxx/PMC3740669.xml
|
Early correction of class III malocclusion with rapid maxillary expansion and face mask therapy
|
A 10-year-old boy came with a complaint of anterior cross bite to our department. The patient had no relevant past dental or medical history and no habits. On extra-oral examination [], patient had a dolico-cephalic head shape, lepto-prosobic facial form, concave profile, anterior divergence and acute nasolabial angle. All functional examination was normal.\nOn intraoral examination [], all soft-tissues and hard tissues were normal. Maxillary arch was constricted while mandibular arch was broad. Molar, canine and incisor relationship were class III on the both right and left side and there was a reverse overjet of 2 mm and overbite of 5 mm and anterior cross bite. The patient had class III skeletal base with retrognathic maxilla and prognathic mandible having average growth pattern with labially tipped mandibular incisors. The objective of the treatment was (1) to intrude and proclined the upper incisors, (2) to retroclined the lower incisors. (3) obtaining class I canine relation. (4) obtaining ideal overjet and overbite. (5) obtaining ideal esthetics.\nPatient was treated with a combination of face mask and RME [Figures -] until 2 mm positive overjet was achieved. The expansion screw was activated one to three turns (0.25 mm/turn) at weekly visits until the desired amount of expansion had been achieved. The face mask was adjusted to rest on the forehead and the chin of the patient. Elastics (5/16 inch by 14 ounces) were worn from hooks located 2-3 cm in front of the lips to the intraoral attachments located on the expansion appliance, approximately at the gingival level of the canine. The force generated by the elastics was 600-800 g bilaterally.\nAfter duration of 9 months of orthopedic correction, then the pre-adjusted edgewise appliance was fixed with extraction of lower 1st premolar and treatment was continued for 12 months.\nMaxillomandibular relations [Figures and ] showed significant improvements during the treatment period, with changes due primarily to the increase in the Sella –nasion- point A angle (SNA) angle. The Sella-nasion-point B (SNB) angle showed no significant changes during protraction. The dental measurements showed a tendency for the upper incisors to flare during treatment; the lower incisors were uprighted significantly. Upper or lower molar angulations did not change during treatment.
|
[[10.0, 'year']]
|
M
|
{'6576652': 1, '26252015': 1, '3328750': 1, '6947695': 1, '19075377': 1, '1092182': 1, '18331935': 1, '267434': 1, '2363406': 1, '21967936': 1, '3075214': 1, '12695770': 1, '8339762': 1, '7484972': 1, '15520688': 1, '23956600': 2}
|
{}
|
162,644 |
3740671-1
| 23,956,602 |
noncomm/PMC003xxxxxx/PMC3740671.xml
|
Nasal prosthesis for a patient with xeroderma pigmentosum
|
A 15-year-old girl was referred to the department of prosthodontics from Otorhinolaryngology Department, Chennai medical College, for nasal prosthesis. Patient had undergone a partial rhinectomy as a treatment for BCC of nose. The bridge of the nose and nasal bone was included in the resection []. Surgical reconstruction and various prosthetic rehabilitation techniques were discussed, general medical complexity of surgical reconstruction such as inward tissue constriction, collapse of tissues and patient refusal to undergo surgery lead to this method of rehabilitation.\nA silicone nasal prosthesis retained using a spectacle glass frame was decided as a treatment plan. The boundary for the impression was outlined on patient face. Necessary precautions taken and a moist gauze was packed to prevent the flow of the material in to the undesired areas of defect, an impression was taken of the defect together with the adjacent tissue, using an irreversible hydrocolloid impression material (Algitex; DPI, Mumbai).\nThe impression was removed, poured with type III dental stone (Kala Stone; Kala Bhai Pvt. Ltd., India). The model prosthesis was sculpted on the facial cast with no. 2 wax (MDM Corporation, India) []. The wax pattern was then tried on to the patient face, it was checked especially in the border areas and the pattern was reviewed to assess the potential areas for prosthesis retention. Tissue texture and relevant contours were evaluated on the face of the patient [].\nFlasking and dewaxing done. Patients skin tone was used as a guide to match the prosthesis. The silicone material mixed with intrinsic colors on a ceramic slab and compared with patient's skin color tone. The mold was then packed with the prepared material and processed according to the manufacturer instructions. After deflasking, the prosthesis was evaluated on the patient and some extrinsic water resistant coloration was added to make the prosthesis more realistic [].\nAfter the final contouring and matching, the prosthesis was attached to the glass frames []. The eye glasses were used to maximize the retention and to improve the esthetic appearance of the patient. The placement of the prosthesis was demonstrated to patient. Patient was scheduled for the first post-insertion adjustment 1 day after the insertion to ensure the health of the tissues and to relieve any pressure areas on the tissues. Patient was then asked to come for recall visit once in every 3 months for evaluation of prosthesis and observation of any recurrence.
|
[[15.0, 'year']]
|
F
|
{'19212487': 1, '23204739': 1, '18687129': 2, '22124061': 1, '15366532': 1, '15674221': 1, '5276856': 1, '17664721': 1, '23956602': 2}
|
{'2529262-1': 1}
|
162,645 |
3740672-1
| 23,956,603 |
noncomm/PMC003xxxxxx/PMC3740672.xml
|
Palatal pyogenic granulomaa
|
A 22-year-old female patient reported to the Department of Oral medicine and Radiology, with a complaint of growth in the palate for the past 8 months. History reveals that the growth started as a small nodular, which gradually increased to the present size. Patient gives a history of occasional bleeding from the lesion and her medical history reveals that she developed growth during her 2nd month of pregnancy and it has retained after pregnancy.\nOn intra oral examination multiple, well-defined, pedunculated growth is evident in the midpalatal region [], measuring around 2 cm × 2 cm in size, irregular margins, surface lobulated and color appears purplish red and certain parts of the lesion are blanched. The growth is firm in consistency, non-tender, smooth surface and has a narrow pedunculated base with evidence of bleeding from the base of the lesion []. Excision biopsy was carried out under local anesthesia and specimen [Figures and ] sent for histopathological study. Histopathological study confirmed it as PG. On 3 months follow-up, healing was satisfactory and there was no recurrence.\nOn microscopic examination, sections show stratified squamous epithelium with ulceration overlying lobules of proliferating vascular channels amidst inflammatory cells. The impression about the lesion was consistent with lobular capillary hemangioma PG [Figures and ].
|
[[22.0, 'year']]
|
F
|
{'1856307': 1, '2945586': 1, '8829057': 1, '10213': 1, '26697068': 2, '15567370': 1, '11335013': 1, '15982213': 1, '2654195': 1, '23956603': 2}
|
{'4678085-1': 1}
|
162,646 |
3740673-1
| 23,956,604 |
noncomm/PMC003xxxxxx/PMC3740673.xml
|
Hypodontia and hypoplasia of mandible: A rare defect caused by combination therapy
|
A 19-year-old female patient reported to the Department of Oral Medicine and Radiology, K.S.R Dental College and Hospital with the chief complaint of missing teeth in the upper and lower jaw since childhood; she had difficulty in mastication and was feeling esthetically ill. Her medical history revealed that in her childhood she had recurrent history of fever followed, which she visited a physician and the investigation was carried out and diagnosed to have Langerhans cell histiocytosis. History reveals that she had lesions in the skull and mandible at the age of 3 years and was treated with a combination of radiotherapy and chemotherapy radiotherapy of 50 Gy was given in divided doses for a period of 1 year and chemotherapy for about 1 year, patient was under review for about 10 years with no recurrence. Her dental history was not contributory; she gave a history of spontaneous exfoliation of her few deciduous teeth, followed by delayed eruption of permanent teeth. On general examination, patient was normal in stature, appearance and gait. On extra oral examination facial asymmetry was noticed on the left side of the face (the radiation exposed side) [] temporomandibular joint movements were normal and on right and left side deep sigmoid notch was present but more prominent on the left side. On intra oral hard tissue examination revealed clinically present 11, 13, 15, 16, 17, 23, 26, 31, 33, 34, 36, 41, 42, 43, 46, 47 and RS in 62. Hence, there was hypodontia, microdontia of all the teeth and spacing between the teeth [Figures and ].\nOrthopantomogram revealed (a) hypodontia (b) hypoplasia of mandible (c) deep sigmoid notch (d) reduced vertical height of ramus (e) stunted roots of all permanent teeth (f) inversed and impacted 34 and 44 []. Lateral and posteroanterior view revealed no bony lesions, but there was hypoplasia of mandible on the left side with multiple missing permanent teeth [Figures and ].\nPatient was subjected to complete hemogram, serum calcium and phosphorus, which were in normal limits.\nOn the basis of clinical history and radiographic examination, a diagnosis of radiation induced biological changes in bone and teeth were made.
|
[[19.0, 'year']]
|
F
|
{'12621240': 1, '3868771': 1, '12799324': 1, '8192008': 1, '19466236': 1, '19834960': 1, '19459580': 1, '12799323': 1, '23956604': 2}
|
{}
|
162,647 |
3740675-1
| 23,956,606 |
noncomm/PMC003xxxxxx/PMC3740675.xml
|
Interdisciplinary approach for bilateral maxillary canine: First premolar transposition with complex problems in an adult patient
|
A 36 years, 10 month old female patient presented to Department of Orthodontics with a chief complaint of generalized spacing in upper and lower front region of the teeth and irregular arrangement in posteriors of the upper arch. Extra oral examination revealed the patient with an average facial form with symmetrical face, mild convex profile, posterior divergence and competent lips. During smile, both upper and lower incisors were visible within her age limits []. Occlusal examination Showed upper retained deciduous canine with bilateral ectopic eruption of canine buccally between 1st and 2nd premolar teeth []. Clinical and radiographic evaluation show it's a case of complete transposition,[] where crown and root of the respective teeth are found parallel in their transposed position []. Interestingly she doesn't have any other dental anomaly or developmental missing tooth except bilateral occurrence of complete canine transposition. Root morphology was altered with external root resorption in the distal aspect of the mid root section was seen in the upper left 1st premolar tooth. Class I molar relation was seen in the right side. She underwent extraction of left side upper 1st molar, both maxillary 3rd molar and right side lower 3rd molar due to gross decayed condition 5 years back. Further, heavily restored amalgam fillings in relation to the lower left 1st molar and right 2nd molar. Grade II mobility[] and class III gingival recession,[] was seen in both lower central incisors. Cephalometric analysis showed a class I skeletal pattern with proclination of both upper and lower incisors with 0.5 mm over jet and overbite relationship [].\nConsidering the class III gingival recession of both the lower central incisors, free gingival graft was planned initially before orthodontic treatment to improve the periodontal status. Free gingival graft of 8 mm × 5 mm was taken from the donor site of palatal tissue in relation to upper left 1st molar region. Graft was placed such that to increase the width of attached gingiva rather than for recession coverage of the lower incisors []. Fixed orthodontic treatment was started with extraction of both retained deciduous canines in the upper arch with 022 Roth prescription along 0.012 niti wire. Since it's a case of complete transposition, maxillary canine and 1st premolar brackets were interchanged with 1st premolar moved mesially in the deciduous canine position. First premolar was recontoured as canine and canine as premolar respectively. After 3 months, brackets were fixed in the lower arch. Leveling and aligning was done up to 0.019 SS × 0.025 SS in both arches. Orthopantamogram was taken and bracket was repositioned in relation to 14, 21, 23, 24 and 2nd molar banding was done []. Recontouring and restoration was done in relation to 11, 13 and 23. Occlusal settling was completed and space in the 26 region was maintained for prosthesis replacement. After final debonding fixed bonded retainer was placed in both upper and lower arch. A removable Hawley type retainer was also placed in the upper arch [Figures -]. Finally, a three unit metal ceramic fixed prosthesis was done in relation to 26 region.
|
[[10.0, 'month']]
|
F
|
{'2718974': 1, '15794040': 1, '8712493': 1, '2688487': 1, '3858267': 1, '5275504': 1, '29034274': 1, '17826609': 1, '11345569': 1, '23956606': 2}
|
{}
|
162,648 |
3740676-1
| 23,956,607 |
noncomm/PMC003xxxxxx/PMC3740676.xml
|
Oral myiasis in a maxillofacial trauma patient
|
A 40-year-old male patient with maxillofacial trauma reported to the Department of Oral and Maxillofacial Surgery with a chief complaint of inability to close the mouth and difficulty in chewing the food. History revealed trauma 3 days back due to physical assault.\nOn clinical examination, patient had a laceration of upper lip and palatal mucosa []. He also had a posterior open bite. In addition, patient had a very poor oral hygiene []. Further, there were multiple maggots crawling out from the lacerated palatal mucosal wound. Orthopantamogram and computed tomography scan showed a fracture of left parasymphysis, bilateral condyle and left coronoid fracture []. After obtaining a detailed case history, clinical, radiographic and hematological investigations, a diagnosis of maxillofacial trauma with oral myiasis was made. The patient was planned for open reduction and internal fixation for fracture and manual removal of maggots under general anesthesia.\nCotton bud impregnated with turpentine oil was applied to the lacerated mucosa for a minimum of 10-12 min. After these maggots were manually removed with the help of blunt tweezer and curved forceps and then sent for entomological examinations [Figures and ]. Further management included surgical removal of necrotic tissue slough present and irrigating the area with saline, H2O2 and then with betadine followed by metronidazole. After debridement of the region, intermaxillary fixation with plating was done in parasymphysis and condylar region []. The patient was put on tablet Ivermectin 6 mg OD for 5 days along with antibiotic cover of doxycycline 100 mg BD and Metronidazole 100 ml 8 h given for 5 days. The patient was advised to maintain proper oral hygiene and rinse the wound with 0.2% Chlorhexidine mouthwash, 3 to 4 times daily.\nAll maggots were removed including dead larvae in approximately 2 days. Patient was discharged on 4th day after informing about wound care. Follow-up appointment was given. Extra oral sutures were removed and patient was recalled periodically. On the 14th day wound had healed completely [Figures and ]. Lab analysis report of maggots, described it as house fly (musca nebulo) common Indian house fly.
|
[[40.0, 'year']]
|
M
|
{'20578665': 1, '29937673': 2, '26884780': 1, '22919224': 2, '11310129': 1, '34654380': 2, '22114438': 2, '22529629': 1, '22144842': 2, '23956607': 2}
|
{'3220154-1': 1, '5996640-1': 1, '5996640-2': 1, '5996640-3': 1, '3227266-1': 1, '8518163-1': 1, '3425107-1': 1}
|
162,649 |
3740677-1
| 23,956,608 |
noncomm/PMC003xxxxxx/PMC3740677.xml
|
Reconstruction of maxillary cemento-ossifying fibroma defect with buccal pad of fat
|
A 35-year, 10 month-old male patient presented to department of oral surgery with a chief complaint of swelling in the left side of the face with visual disturbances []. Further, he complaints of a huge mass in the upper left dental arch region for past 1 year, which gradually increasing in size with difficulty in mastication and bleeding on touch without any difficulty in pain and swallowing. Past medical history reveals he was affecting nasal obstruction for past 6 months. Visual evaluation shows he was suffering from diplopia. Extra oral examination showed along with swelling in the left region off the face an altered infra orbital bony contour and proptosis. On intra oral examination, a large circumscribed mass involving the left posterior region of hard palate from midline and extended bilaterally displacing the left upper molars and premolars []. Swelling was firm and well-demarcated margin. 2nd and 3rd molar teeth was having grade 3 mobility, displaced, extruded severely below the occlusal plane, bleeding on probing without pain and tenderness.\nOrthopantomogram and contrast enhanced computed tomography scan showed expansible lytic lesion with osseous fragments involving the posterior 1/3 of the hard palate and alveolar ridge corresponding to premolar and molar regions [Figures and ]. Further, it invades the left maxillary sinus involving the floor of the orbit and part of ethmoid. Anteriorly, it involves the right nasal passage abutting the inferior turbinate and blocking the airway. Histopathology report confirmed as COF.\nWeber-Fergusson approach was carried out with en-bloc resection of the tumor [Figures and ]. Following resection closure of palatal defect was carried out using ipsilateral buccal pad of fat by careful, gentle dissection and reconstruction []. Remaining portion was packed with Bismuth Iodoform Paraffin Paste pack and secured with an acrylic stent. Post-operative period was uneventful and healing was favorable and good [].
|
[[10.0, 'month']]
|
M
|
{'14625814': 1, '7677026': 1, '7092025': 1, '20580275': 1, '23956608': 2}
|
{}
|
162,650 |
3741440-1
| 23,946,763 |
noncomm/PMC003xxxxxx/PMC3741440.xml
|
Paranoid Adipsia-induced Severe Hypernatremia and Uremia treated with Hemodialysis
|
A 40 year-old-female\nAltered mentality\nThis previously healthy 40-year-old female was transported to the emergency room by her neighbors, who heard her moaning in her house. She lived alone, and 1 month prior to her admission, she developed the paranoid idea that her water was poisoned, and did not drink any water or beverages since then.\nNon-contributory\nNon-contributory\nHer blood pressure was 100/60 mmHg, pulse rate 106/min, respiration rate 16/min, and body temperature 36.5℃. She looked chronically ill, and her skin and mucosa were extremely dehydrated. There was no evidence of trauma. A chest examination revealed a regular heart beat and clear breathing sounds. The abdomen was soft and flat with no palpable mass.\nShe was light, drowsy and disorientated. Her pupils were intact and reactive. The Glasgow Coma Scale was 11. No cranial nerve problem or peripheral nerve dysfunction was found.\nWhite blood cell count 21,900/mm3 (4000-10,000/mm3), hemoglobin 11.2 g/dL(men 13-17 g/dL: women 12-16 g/dL), hematocrit 51%(men: 42-50%: women 36-44%), and platelets 207,000/mm3 (150,000-400,000/mm3). Her coagulation profile showed an international normalized ratio of 1.71 (1.2 below) and activated partial thromboplastin time of 177.4 sec (24-33 sec). Laboratory chemistry showed blood urea nitrogen 208mg/dL (8.0-20 mg/dL), creatinine 4.90mg/dL(0.6-1.2mg/dL), serum osmolality 452mOsm/L(289-302mOsm/L), protein 7.5 g/dL (6.5-8.2mg/dL), albumin 4.5 g/dL(3.5-5.1 g/dL), ionized calcium 4.6mg/dL (4.2-5.4mg/dL), magnesium 4.5mg/dL (1.9-2.5 mg/dL), serum sodium 172mEq/L(135-145mEq/L), potassium 4.4mEq/L(3.5-5.5mEq/L), chloride 127mEq/L(98-110 mEq/L), total CO2 21mEq/L (24-31mEq/L), aspiratetransaminase 22 IU/L (0-40 IU/L), alanine aminotransferase 16 IU/L (0-40 IU/L), total bilirubin 1.1mg/dL(0.2-1.1 mg/dL), myoglobin 1,949 ng/mL (28-72 ng/mL), creatine phsphokanase 389 IU/L (190 below IU/L), anti-diuretic hormone 8.95 pg/mL(0.0-6.7 pg/mL), adrenocorticotropic hormone (ACTH) 111 pg/mL(10-60 pg/mL), and cortisol 71 g/mL (morning 9.4-26.1/evening 1.8-12.7 g/mL). Breathing room air, the arterial blood gas analysis revealed pH 7.422, PaCO2 35.4mmHg, PaO2 106mmHg, and bicarbonate 22.6mEq/L. Urinalysis showed specific gravity was >1.030, urine pH 5.0, urine osmolality 698mOsm/L (300-900mOsm/L), and urine sodium/potassium/chloride34/85.6/8mEq/L.\nBrain computerized tomography (CT) was normal.\nShe was diagnosed with uremic encephalopathy due to severe prerenal acute renal failure. Her estimated water deficit was 5.94 L. We started intravenous dextrose for 4h, but the changein serum sodium was minimal (171mEq/L). We therefore started hemodialysis to treat the uremic encephalopathy. The dialysate sodium level was 150mEq/L. After dialysis, the serum sodium decreased to 160mEq/L, potassium was 4.2mEq/L, chloride 124 mEq/L, and total CO2 23mEq/L. After a second dialysis treatment, the sodium was 150mEq/L and she became alert without neurological sequelae. We continued an intravenous dextrose fluid infusion with oral hydration, and the sodium level normalized on day 3 of hospitalization (). After discharge, her sodium and chemistry profile remained normal.
|
[[40.0, 'year']]
|
F
|
{'15567546': 1, '10816188': 1, '2368698': 1, '4729012': 1, '11194198': 1, '19837653': 1, '22515501': 1, '15985507': 1, '3718109': 1, '7477631': 1, '28149505': 2, '23946763': 2}
|
{'5265699-1': 1}
|
162,651 |
3741470-1
| 23,946,755 |
noncomm/PMC003xxxxxx/PMC3741470.xml
|
Normalization of Elevated CA 19-9 Level after Treatment in a Patient with the Nodular Bronchiectatic Form of Mycobacterium abscessus Lung Disease
|
A 40-year-old man was referred to our hospital because of chronic cough and sputum. He had been healthy until five years earlier, when cough and sputum developed. He had no history of pulmonary tuberculosis. The patient had no smoking history or other medical history. He appeared relatively healthy, and no signs of fever, chills, weight loss, or digestive symptoms were observed at the time of visit. He was suffering from productive cough, purulent sputum, and right pleuritic pain. His blood pressure was 134/90 mm Hg, pulse rate 78/min, respiratory rate 20/min, and body temperature 36.1℃. Bronchial breathing sound with inspiratory rhonchi was auscultated on the right upper lung field in the thoracic examination. Laboratory results, including immunoglobulin levels, were normal with the exception of elevated serum CA 19-9 to 142.35 U/mL (normal range, <37 U/mL). Pancreas computed tomography (CT) yielded no specific abnormal findings.\nChest radiography revealed cystic changes in the right upper and middle lung zones. A chest CT scan revealed severe bronchiectasis in the right upper lobe and right middle lobe (). There was no evidence of cystic fibrosis or other common causes of bronchiectasis. A sputum Gram stain shows normal flora and routine bacterial culture reveals no pathogens. Numerous acid-fast bacilli were seen in multiple sputum specimens (4+). Nontuberculous mycobacteria were isolated repeatedly from three expectorated sputum specimens and all isolates were identified as M. abscessus by a polymerase chain reaction-restriction fragment length polymorphism method based on rpoB and sequence analysis targeting the rpoB and hsp65 genes. Drug susceptibility testing was performed at the Korean Institute of Tuberculosis by using a broth microdilution method. The isolated M. abscessus was susceptible to amikacin, cefoxitin, clarithromycin, and ciprofloxacin, but resistant to doxycyline.\nThe patient was diagnosed with M. abscessus lung disease, according to the diagnostic guidelines, and began antibiotic therapy with a two-drug oral regimen that included clarithromycin (1,000 mg/day) and ciprofloxacin (1,000 mg/day), along with an initial 4-week course of amikacin (15 mg/kg/day in two divided doses) and cefoxitin (200 mg/kg/day, maximum 12 g/day in three divided doses). Right upper and middle lobectomy was performed because sputum culture was persistently positive after 5 months of antibiotic treatment. Pathologic examinations showed severe bronchiectasis and associated chronic granulomatous inflammation with caseous necrosis. Antibiotics were continued 12 months after surgery. Negative sputum culture conversion was achieved immediately after surgery and was maintained until the completion of antibiotic treatment. The serum CA 19-9 levels returned to the normal range (13.56 U/mL) 1 month after surgery and remained within the normal range (15.51 U/mL) 12 months after surgery ().
|
[[40.0, 'year']]
|
M
|
{'17277290': 1, '33531571': 1, '20833823': 1, '32483216': 1, '10588596': 1, '12153695': 1, '19494536': 1, '19661243': 1, '10436809': 1, '8103656': 1, '33634243': 1, '16832130': 1, '17385665': 1, '19402792': 1, '23946755': 2}
|
{}
|
162,652 |
3741471-1
| 23,946,756 |
noncomm/PMC003xxxxxx/PMC3741471.xml
|
Mycobacterium intracellulare Pulmonary Disease with Endobronchial Caseation in a Patient Treated with Methotrexate
|
A 58-year old woman was admitted to our hospital with a two month history of a worsening productive cough, fatigue and fever. The patient had a 20 year history of RA involving primarily her hands and wrists, and her disease had become refractory to multiple non-steroidal anti-inflammatory drugs over the past several years. Three year ago, the patient had commenced treatment with MTX at a dose of 12.5 mg per week with concomitant acetaminophen 650 mg twice daily. She had achieved control with these medications. She has never had a similar respiratory problem before. She also complained of mild chest pain, shortness of breath, night sweats and anorexia. The shortness of breath was progressive in nature and it was aggravated by strenuous activities and it subsided when taking a rest.\nOn physical examination, the patient appeared chronically ill. She was appropriately alert and oriented. She has a body temperature of 37.8℃ and regular heart rhythm with a rate of 80 beats/min. Her blood pressure was 140/80 mm Hg and the respiratory rate was 25 breaths/min. The respiratory system examination was entirely normal except for bibasilar crackles noted on auscultation.\nAt the time of presentation a complete blood cell count showed a hemoglobin level of 10.9 g/dL and a white blood cell of 6,380 cells/mm3 with 74% neutrophils, and 20% lymphocytes. The other laboratory results were as follows: the erythrocyte sedimentation rate was 28 mm/hr, the C-reactive protein was 6.33 mg/dL, the RA factor was 27.7 IU/mL and the anti nuclear antibody, the anti-neutrophil cytoplasmic antibodies and the anti-ds-DNA were all negative. The anti-human immunodeficiency virus (HIV) antibody was also negative. A chest X-ray revealed multifocal nodular consolidation and ill-defined nodules in both lungs, and this was more prominent in the mid-lung field of the right lung and there was no evidence of mediastinal lymphadenopathy (). Bronchoscopy at this time revealed diffuse actively caseating endobronchial lesions in the left main and left upper lobar bronchus (). The bronchial biopsy specimen from the left main bronchus showed granulomatous inflammation with caseating necrosis (). Ziehl-Neelsen staining of the bronchial washing fluid and expectorated sputum showed acid-fast bacilli (AFB). The polymerase chain reaction test for the specific sequences of M. tuberculosis was negative.\nThe MTX was discontinued. Her RA was treated with hydroxychloroquine sulfate 100 mg twice daily, nambumetone 500 mg twice daily and acetaminophen 650 mg twice daily. She was empirically treated with isonizid (300 mg/day), rifampin (600 mg/day), ethambutol (800 mg/day), and pyrazinamide (1,500 mg/day) for tuberculosis pending the AFB culture results. Subsequently, the fever and cough subsided, and the fatigue and shortness of breath regressed. After 6 weeks, the mycobacterium culture of the sputum and bronchial washing fluid yielded M. intracellurare. The isonizid and pyrazinamide were discontinued. Antimycobacterial therapy was continued with rifampicin, ethambutol, and clarithromycin (500 mg twice daily) for 18 months with a good response. Follow up bronchoscopy after 2 months of therapy revealed that the actively caseating endobronchial lesion had completely resolved. At the return visits 3 and 6 months later, the patient was able to do most of her daily activities without respiratory symptoms, and she well tolerated the antimycobacterial medications without any adverse reactions. The chest X-ray checked at the end of the treatment showed normal findings.\nAt eight months after completing the antimycobacterial medications, the patient was still totally free of respiratory symptoms and the sputum culture for AFB was negative.
|
[[58.0, 'year']]
|
F
|
{'15661020': 1, '17277290': 1, '19033291': 1, '9042656': 1, '25337995': 1, '3579001': 1, '33896863': 1, '3376086': 1, '12468815': 1, '34539814': 1, '20299630': 1, '2736976': 1, '16430744': 1, '16478850': 1, '10524688': 1, '28740687': 1, '17039308': 1, '14969073': 1, '23946756': 2}
|
{}
|
162,653 |
3741472-1
| 23,946,757 |
noncomm/PMC003xxxxxx/PMC3741472.xml
|
Late-Onset Distant Metastatic Upper Urinary Tract Urothelial Carcinoma Mimicking Lung Adenocarcinoma
|
A 50-year-old man was referred to our hospital with presumed lung cancer. He reported blood-tinged sputum for 5 days but was otherwise well. He had a 40-pack-year history of cigarette smoking. Twelve years earlier, after two episodes of gross hematuria, a diagnosis of UC of the renal pelvis had been made at our hospital. Right nephroureterectomy with bladder cuff excision was performed. Pathological examination revealed a UC in the renal pelvis (T1N0M0, grade 2) (), and a tumor involving the ureteral margin. The patient underwent adjuvant chemotherapy (methotrexate, vinblastine, doxorubicin, and cisplatin: three cycles for 3 months). Thereafter, he was followed up through regular cystoscopy and/or abdominal computed tomography (CT) at the urology clinic for 10 years, and no additional tumors were identified.\nAt admission, the serum level of carcinoembryonic antigen was 9.73 ng/mL (reference range, 0.0-6.0 ng/mL). Other laboratory test results were normal. A chest CT scan showed a mass lesion in the left lower lobe of the lung and lymphadenopathy in the left lower paratracheal and subcarinal areas. Bronchoscopic examination revealed no endobronchial lesions. A CT-guided fine-needle biopsy of lung demonstrated histologic features suggestive of adenocarcinoma (). No other primary lesions were found by 18F-fluorodeoxyglucose positron emission tomography/computed tomography, digestive endoscopy, abdominal CT or urine cytology. Brain magnetic resonance imaging revealed brain metastases. Therefore, we diagnosed the patient with advanced lung adenocarcinoma. After brain CyberKnife radiosurgery, he underwent two cycles of cisplatin-based combination chemotherapy, which had no effect. After chemotherapy, a small nodule in the mid-trachea was noted on bronchoscopic examination. Pathological analysis of a bronchoscopic biopsy showed a poorly differentiated carcinoma (). Immunohistochemical analysis showed the tumor cells to be positive for cytokeratin 7 and p63 (), and negative for thyroid transcription factor 1 (TTF-1). These findings suggested possible metastatic UC. All histopathological samples, including the previous UC of the renal pelvis (), CT-guided fine-needle biopsy of the lung (), and tracheal biopsy (), were reviewed. The results of pathologic analysis revealed a high-grade metastatic UC following a previous low-grade UC of the renal pelvis. Systemic re-evaluation revealed concomitant aggravation of lung, esophagus, and bone metastases (). In spite of radiotherapy and supportive care, the patient died as a result of aggravation of multiple metastasis.
|
[[50.0, 'year']]
|
M
|
{'18372021': 1, '21164283': 1, '16707367': 1, '7490804': 1, '21269756': 1, '28144859': 2, '11025695': 1, '5047417': 1, '9301692': 1, '18580098': 1, '21555688': 1, '17957189': 1, '11764070': 1, '19494856': 1, '9763077': 1, '23946757': 2}
|
{'5285295-1': 1}
|
162,654 |
3741473-1
| 23,946,758 |
noncomm/PMC003xxxxxx/PMC3741473.xml
|
A Case of Capillary Hemangioma of Lingular Segmental Bronchus in Adult
|
A 61-year-old man visited to outpatient clinic due to small amount of fresh blood in sputum lasting for a week. He had been treated with asthma and emphysema with inhaled long-acting anticholinergics (Spiriva; Boehringer Ingelheim Pharmaceuticals, Inc., Ridgefield, CT, USA), inhaled corticosteroids (Alvesco; Nycomed GmbH, Milford, MA, USA) and oral theophylline from a year ago in our clinic. He was treated with pulmonary tuberculosis about 30 years ago and had tuberculosis sequelae in right upper lobe. He had smoked 30 pack-year of cigarettes and quit smoking 10 years ago. He had history of hypertension and diabetes mellitus, but has taken neither anti-platelet agent nor anticoagulant.\nOn physical examination, blood pressure was 140/80 mm Hg, heart rate was 88 beats/min, respiratory rate was 20 breaths/min, and body temperature was 36.1℃. The findings of auscultation were not significant. Laboratory tests revealed normal values of complete blood cell count, electrolytes, chemistry profile, arterial blood gas analysis, erythrocyte sedimentation rate, and C-reactive protein concentration.\nSimple chest radiograph showed irregular nodular and linear opacities with volume loss in right upper lobe, which was compatible with inactive pulmonary tuberculosis. The opacities have not been changed in comparison with chest radiograph examined two-months ago. Chest computed tomography showed centrilobular and paraseptal airspace enlargement in both lungs and irregular linear and nodular opacities with distortion of surrounding architecture in right upper lobe. A tiny enhancing nodule was seen at bronchial wall of lingular segment of left upper lobe ().\nFlexible bronchoscopy was performed under local anesthesia and a 3 mm sized polypoid lesion with pinkish color was found on the medial side of left lingular segmental bronchus (). Forcep biopsy was performed to examine and remove the lesion and small amount of bleeding was followed. The amount of bleeding was minimal and the bleeding stopped after endobronchial instillation of 1:10,000 diluted epinephrine. Small amounts of hemoptysis appeared one time after bronchoscopy, then no more hemoptysis was found till 4 weeks after bronchoscopy.\nLight microscopic findings revealed small polypoid nodule which showed proliferation of blood vessels of capillary caliber and surface bronchial epithelium. The bronchial epithelium was partly eroded. Immunohistochemical stain for CD31 demonstrated vascular endothelial cells ().
|
[[61.0, 'year']]
|
M
|
{'10612575': 1, '22722797': 1, '22563274': 2, '25861344': 2, '26982046': 1, '482999': 1, '1137250': 1, '17268168': 1, '11374256': 1, '23946758': 2}
|
{'3337873-1': 1, '4388893-1': 1}
|
162,655 |
3741975-1
| 23,960,347 |
noncomm/PMC003xxxxxx/PMC3741975.xml
|
Acute renal failure as an initial manifestation of acute lymphoblastic leukemia
|
An 8-year-old boy presented with fever, arthralgia, and oliguria. He was treated elsewhere symptomatically. On examination, he had pallor, no lymphadenopathy or hepatosplenomegaly. His blood pressure was 110/70 mm Hg. Investigations showed hemoglobin of 5.2 g/dl; white blood cell count 5,410/cumm; differential count – polymorph 54.8%, lymphocytes 27.2%, monocytes 4.4%, basophils 0.4%, eosinophils 0.2%, platelets 90,000/cumm; and renal functions showed BUN 48 mg/dl and creatinine 3 mg/dl. The peripheral smear was normal. Urine analysis was normal. Serum electrolytes and arterial blood gas analysis were normal. He was given peritoneal dialysis for a week. In view of severe pain in the joints, considering leukemia, uric acid was found to be 18.4 mg/dl and lactate dehydrogenase (LDH) 1,658 U/L. Ultrasound abdomen showed mild nephromegaly. In view of fever, cytopenia involving two cell lineages (anemia and thrombocytopenia), hyperuricemia, and elevated LDH levels, bone marrow biopsy was performed which showed acute leukemia. Flow cytometry confirmed Pre B-cell ALL. Renal parameters normalized within a week of treatment with steroids as per induction protocol, hydration, rasburicase therapy indicating uric acid nephropathy as a cause of renal failure. Currently he is on chemotherapy and is doing well since past 1 year.
|
[[8.0, 'year']]
|
M
|
{'28401105': 2, '18846803': 1, '1068267': 1, '32425404': 1, '31065357': 2, '17251998': 1, '8846137': 1, '5283710': 1, '16844565': 1, '9658725': 1, '29901649': 2, '12928576': 1, '26937086': 1, '23960347': 2}
|
{'3741975-2': 2, '3741975-3': 2, '6024069-1': 1, '6487745-1': 1, '5383591-1': 1}
|
162,656 |
3741975-2
| 23,960,347 |
noncomm/PMC003xxxxxx/PMC3741975.xml
|
Acute renal failure as an initial manifestation of acute lymphoblastic leukemia
|
A 7-year-old girl was brought with complaints of fever, joint pain, and decreased urine output for 3 days. On examination, she was pale, had cervical lymphadenopathy, but no hepatosplenomegaly. She was normotensive. Investigations showed hemoglobin 7.1 g/dl; white blood cell count 24,700/cumm; differential count: Polymorph 30.2%, lymphocytes 68.1%, monocytes 2.2%, eosinophils 0.3%, basophils 0.2%, and platelets 80,000/cumm. Renal function tests showed BUN of 44 mg/dl and creatinine 2.9 mg/dl; renal ultrasound was normal. Peripheral smear showed occasional blast cells. Uric acid was 30 mg/dl and LDH 2,163 U/L. Serum electrolytes, arterial blood gas analysis, and urine analysis were normal. In view of fever, lymphadenopathy, anemia, leukocytosis, blasts in the peripheral smear, hyperuricemia, and raised LDH levels, bone marrow biopsy was planned to rule out hematologic malignancies. Bone marrow biopsy showed acute leukemia and flow cytometry was suggestive of T-cell ALL. She was treated with steroids as per induction protocol with rasburicase and hydration therapy. Renal parameters were normalized after 2 days, which indicates that renal failure was due to uric acid nephropathy. Currently she is receiving chemotherapy and is doing well since 1 year.
|
[[7.0, 'year']]
|
F
|
{'28401105': 2, '18846803': 1, '1068267': 1, '32425404': 1, '31065357': 2, '17251998': 1, '8846137': 1, '5283710': 1, '16844565': 1, '9658725': 1, '29901649': 2, '12928576': 1, '26937086': 1, '23960347': 2}
|
{'3741975-1': 2, '3741975-3': 2, '6024069-1': 1, '6487745-1': 1, '5383591-1': 1}
|
162,657 |
3741975-3
| 23,960,347 |
noncomm/PMC003xxxxxx/PMC3741975.xml
|
Acute renal failure as an initial manifestation of acute lymphoblastic leukemia
|
A 13-year-old boy presented with bilateral swelling in the neck for one week, cough, dyspnea, and reduced urine output for 3 days. Physical examination showed cervical lymphadenopathy and hepatosplenomegaly. He was found to have hypertension, which was controlled with nifedipine. Investigations revealed hemoglobin of 5 g/dl; white blood cell count 300,100/cumm; platelet count 75,000/cumm; uric acid 32.2 mg/dl; LDH 12,720 U/L; and peripheral smear showed 90% blast cells. Renal functions showed BUN 38 mg/dl and creatinine 2.4 mg/dl; urine analysis was normal. Serum electrolytes and arterial blood gas analysis were normal. Renal ultrasound was normal. Bone marrow biopsy and flow cytometry showed features suggestive of ALL (T-cell type). He was started on dialysis, chemotherapy, and tumor lysis supportive measures. Renal parameters normalized after 2 weeks, indicating again the possibility of uric acid nephropathy. Currently he is on chemotherapy.\nA renal biopsy was not performed in our patients as there was complete resolution of renal failure and a definite diagnosis of leukemia was obtained.
|
[[13.0, 'year']]
|
M
|
{'28401105': 2, '18846803': 1, '1068267': 1, '32425404': 1, '31065357': 2, '17251998': 1, '8846137': 1, '5283710': 1, '16844565': 1, '9658725': 1, '29901649': 2, '12928576': 1, '26937086': 1, '23960347': 2}
|
{'3741975-1': 2, '3741975-2': 2, '6024069-1': 1, '6487745-1': 1, '5383591-1': 1}
|
162,658 |
3741976-1
| 23,960,348 |
noncomm/PMC003xxxxxx/PMC3741976.xml
|
Type IV renal tubular acidosis following resolution of acute kidney injury and disseminated intravascular coagulation due to hump-nosed viper bite
|
A 51-year-old male was admitted to the local hospital after a hump-nosed viper bite on his hand while weeding his garden. Since the viper was brought alive by the neighbors, primary care physician was able to make a positive identification of the snake as Merrem's hump-nosed viper (Hypnale hypnale). The patient had severe pain and swelling in the hand. The next day his urine output was reduced and he was transferred to a tertiary care institute for hemodialysis. On admission, patient was conscious and rational, febrile, and he was in pain. He was pale and mildly icteric. He had marked swelling and redness in his right hand with blistering at the bite site.\nHis pulse rate was 92 beats per minute and blood pressure was 118/78 mmHg. On auscultation of the heart, S1 and S2 were heard in normal intensity with no murmurs. Respiratory system examination was normal except for few fine basal crepitations. Abdominal examination was normal with no organ enlargement or free fluid. Neurological examination was normal with no ophthalmoplegia or other cranial nerve paralysis.\nHis investigation results were as follows: white cell count, 12,700 (80% neutrophils); platelet count, 40,000/μl; hemoglobin, 9.9 g/dl; International normalized ratio, 1.46; activated partial thromboplastin time, 43 s; serum creatinine, 1,040 μmol/l; Na, +130 mmol/l; K+, 5.4 mmol/l; erythrocyte sedimentation rate, 10 mm/Hr; C-reactive protein, 1 mg/L; aspartate transaminase, 54 u/l; alanine transaminase, 42 u/l; serum bilirubin, 22.7 μmol/l; total protein, 52 g/l (albumin 33 g/l). Peripheral blood smear revealed marked red cell fragmentation, polychromasia and reduced number of platelets indicating disseminated intravascular coagulation. Serum calcium, 7.7 mg/dl; serum phosphate, 3.1 mg/dl; creatine phosphokinase, 122 u/l; urine microscopy showing 10-12 pus cells and 1-2 red cells per high power field with no casts. Protein was present in urine in trace amounts. Abdominal ultrasound scan revealed enlarged and globular kidneys suggestive of acute renal parenchymal disease. Venom-induced acute tubular necrosis was suspected.\nHe was commenced on hemodialysis. After 12 sessions of hemodialysis, he was dialysis dependent and renal biopsy was performed 8 weeks after the viper bite. The biopsy revealed patchy areas of tubular atrophy with interstitial edema and patchy interstitial chronic inflammation suggesting subacute interstitial nephritis. There was no evidence of acute tubular necrosis possibly because biopsy was performed very late after the onset of AKI. Glomeruli were normal.\nTen weeks after the viper bite, the patient's renal functions and urine output were improved. He was discharged from the hospital to be reviewed in clinic as an outpatient. At the time of discharge, he had a serum creatinine of 1.9 mg/dl and serum potassium of 3.9 mmol/l.\nEighteen weeks after the initial viper bite, he was admitted with sudden onset bilateral lower limb weakness. There was no respiratory muscle paralysis. Both lower limbs had grade two muscle power and upper limbs grade four. Reflexes were diminished and Babinski sign was negative. There was no objective sensory loss.\nDuring this admission, he was found to have acidotic breathing. Arterial pH was 7.31 and PCO2 18 mmHg, PO2 121 mmHg, and HCO3\n− 10.3 mmol/l. His serum potassium level was 7.0 mmol/l with sodium 130 mmol/l and chloride 114 mmol/l. ECG showed tall tented T waves suggestive of hyperkalemia. Serum creatinine was 114 μmol/l with an estimated glomerular filtration rate of 76 ml/min. He was given intravenous calcium gluconate, nebulized with salbutamol and started on insulin-dextrose infusion until an urgent hemodialysis was arranged. There was no history of use of angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), or diuretics like spironolactone.\nBlood anion gap was normal at 5.7 mmol/l. Urine pH was 5.0. Urinary electrolytes were as follows: Na+ 77 mmol/l, K+ 16 mmol/l, Cl− 84 mmol/l, pH 5.0, serum osmolality 300 mosm/kg, urine osmolality 380 mosm/kg, and urinary anion gap was 9 mmol/l. Transtubular potassium gradient (TTKG) was 1.80.\nPresence of hyperchloremic metabolic acidosis and hyperkalemia with normal serum creatinine level was suggestive of type IV renal tubular acidosis. The ability to lower the urine pH to 5.0, positive urinary anion gap, and the low TTKG (less than five) were all supportive evidence for type 4 renal tubular acidosis.\nPatient had a good response to fludrocortisone 100 μg twice daily with the correction of hyperkalemia and the metabolic acidosis. He was discharged while on fludrocortisone with serum potassium of 4.3 mmol/l. Three weeks later, fludrocortisone was stopped as serum potassium was 3.5 mmol/l and he was closely observed for the development of hyperkalemia or acidosis. Eight weeks after discharge, he had potassium of 4.2 mmol/l without any potassium-lowering drug therapy.
|
[[51.0, 'year']]
|
M
|
{'3118260': 1, '25073710': 1, '26099916': 1, '9660472': 1, '1259022': 1, '6386199': 1, '19193780': 1, '33290400': 1, '6679805': 1, '18455743': 1, '10895268': 1, '5476148': 1, '32602439': 1, '8036678': 1, '8758082': 1, '23960348': 2}
|
{}
|
162,659 |
3741977-1
| 23,960,349 |
noncomm/PMC003xxxxxx/PMC3741977.xml
|
Acute oxalate nephropathy due to ‘Averrhoa bilimbi’ fruit juice ingestion
|
A 38-year-old man, who was working abroad and came to India on a vacation, underwent a health check up, which showed normal renal functions and hypercholesterolemia. He consumed a glass of I. puli fruit juice daily for 4 days for control of hypercholesterolemia. After 4 days, the patient developed abdominal discomfort, nausea, and loss of appetite. He presented to our center with the above-mentioned symptoms; he had normal urine output. On examination, the patient was conscious, oriented, blood pressure 150/90 mmHg; he had no edema, and his systems were normal. Investigations showed severe renal failure with serum creatinine of 6.4 mg/dl, with normal hemogram and liver function tests; urine analysis showed no albuminuria, and microscopy showed oxalate crystals. Ultrasonogram of abdomen was normal. The patient underwent two sessions of hemodialysis, following which a left percutaneous kidney biopsy was done. Kidney biopsy showed acute tubular necrosis with many polarizable fractured crystals in the tubular lumina (calcium oxalate crystals) [Figure and ]. 24-h urinary oxalate was 60 mg/day. The oxalate content of the fruit was 25.1 mg per 100 g of the fruit, when analyzed in our lab by spectrophotometry method. He was on hemodialysis for 10 days. His renal functions improved to normal in 6 weeks (serum creatinine: 0.9 mg/dl).
|
[[38.0, 'year']]
|
M
|
{'18335167': 1, '33924791': 1, '2645433': 1, '16925274': 1, '28216948': 1, '12480969': 1, '28975090': 2, '24995136': 2, '30450463': 1, '16408105': 1, '27942177': 1, '9550629': 1, '15808883': 1, '28203564': 2, '11157385': 1, '17185156': 1, '19031370': 1, '8311084': 1, '25374807': 1, '23458924': 1, '17136702': 1, '19356376': 1, '23960349': 2}
|
{'3741977-2': 2, '5607971-1': 1, '5301110-1': 1, '4065667-1': 1, '4065667-2': 1}
|
162,660 |
3741977-2
| 23,960,349 |
noncomm/PMC003xxxxxx/PMC3741977.xml
|
Acute oxalate nephropathy due to ‘Averrhoa bilimbi’ fruit juice ingestion
|
A 57-year-old man, known to have type 2 diabetes mellitus (on diet control) and dyslipidemia (on statins) presented to us with a history of anorexia, nausea, and fatigue for 2 weeks after intake of I. puli fruit juice for 5 days; he was oliguric. He had a normal hemogram, with serum creatinine: 9.3 mg/dl, serum cholesterol: 180 mg/dl. Urine analysis showed 1+ Protein, and microscopic examination of the urine sample showed plenty of oxalate crystals. He was initiated on hemodialysis and subsequently underwent a left percutaneous kidney biopsy which showed acute tubular necrosis with intra tubular calcium oxalate crystals. He needed six sessions of hemodialysis. His renal functions became normal in about 5 weeks’ time.\nSimilar cases have been reported in other hospitals of Kerala. All the patients had history of consuming I. puli juice and developed renal failure. None of the patients had history of renal failure before consuming the fruit juice. The details of these ten patients are given in . All the patients were male, age ranging from 38 to 72 years. Six patients had pre-existing problems like diabetes mellitus or hypertension. Eight out of 10 patients had plenty of oxalate crystals in urine; all the patients had severe renal failure with serum creatinine ranging from 5.5 to 12.3 mg/dl. Seven patients required hemodialysis in view of severe renal failure; the remaining three patients were treated conservatively and renal functions returned to normal. Kidney biopsy was performed in seven patients. All the patients showed acute tubular necrosis with polarizable tubular crystals consistent with oxalate crystals []. The time taken for Serum creatinine to reach the normal level ranged from 2 to 6 weeks.
|
[[57.0, 'year']]
|
M
|
{'18335167': 1, '33924791': 1, '2645433': 1, '16925274': 1, '28216948': 1, '12480969': 1, '28975090': 2, '24995136': 2, '30450463': 1, '16408105': 1, '27942177': 1, '9550629': 1, '15808883': 1, '28203564': 2, '11157385': 1, '17185156': 1, '19031370': 1, '8311084': 1, '25374807': 1, '23458924': 1, '17136702': 1, '19356376': 1, '23960349': 2}
|
{'3741977-1': 2, '5607971-1': 1, '5301110-1': 1, '4065667-1': 1, '4065667-2': 1}
|
162,661 |
3741978-1
| 23,960,350 |
noncomm/PMC003xxxxxx/PMC3741978.xml
|
Acute renal failure secondary to ingestion of ayurvedic medicine containing mercury
|
A 2-year-old girl presented with anuria of 4 days duration. The anuria was preceded by intermittent vomiting for 2 days. She had no preceding fever, diarrhea, skin rash, or red urine. Her physical growth and motor milestones were normal. She was not yet speaking a single word, did not interact with other children, and avoided eye contact. On enquiry, there was a history of intake of medications from a traditional healer for the past 5 months, which according to parents were given to promote normal growth. Physical examination was unremarkable except for a blood pressure of 130/80 mmHg. Her investigations revealed blood urea nitrogen 71 mg/dL, serum creatinine 11 mg/dL, estimated glomerular filtration rate (eGFR) 4.7 mL/min, Na 127 mEq/L, K 5.7 meq/L, hemoglobin 11.1 g/dL, platelet count 3.7 × 103/μL, total leucocyte count 13,900 × 103/μL, and serum lactate dehydrogenase 2000 U/L. Peripheral smear revealed no schistocytes or malarial parasites. Her C3 levels were normal and the antinuclear antibody, anti neutrophilic cytoplasmic antibody and anti-glomerular basement membrane antibodies were negative. Serology was negative for IgM antibodies to leptospira. Ultrasound of the kidneys revealed enlarged kidneys. Renal biopsy [] revealed normal-looking glomeruli, tubules showed moderate neutrophilic infiltration, dilation, and cellular casts comprising neutrophils and tubular epithelial cells. There was no evidence of crystals, viral inclusions, or rupture of tubular basement membrane. Interstitium revealed edema along with mixed infiltration with neutrophils, lymphocytes, and occasional eosinophils, without any evidence of granulomas or fungal elements. Histopathology was suggestive of acute tubulointerstitial nephritis.\nShe was started on peritoneal dialysis and given three intravenous pulses of dexamethasone on alternate days. Subsequently she was put on oral prednisolone at 2 mg/kg/day and was shifted to hemodialysis. She remained dialysis dependent for a total period of 17 days. During this period, she had multiple episodes of convulsions with altered sensorium due to severe hypertension, which required four antihypertensive agents for control. Neuroimaging and electroencephalograph were normal. She developed hemodialysis catheter-related Acinetobacter sepsis, requiring catheter removal and antibiotic therapy. There was a drop in hemoglobin, requiring one packed red blood cell transfusion. The urine output improved after 2 weeks to 1 liter/day over a period of 4 weeks. There was a progressive decrease in creatinine levels to 1 mg/dL (eGFR – 51.7 mL/min) at the time of discharge.\nThe ayurvedic medications were retrieved and sent for heavy metal toxicological screen. The analysis reported 2066.6 ppm of mercury, which amounted to a daily intake of 289.324 micrograms of mercury as against an average daily human intake 2.31 microgram. Lead and arsenic were undetectable. Chelation with D-penicillamine was started and continued for 6 months. Mycophenolate mofetil was added and oral steroids were continued in gradually tapering doses for 6 months. On follow-up, the urine mercury levels were within normal levels. She is now normotensive without medications, has normal creatinine levels (0.7 mg/dL), eGFR-73.8 mL/min, and no proteinuria.\nOn 6-month follow-up, she had begun talking, was friendly, and had started attending play school.
|
[[2.0, 'year']]
|
F
|
{'20721700': 1, '12197264': 1, '29720798': 1, '7563649': 1, '31687105': 1, '27194836': 2, '33840969': 1, '25734058': 1, '31172119': 2, '25253924': 1, '25120305': 1, '30613523': 1, '5432201': 1, '10699136': 1, '25249731': 1, '26730144': 1, '23960350': 2}
|
{'4862267-1': 1, '6548077-1': 1}
|
162,662 |
3741979-1
| 23,960,351 |
noncomm/PMC003xxxxxx/PMC3741979.xml
|
Acute interstitial nephritis due to proton pump inhibitors
|
Our first index case was a 49-year-old female who was on follow-up for hypothyroidism, bronchial asthma, and acid peptic disease. She was taking omeprazole, eltroxin, deriphyllin for 8 weeks before being admitted with complaints of dysphagia and heart burn for 4 days. Here was no fever, loin pain or skin rash. Blood pressure was 140/80 mmHg. On admission, dipstick urinalysis showed 1+ protein and with 4-6 WBCs/hpf. Blood urea was 45 mg/dl and serum creatinine 1.6 mg/dl. Oliguria developed after 48 h and renal failure worsened. Renal ultrasonogram showed enlarged kidneys with increased cortical echoes. In renal biopsy the glomeruli were normal, but interstitium showed diffuse and dense lymphocytic infiltrates covering >90% of the core [].\nOmeprazole was stopped. She was treated with 10 mg/kg of intravenous methyl prednisolone for 3 days followed by oral prednisolone 1 mg/kg tapered to 0.5 mg/kg over 3 months. Her renal parameters gradually improved, but she is left with residual renal impairment with serum creatinine of 1.6 mg % after 1 year.
|
[[49.0, 'year']]
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F
|
{'29854491': 2, '11774962': 1, '9027776': 1, '32128193': 2, '11473672': 1, '33273914': 1, '29502481': 1, '6604293': 1, '32996701': 1, '19520747': 1, '8820506': 1, '16630752': 1, '28571164': 1, '1341422': 1, '31808445': 1, '17722704': 1, '31748498': 1, '30010692': 1, '30155380': 1, '15004262': 1, '29805547': 1, '17635502': 1, '17014549': 1, '30463778': 1, '23960351': 2}
|
{'3741979-2': 2, '3741979-3': 2, '3741979-4': 2, '5952557-1': 1, '7044375-1': 1}
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162,663 |
3741979-2
| 23,960,351 |
noncomm/PMC003xxxxxx/PMC3741979.xml
|
Acute interstitial nephritis due to proton pump inhibitors
|
A 53-year-old female was admitted with a history of vomiting, loin pain for the 2 weeks and oliguria for 4 days. She was a known case of pulmonary tuberculosis who was receiving anti-tuberculosis therapy for the past 2 months. Pantoprazole was started for nausea 3 weeks ago. On examination, she appeared sick, febrile (100.5°F), tachypneic with a blood pressure of 130/80 mmHg. Blood urea was 76 mg/dl, serum creatinine 4.9 mg/dl and serum bicarbonate 14 mEq/L. She was started on daily hemodialysis for 4 days after which her general condition improved. Renal biopsy revealed AIN with dense lymphocyte and eosinophilic infiltrates in the interstitium []. PPI was stopped and she was started on oral corticosteroids for 8 weeks with continuation of anti-tuberculosis therapy. After 4 months her serum creatinine remained high at 1.6 mg/dl. Rifampicin induced AIN was considered unlikely given the temporal profile of events after start of pantoprazole and the fact that renal function rapidly recovered, after withdrawal of the latter with steroid therapy.
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[[53.0, 'year']]
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F
|
{'29854491': 2, '11774962': 1, '9027776': 1, '32128193': 2, '11473672': 1, '33273914': 1, '29502481': 1, '6604293': 1, '32996701': 1, '19520747': 1, '8820506': 1, '16630752': 1, '28571164': 1, '1341422': 1, '31808445': 1, '17722704': 1, '31748498': 1, '30010692': 1, '30155380': 1, '15004262': 1, '29805547': 1, '17635502': 1, '17014549': 1, '30463778': 1, '23960351': 2}
|
{'3741979-1': 2, '3741979-3': 2, '3741979-4': 2, '5952557-1': 1, '7044375-1': 1}
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162,664 |
3741979-3
| 23,960,351 |
noncomm/PMC003xxxxxx/PMC3741979.xml
|
Acute interstitial nephritis due to proton pump inhibitors
|
A 22-year-old male was admitted with history of oliguria and back pain of 1-week duration. He had received pantoprazole and paracetamol for 10 days as treatment for dyspepsia and body ache. On examination, there was no fever, BP was 140/80 mm Hg, blood urea was 123 mg/dl, and serum creatinine 10.7 mg/dl. Hemodialysis was started. Renal biopsy showed AIN with lymphocytic and eosinophilic infiltrations in the interstitium with normal appearing glomeruli. PPI was stopped and he was started on pulse methyl prednisolone for 3 days followed by oral prednisolone for 12 weeks. His renal function normalized after 8 weeks and remained at 0.9 mg /dl after 12 months.
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[[22.0, 'year']]
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M
|
{'29854491': 2, '11774962': 1, '9027776': 1, '32128193': 2, '11473672': 1, '33273914': 1, '29502481': 1, '6604293': 1, '32996701': 1, '19520747': 1, '8820506': 1, '16630752': 1, '28571164': 1, '1341422': 1, '31808445': 1, '17722704': 1, '31748498': 1, '30010692': 1, '30155380': 1, '15004262': 1, '29805547': 1, '17635502': 1, '17014549': 1, '30463778': 1, '23960351': 2}
|
{'3741979-1': 2, '3741979-2': 2, '3741979-4': 2, '5952557-1': 1, '7044375-1': 1}
|
162,665 |
3741979-4
| 23,960,351 |
noncomm/PMC003xxxxxx/PMC3741979.xml
|
Acute interstitial nephritis due to proton pump inhibitors
|
A 68-year-old female was admitted with bilateral loin pain and recurrent vomiting for 1 week. She was prescribed esomeprazole for dyspepsia 3 weeks ago. She was afebrile, mildly volume depleted with a BP of 100/70 mmHg Intravenous saline was started. Serum creatinine was 2.6 mg/dl with trace proteinuria and pyuria. Renal biopsy showed AIN with dense interstitial infiltrates of lymphocytes, plasma cells, and eosinophils. Urine culture grew E. coli which was treated by antibiotics. PPI was stopped and oral prednisolone was started on 1 mg/kg dose for 8 weeks, which resulted in excellent recovery of her renal function. Her serum creatinine stabilized at 1.2 mg/dl at 4 months.
|
[[68.0, 'year']]
|
F
|
{'29854491': 2, '11774962': 1, '9027776': 1, '32128193': 2, '11473672': 1, '33273914': 1, '29502481': 1, '6604293': 1, '32996701': 1, '19520747': 1, '8820506': 1, '16630752': 1, '28571164': 1, '1341422': 1, '31808445': 1, '17722704': 1, '31748498': 1, '30010692': 1, '30155380': 1, '15004262': 1, '29805547': 1, '17635502': 1, '17014549': 1, '30463778': 1, '23960351': 2}
|
{'3741979-1': 2, '3741979-2': 2, '3741979-3': 2, '5952557-1': 1, '7044375-1': 1}
|
162,666 |
3741980-1
| 23,960,352 |
noncomm/PMC003xxxxxx/PMC3741980.xml
|
IgG4 related interstitial nephritis: A case report and review of literature
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A 39-year-old man was referred for evaluation of renal failure. He complained of weight loss of about 8 kg and intermittent fever during the previous 3 months. There was no history of dry mouth or eyes. Examination revealed cervical, axillary and inguinal lymphadenopathy, bilateral parotid enlargement, and hepatosplenomegaly. There was trace ankle edema. Blood pressure was 140/90 mmHg. Examination of heart, lung, and nervous system revealed no abnormalities. Investigations: Urine analysis-trace proteinuria, spot urine protein-creatinine ratio: 0.53, no active sediments. Blood: Hemoglobin 11.8 g/dl; Total count 7800/mm3 (polymorphs 64%, lymphocytes 27%, monocytes 2%, eosinophils 7%), erythrocyte sedimentation rate 64 mm-1st h, peripheral smear revealed no abnormal immature white blood cells. Urea 56 mg/dl; creatinine 2.4 mg/dl; sodium 134 mEq/L, potassium 3.8 mEq/L, total serum protein 8.6 g/dl, albumin 3 g/dl, globulin 5.6 g/dl, serum transaminases were within the normal limits. Serology for HIV, HBsAg, and anti-HCV antibody were negative. Ultrasonogram of abdomen revealed large kidneys (right-18.2 × 7.2 cm; left-18.4 × 7.4 cm). CT abdomen confirmed the ultrasound findings, and no abnormalities were noted in pancreas. Renal biopsy: light microscopic examination revealed massive interstitial infiltration of lymphocytes, plasma cells, and a significant number of eosinophils with extensive fibrosis and tubular atrophy. Glomeruli were normal. Immunofluorescence for IgG showed intense positivity in the capillary walls. Stains for IgM, IgA, C3, C4, C1q, Kappa, and Lambda light chains were negative. Immunohistochemical stain for IgG4 was diffusely positive with most of the cells showing positivity (more than 50 cells/hpf) [Figures –].
|
[[39.0, 'year']]
|
M
|
{'25983998': 2, '26628798': 1, '22316447': 1, '21705127': 1, '11236777': 1, '20720530': 1, '7628283': 1, '20213336': 1, '21898030': 1, '22654915': 1, '21030970': 1, '25484534': 2, '23960352': 2}
|
{'4244720-1': 1, '4244720-2': 1, '4244720-3': 1, '4421185-1': 1}
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162,667 |
3741981-1
| 23,960,353 |
noncomm/PMC003xxxxxx/PMC3741981.xml
|
Renal disease masquerading as pyrexia of unknown origin
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A 57-year-old gentleman was referred with high grade intermittent fever with chills since 3 months. He was a longstanding type 2 diabetic, on oral hypoglycemic agents with a fairly good sugar control. He did not have any constitutional symptoms like weight loss or anorexia. He was normotensive and had no specific urinary symptoms. Other than the fever for which he consumed paracetamol, he was fairly asymptomatic. There were no clinical clues to the etiology for the fever on systemic examination.\nThe complete blood count of the patient showed an Hemoglobin 11 g/dL, total leukocyte count 10,100 (polymorphs 85, lymphocytes 13% and eosinophils 2%) and a normal platelet count of 2.73 lacs. Liver function tests were essentially normal with a bilirubin of 0.7 mg/dL, alanine aminotransferase/ALT of 36 and 31 IU/L, serum albumin 3.84 g/dL, and serum globulin 2.46 g/dL. Renal function tests showed BUN 55 mg/dL, serum creatinine 1.5 mg/dL, and normal serum electrolytes. The urine analysis was essentially bland with no albumin, 1-2 pus cells, and no red cells.\nTest results during these 3 months revealed an erythrocyte sedimentation rate of 90 mm at the end of 1 h and two high C-reactive protein levels of 35.8, 24, and 18.5 mg/L (Normal up to 6 mg/L). Complete blood count, urine examination, chest radiology, and 2D Echo performed to investigate the cause of the fever were all normal. Blood and urine cultures were also negative. Serum Ferritin and complement levels were normal. anti-nuclear antibodies and anti-neutrophil cytoplasmic antibody were negative. angiotensin converting enzyme levels were normal. Tumor marker profile was negative. Enzyme immunoassays for tuberculosis and brucellosis were negative. He was treated empirically with antibiotics during this period with no permanent relief.\nThe abdominal ultrasound was also essentially normal. A whole body computed tomography (CT) scan revealed multiple lymph nodes measuring 1.5-4 cm in the mediastinum and retrocarinal region reported to be of inflammatory/infective etiology. Fine needle aspiration of the lymph node was reported as non-specific lymphadenitis. The contrast CT abdomen revealed heterogeneous enhancement of both kidneys with hypodensities at the lower pole [].\nGiven the clinical presentation and the clinical possibilities of vasculitis and lymphoma, and the kidney findings on CT, a renal biopsy was performed. The conspicuous feature was presence of expansile interstitial fibrosis with a plasma cell rich interstitial infiltrate that were accompanied by a few lymphocytes and occasional eosinophil []. Some areas of the biopsy showed storiform fibrosis. There were neither neutrophils nor granulomas. The fibro inflammatory process was seen to extend into the peri-nephric tissue and had resulted in significant tubular loss. The remaining tubules showed thickening of their basement membranes. The glomeruli revealed diffuse capillary wall thickening but there were no changes of diffuse or nodular diabetic glomerulopathy. The arteries revealed mild medial thickening. The pathologic features raised the suspicion for IgG4 related tubulointerstitial nephritis. Immunofluorescence was negative for IgG, IgA, IgM, C3 and C4. IgG4 immunohistochemistry was performed which showed numerous IgG4 expressing plasma cells amounting to at least 15 per high power field (HPF) []. The pathologic diagnosis was IgG4 related tubulointerstitial nephritis. Corresponding serum IgG4 level was 5.9 g/L (N-0.01-1.3 g/L). The diagnosis of IgG4 mediated nephropathy was made on the basis of the clinical history, CT scan findings, histopathology, immunohistochemistry, and serology. He was initiated on a dose of 40 mg prednisolone (0.5 mg/kg/day) and his fever defervesced within 24 h. The steroids were continued and tapered over the next 5 months. His serum creatinine touched a baseline of 1.2 mg/dL at the end of 2 months therapy with steroids. Although an attempt was being made to taper down the steroids further, his fever recurred at a steroid dose of 5 mg/day. He was therefore initiated on Mycophenolate Mofetil (MMF) with a dose of 1 g b.i.d to which his fever responded again. Steroids were stopped by the end of the 5th month and MMF was continued. The serum IgG4 levels progressively declined from a peak of 5.9 g/L to 2.04 followed by 1.55 g/L by the end of the 4th month. The patient continued to be on a dose of 2 g of MMF per day. The CT scan repeated after 6 months showed a significant regression in the mediastinal and retrocarinal lymphadenopathy and resolution of the original hypodense foci in the kidneys.
|
[[57.0, 'year']]
|
M
|
{'26628798': 1, '18344866': 1, '21124093': 1, '19398440': 1, '21124086': 1, '22316447': 1, '18376303': 1, '11236777': 1, '20720530': 1, '20191576': 1, '8227892': 1, '19258916': 1, '23960353': 2}
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{}
|
162,668 |
3741982-1
| 23,960,354 |
noncomm/PMC003xxxxxx/PMC3741982.xml
|
Oxalate nephropathy: An important cause of renal failure after bariatric surgery
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A 54-year-old male was seen in our nephrology clinic for progressive increase in his serum creatinine from 1.38 to 3.66 mg/dl over 9 months. There was no history of fever, diarrhea, steatorrhea, urinary tract symptoms, renal stones, or use of nephrotoxic agents. His past medical history included hypertension for 15 years, type 2 diabetes for 11 years, obstructive sleep apnea, depression, and treated cellulitis. He had undergone a duodenal switch procedure for morbid obesity (body mass index >50 kg/m2) 20 months earlier. Subsequently, he had lost more than 100 kg of body weight, and there was significant improvement in the control of blood pressure, sleep apnea, and blood sugar. His serum creatinine was 1.38 mg/dl and urinalysis was normal at the time of surgery.\nHis clinical examination was unremarkable. Laboratory investigations showed hemoglobin of 9.9 g/dl, white cell count of 6.9 × 103/μl, blood urea nitrogen of 51.82 mg/dl, and serum creatinine of 3.66 mg/dl. Serum electrolytes, calcium, phosphate, and bicarbonate were within normal limits. Urinalysis showed 5-10 white cells/hpf and 1-2 white cell casts without any proteinuria or hematuria. Ultrasound of kidneys showed normal sized kidneys with a few small bilateral calculi without any evidence of obstruction. Doppler of renal arteries was normal.\nIn view of progressive unexplained increase in creatinine, a kidney biopsy was done. The kidney biopsy [Figures and ] demonstrated 13 glomeruli of which six were globally sclerosed. The remaining glomeruli were histologically normal. The tubular interstitial compartment showed foci of tubular damage with deposition of translucent crystals of different shapes which are predominantly intraluminal with few intracellular and focal interstitial distributions. Under polarized light, the deposits appeared strongly birefringent forming fan-like, sheaf-like, or irregular shapes consistent with calcium oxalate crystals. There was an associated mild interstitial inflammation with moderate interstitial fibrosis and tubular atrophy. Blood vessels exhibited moderate arteriosclerosis and arteriolar hyalinosis. The immunofluorescence was negative and electron microscopy did not show any electron dense deposits but did reveal tubular damage with intratubular crystal deposition. His 24-h urinary oxalate level was found to be significantly elevated at 98.7 mg/day (normal range upto 40 mg/day). Urinary calcium and citrate were undetectable.\nA diagnosis of oxalate nephropathy secondary to enteric hyperoxaluria post-duodenal switch operation was made and he was started on low-oxalate, low-fat diet, with high-fluid intake (>3 liters per day). In addition, he was prescribed calcium citrate 1000 mg tid with meals as an oxalate binder. He was also started on cholestyramine 4 g twice daily and repeat urine oxalate improved markedly to 63 mg/day and his serum creatinine stabilized.
|
[[54.0, 'year']]
|
M
|
{'2062767': 1, '19375090': 1, '20071471': 1, '20217955': 1, '18701613': 1, '17377509': 1, '17715408': 1, '16925274': 1, '19359221': 1, '25097346': 1, '19846351': 1, '19762043': 1, '23960354': 2}
|
{}
|
162,669 |
3742063-1
| 23,986,853 |
noncomm/PMC003xxxxxx/PMC3742063.xml
|
Iron deposits in the knee joints of a thalassemic patient
|
A 45-year-old white man with β-thalassemia major was referred for MRI of the left knee due to prominent non-traumatic chronic medial and lateral pain (past 1–2 years), as well as partial locking and restriction in the range of motion. Neither previous nor recent traumatic knee injury nor other suspicious events were reported. The patient had been undergoing regular blood transfusions twice a month maintaining a hemoglobin level of about 9.5 mg/dl and a ferritin level of 3000 ng/mL. The patient reported receiving chelation therapy with only oral deferiprone for the past 13 years at a dose of 75 mg/kg/day. Occasional chelation with desferioxamine was also used during the same time period. T2* measurements from previous MRI examinations on heart and liver are presented in Table . It was evident from the decreasing T2* measurements of heart and liver, that there was progressive increase in the degree of iron deposits in the above two organs in parallel with clinical observations of poor adherence to chelation therapy compatible with high levels of plasma ferritin. Following regular assessment, the patient underwent MRI of the left knee. Subsequent MR scanning of the right knee was also performed for comparison purposes. Written informed consent was obtained from the patient for publication of this manuscript and accompanying images.\nMRI was performed with a 3.0 Tesla scanner (Achieva, Philips Medical Systems, Best, The Netherlands) to assess arthropathy including potential iron deposits in the knee joints. We used the built-in quadrature radiofrequency (RF) body coil and a phased array 8-channel knee coil for proton excitation and signal detection, respectively. MRI scanning protocol included several multislice pulse sequences routinely performed for morphological imaging (in each case, 28 slices were acquired with a field-of-view of 170 mm, a section thickness of 2.8 mm, and a pixel size of 0.6 × 0.7 mm); T1-weighted (T1-w) (repetition time [TR], 674 ms; echo time [TE], 18 ms; total scan time [ST], 2.5 min) turbo spin echo (TSE) in the sagittal plane; T2*-weighted (T2*-w) (TR, 575 ms; TE, 12 ms; ST, 2.4 min) gradient recalled echo (GRE) in the axial plane; proton density-weighted (PD-w) (TR, 2342 ms; TE, 35 ms; ST, 2.9 min) TSE with spectral fat suppression in the coronal and axial planes. Three-dimensional (3D) susceptibility weighted imaging (SWI) and ultra short echo time (UTE) GRE pulse sequences were also prescribed in the axial plane. The former utilizes an echo-shifting technique that allows the employment of relatively long echo times (TE, 21 ms) in a time-efficient way (TR, 15 ms; ST, 1.5 min for 100 slices with an acquisition resolution of 1 × 1× 2 mm). The latter uses a radial data sampling technique achieving an ultra short TE of 14 μs (TR, 7.5 ms; ST, 9.8 min; 144 slices; 1 mm3 acquisition voxel size). The sequence used for quantitative T2 measurements was also prescribed in the sagittal plane. A single-slice (acquisition voxel size of 0.5 × 0.5 × 5.0 mm) Carr Purcel Meibomm Gill (CPMG) spin echo sequence employing 16 equidistant echoes, a short echo spacing of 6 ms and a TR of 2s was used (ST, 5.7 min).\nLeft knee MR images revealed several pathological findings compatible with the prominent clinical symptomatology. The imaging findings included a flap tear of the medial meniscus with a displaced meniscal fragment in the medial intercondylar notch (Fig. ). In addition, osteoarthritis was noted in the medial joint compartment with marked attenuation of the articular cartilage, reactive subcortical bone marrow edema in the medial tibial plateau, and minimal subcortical cystic changes (Fig. ). Furthermore, there was mild attenuation of the patellar cartilage indicating chondromalacia patellae grade II. Foci of iron deposits were identified macroscopically within the supra-patellar pouch right above the superior pole of the patellae and also in contact with the patellae cartilage at the upper pole, as well as within the Hoffa's fat pad in contact with the patellae cartilage in its inferior pole and in the cartilage surface over the trochlea (Fig. a). Finally, iron deposits were also noted along the surface of the medial plica in the supra-patellar pouch. The iron deposits were detected as low signals intensity foci in all MRI sequences used. However, iron deposits were less conspicuous on the T1-w and PD-w sequences, with particular signal loss on gradient echo (Fig. B). During the above study we also noticed further exaggeration of the signal loss on the SWI and UTE sequences (Fig. ). In Table we present mean T2 measurements for regions of interest prescribed in different areas of the cartilage in the left knee. The T2 measurement of normal Hoffa's fat pad was 215 ms (18.8 SD), while in Hoffas fat pad with iron deposits T2 measurement was 54.8 ms (11 SD) and in the supra-patellar pouch with iron deposits T2 was 51.1 ms (4.4 SD), respectively. Such findings indicate iron deposits in the above regions with decreased T2 measurements.\nMRI of the right knee was also performed mainly for comparison purposes. Iron deposits were also noted in the right knee (Fig. ). Iron deposits were noted in contact with the inferior pole of the patellar cartilage, as well as in contact with the anterior articular surface of the lateral femoral condyle.\nFollowing MRI studies, the patient underwent an arthroscopy of the left knee in order to explore the pathological imaging findings and repair the meniscal tear. Biopsy of the synovium showed edema of the basal membrane with papillary morphology and hemosiderin deposits. Histiocytes with hemosiderin moieties were also noted along with hyperplastic serous cells.
|
[[45.0, 'year']]
|
M
|
{'19881074': 2, '15491298': 1, '16424659': 1, '7911181': 1, '15010381': 1, '22213195': 1, '15385291': 1, '26420500': 1, '11090375': 1, '21501938': 1, '23986853': 2}
|
{'2765185-1': 1}
|
162,670 |
3742064-1
| 23,986,855 |
noncomm/PMC003xxxxxx/PMC3742064.xml
|
Successful removal of a Gunther tulip vena cava filter with wall-embedded hook and migration during a retrieval attempt
|
Written informed consent for placement and retrieval of the vena cava filter was obtained from the patient for use of the standard procedure as well as modified procedures if difficulties were encountered.\nA 32-year-old man presented with a thrombus in the IVC. This was incidentally noticed on enhanced CT images obtained to follow-up findings from a routine chest X-ray as part of a medical check-up. The thrombus was also distributed in the proximal portion of the right common iliac vein. Pulmonary embolism was not seen. D-dimer was elevated to 1.8 μg/mL. The patient was in apparent good health and had experienced no specific episode that could have caused deep venous thrombosis. A review of the entire family tree revealed no inherited disorder, and results of blood studies suggested no genetic causative factors.\nA GTF (Cook, Bjaeverskov, Denmark) was prophylactically implanted to prevent development of a pulmonary embolism by movement of the released thrombus. Because the top of the thrombus distributed in the IVC just below the level of the renal veins, the GTF was positioned at the suprarenal IVC through the right jugular vein with the patient under local anesthesia. Anticoagulation therapy with intravenous heparin followed by warfarin sodium given by mouth was administered.\nEighteen days later, enhanced CT revealed that the venous thrombus had decreased and the risk of pulmonary embolism had lessened. Thus retrieval of the GTF was attempted.\nAt first, we used the standard method of retrieval using the GTF retrieval set supplied by the manufacturer (Cook). Details of techniques to retrieve the GTF are described elsewhere (). Devices for retrieval were inserted from the right jugular vein. However, retrieval was impossible in spite of perseverance. The filter had become slightly tilted from the position of implantation. The hook had attached to one side wall of the IVC and could not be snared. It was considered that, in implanting the GTF, more meticulous care should have been taken to orient the filter so that the hook pointed away from the contralateral IVC wall with the open side of the hook directed toward the IVC lumen. We then attempted retrieval using a modification of the standard method as described by Kuo et al. (). We inserted a 4-French angled catheter (Clinical Supply, Gifu, Japan) slowly into the retrieval catheter included in the GTF retrieval set (Cook) to enter the inside of the cone from an interstice between the filter struts and to emerge from another interstice. A 0.035-inch, 260-cm-long, hydrophilic guide wire (Terumo, Tokyo, Japan) was inserted into the previously inserted 4-French angled catheter. Then another 4-French angled catheter (Create Medics, Kanagawa, Japan) was coaxially advanced from the retrieval catheter to near the distal end of the hydrophilic guide wire. A multi-snare (10 mm in diameter, pfm, Koln, Germany) was advanced into this 4-French catheter (Create Medics) and captured the distal edge of the hydrophilic guide wire that had been advanced from the 4-French angled catheter (Clinical Supply) through the inside of the GTF'S cone (Fig. a). After access was established across and through the filter struts, both the hydrophilic guide wire that was inserted through the 4-French angled catheter (Clinical Supply) and the multi-snare that was inserted through another 4-French catheter was pulled toward the cephalad site with tension maintained at both ends. The hook of the GTF was released from the attached IVC wall and the GTF began to move. Then when we attempted to advance the vascular sheath slowly over the filter, the GTF was immediately observed to be floating up the IVC and moving into the right atrium. A strut of the GTF was quickly grasped by pulling tightly both the hydrophilic guide wire and multi-snare into the retrieval catheter and sheath. Through this maneuver, further migration of the GTF was prevented. Finally, another GTF retrieval set was inserted from the left jugular vein and the hook of the GTF was successfully grasped with the retrieval snare that was included in the GTF retrieval set (Fig. b). The GTF was then retrieved.\nDuring these actions, the patient experienced transient arrhythmias and mild back pain, but no serious complication occurred.
|
[[32.0, 'year']]
|
M
|
{'16517787': 1, '14512331': 1, '17142717': 1, '16371548': 1, '10693717': 1, '9459643': 1, '14514816': 1, '8994718': 1, '10693718': 1, '17205364': 1, '23986855': 2}
|
{}
|
162,671 |
3742065-1
| 23,986,854 |
noncomm/PMC003xxxxxx/PMC3742065.xml
|
Right aortic arch and Kommerell's diverticulum associated with acute aortic dissection and pericardial tamponade
|
A 62-year-old female patient arrived at our emergency department after collapsing during her household routine. After intubation, peripheral oxygenation decreased to 59%, followed by bradycardia and low blood pressure. Fifteen minutes later, the patient developed a cardiac arrest. The patient was stabilized with 3 mg of atropine and 4 mg of adrenaline. Cranial computed tomography (CCT) with perfusion imaging at the level of the basal ganglia and carotid CT angiography (120 kVp, 95 mAs, pitch of 1.2, standard image reconstruction in 0.6 mm thickness, and multiplanar reconstructions in 5 mm thickness for the carotid artery) was performed to exclude intracranial bleeding, ischemic stroke, and carotid obstruction. CT images showed no signs of intracranial or cervical pathology. However, the upper mediastinum was seen markedly enlarged. Therefore, CT angiography with coronal and sagittal reconstructions of the thoracic aorta was appended (100 kVp, 150 mAs, pitch of 1.25, 1.5, and 5 mm reconstructions). We found a complex vascular anomaly of the aorta and the supra-aortic branches with right-sided aortic arch and aneurysmal dilatation of the vascular origin of the aberrant left subclavian artery (Figs. –). Furthermore, there was a dense pericardial effusion (45 HU), strongly indicating a dissection of the ascending aorta including a hemopericardium. Due to motion artifacts at the level of the aortic root, no intimal flap was evident (Fig. a). Further electrocardiography-triggered CT of the thorax revealed a dissection of the aorta type A following the Stanford classification (DeBakey type II) with pericardial tamponade (Fig. b). Surgery with graft replacement was performed immediately. Because of the long-lasting, cerebral perfusion deficiency, the patient developed a massive cerebral ischemia with associated edema 3 days after surgery. On a follow-up CT, there was brain swelling with loss of differentiation of the cortex. The patient died 4 days after the initial event.
|
[[62.0, 'year']]
|
F
|
{'32542187': 1, '24421931': 1, '5722774': 1, '12232456': 1, '16091992': 1, '16515907': 1, '14718830': 1, '26306929': 1, '27508212': 1, '18877614': 1, '19467953': 1, '8231269': 1, '23986854': 2}
|
{}
|
162,672 |
3742348-1
| 23,950,650 |
noncomm/PMC003xxxxxx/PMC3742348.xml
|
Clinical features and imaging findings in a case of Capgras syndrome
|
A 53-year-old Caucasian woman was referred to our Psychiatry Unit for hospitalization by her general practitioner. Anamnestic data collection revealed that the patient had had a difficult adolescence, due to the fact that her father had had a mistress and suffered from pathologic gambling. Notwithstanding, she had not experienced any previous psychopathologic problems in the past. She was a housewife with two daughters, and the eldest daughter had always been in conflict with her mother. On the day of her admission to hospital, the patient had a fatuous expression, seemed apathetic, and was suffering from considerable psychomotor retardation. She was distrustful of other patients because they were “too intrusive”. However, when approaching other patients, she showed a childish attitude and was disrespectful of conventional interpersonal distances. The patient had the delusional belief that her eldest daughter, whom she thought had disappeared for 12 months, had been replaced by an impostor. In fact, the previous year the patient’s daughter had left her house without telling her mother. The patient tried to get in touch with her, and the girl answered the phone saying that she was at work. Because her workplace was quite far off from her house, the patient thought that it was not possible for her daughter to arrive at work in such a short time. Hence, she believed that the person she had spoken to over the phone was an impostor who was replacing the daughter whom she thought had disappeared.\nHer delusional belief was characterized by incorrigibility and unwarranted subjective conviction. The patient had two “proofs” to justify her belief: the distance of the workplace and the impostor’s makeup, which was heavier than that worn by her daughter.\nThe patient was experiencing not only the tragedy of a mother who had lost her daughter, but also the frustration of continuous deception by the “double”/impostor. Indeed, the patient thought that the “double” was imitating her daughter’s way of speaking so as to convince her (the patient) that she (the “double”) was her daughter. The patient had no idea where her daughter could be. However, she did nothing to find out where she was. In addition, even though she considered the impostor to be a menacing presence, the patient had a passive attitude towards the impostor, and treated her with indifference. Her mood was deflected owing to her daughter’s disappearance. Obviously, the patient had no insight into her illness. The Capgras delusion was the only unusual belief presented by this patient, who did not show any other psychotic symptoms. The clinical picture of this patient was peculiar: she was tormented by the thought of the “double” who, in addition, provoked a feeling of disgust. This feeling was caused by the fact that the “double” treated the patient in a confidential way in order to deceive her without feeling any real affection. This thought, which was particularly intrusive, caused her considerable distress and even disturbed her sleep; almost every night, she had difficulty in falling asleep at the thought of the painful condition of deception that she had to endure. In addition, this delusional belief was presented to the medical interviewers in an obsessive way, with perseveration regarding the subject (she constantly repeated that the woman was not her daughter), and the thought content restricted to it. The story about her daughter was the answer to simple questions that had nothing to do with the topic. The intrusive thoughts pertaining to her daughter’s disappearance and to the impostor were always present and did not fluctuate much over time.\nGeneral physical examination was within normal limits. She did not drink alcohol or coffee, and did not use any illicit or recreational drugs. The Mini-Mental State Examination (MMSE) was 27/30, indicating normal cognition. Items of the MMSE that the patient was less able to complete pertained to calculation and to short-term and long-term memory. The Structured Clinical Interview for DSM-IV Axis II Personality Disorders indicated an unspecified personality disorder, with a preponderance of paranoid and obsessive-compulsive personality traits. The electroencephalogram was characterized by background alpha activity and rapid rhythms in the frontocentral regions, bilaterally, as shown in . Magnetic resonance imaging (images obtained through fluid-attenuated inversion recovery, spin echo, and turbo field echo techniques, diffusion weighted in axial, sagittal, and coronal planes) showed moderate lesions in the frontal subcortical white matter and in the semioval centers on both sides. In particular, in long repetition time sequences, these cerebral areas showed hyperintensities compatible with a picture of gliosis, as shown in .
|
[[53.0, 'year']]
|
F
|
{'7846238': 1, '2224375': 1, '3337924': 1, '9385782': 1, '29707400': 1, '23186382': 2, '3629249': 1, '22922811': 1, '3651660': 1, '6625025': 1, '19650368': 1, '18442878': 1, '21944325': 1, '20975828': 1, '3812829': 1, '16122573': 1, '20945171': 1, '19956472': 1, '1790464': 1, '1448540': 1, '1202204': 1, '17040174': 1, '9263474': 1, '20387212': 1, '3690120': 1, '17097073': 1, '26909325': 1, '23355784': 1, '23950650': 2}
|
{'3520716-1': 1}
|
162,673 |
3742910-1
| 23,956,833 |
noncomm/PMC003xxxxxx/PMC3742910.xml
|
Squamous Cell Carcinoma in Exstrophy of the Bladder
|
The patient, a 36-year-old woman with a known case of exstrophy of the bladder had undergone repair of the defect 17 years previously. However, dehiscence of the repair had occurred and the patient continued to leak urine from the lower abdominal wall. Six months following this, an ileal conduit urinary diversion was done to prevent the continuous leakage of urine. Six month prior to presentation, the patient had noticed an irregular mass arising from the exposed bladder mucosa that was rapidly increasing in size. On examination, a hemispherical growth with an irregular surface was seen in the region of the exposed bladder mucosa (). The computed tomography scan showed a mildly enhancing nodular lesion on the right side of the lower abdomen superficially. The lesion was confined to the urinary bladder. A wedge biopsy was taken from the growth, and the results were suggestive of squamous cell carcinoma. The results of a routine hematological evaluation, liver function tests, and a chest radiograph were normal. The patient thus underwent removal of the urinary bladder along with a cuff of the surrounding abdominal wall and pelvic lymph node dissection (radical cystectomy). After resection, there was a full thickness defect of the lower abdomen about 8 cm×9 cm in size. To cover this defect, the peritoneum was mobilized on both sides and was sutured in the midline. Both recti were also mobilized and sutured in the midline. The skin defect was resurfaced with an extended groin flap from the left side and the secondary defect thus created was covered by a split thickness skin graft (, ). Histopathological examination of the resected specimen was suggestive of well-differentiated squamous cell carcinoma infiltrating the underlying muscle (stage pT2a) with dense lymphocytic infiltration of the stroma. All the resected margins and deeper plane of resection were free of tumor (). In the postoperative period, the patient developed a small collection beneath the flap that was drained by removal of two stitches, and daily dressings were done. This site granulated well and healed without any significant additional scaring. The patient is on regular follow-up and is doing well without any evidence of recurrence to date (5 months postoperatively) ().
|
[[36.0, 'year']]
|
F
|
{'10671791': 1, '5906001': 1, '963399': 1, '16413365': 1, '19418846': 1, '30061975': 1, '26169528': 1, '10458349': 1, '34717273': 1, '27583267': 1, '17614317': 1, '2822077': 1, '3721776': 1, '11560227': 1, '23956833': 2}
|
{}
|
162,674 |
3742911-1
| 23,956,834 |
noncomm/PMC003xxxxxx/PMC3742911.xml
|
Corticosteroid Therapy Improves the Outcome of Semen Analysis in an Oligozoospermic Patient With Epididymal Sarcoidosis
|
We report on the case of a 25-year-old Caucasian man who presented to the outpatient clinic complaining of right scrotal stiffness for 1 year and new left scrotal pain and tenderness. He had been diagnosed with sarcoidosis by a mediastinal lymph node biopsy owing to a hilar lymphadenopathy 2 years previously after presenting with an acute onset and progressive course of fatigue and cough. The physical examination revealed multiple, painless subcutaneous nodules on his arms and upper thighs in addition to large, bilateral epididymal masses. The consistency and size of the testes were normal and there were no signs of varicocele on the physical examination. Laboratory investigations revealed a normal blood sugar concentration and normal liver and kidney functions with a slightly elevated erythrocyte sedimentation rate (14 mm/h). Moreover, serum α-fetoprotein and β-human chorionic gonadotropin were within the normal range. The urine was negative for acid-fast bacilli by Ziehl-Neelsen stain, which was repeated three times. Biochemical analysis revealed normal serum testosterone (15.85 nmol/L; normal range, 10.07 to 38.76 nmol/L) and luteinizing hormone levels (3 IU/L; normal range, 0.9 to 7.0 IU/L) and elevated serum follicle-stimulating hormone levels (15.4 IU/L; normal range, 1.5 to 12.4 IU/L). Semen analysis showed severe oligospermia (2×106/mL, ).\nT1-weighted post-contrast magnetic resonance imaging (MRI) revealed an enlarged and enhanced epididymis on both sides (). The sizes of the lesions in the right and left epididymis were 3.1 cm and 1.3 cm, respectively.\nThe patient underwent inguinal exploration to differentiate the scrotal malignancy. Exploration revealed enlargement of both epididymides with increased bilateral vascularity and firm consistency of the mass. The masses extended from the epididymis through the testis with thick adherent coverings. Incision of the tunica albuginea demonstrated normal seminiferous tubules with no mass in the testis. A biopsy sample was obtained from the epididymal mass for frozen section analysis. The sample revealed multiple noncaseating epithelioid granulomas (). Because the patient had been diagnosed with pulmonary sarcoidosis 2 years ago, malignancy of the testis and epididymis was ruled out easily and medical treatment considered.\nThe patient was given 40 mg of prednisone/d for 1.5 months. Subsequently, the dosage was reduced to 20 mg/d, which was administered for another 1.5 months. After the first 3 months, the prednisone dose was tapered every month and the patient received the drug as 10-mg, 5-mg, and 2.5-mg tablets during the fourth, fifth, and sixth months, respectively. As a result, the prednisone was gradually reduced to a maintenance dose of 2.5 mg/d at the end of 6 months (). The patient discontinued the medicine 1 month after the maintenance dose was achieved. During the follow-up period, the patient underwent physical examination with repeated semen and biochemical analysis every 3 months (). The results of the semen analysis at the end of therapy showed a dramatically increased sperm count of 34.7×106/mL with normal follicle-stimulating hormone and testosterone levels.
|
[[25.0, 'year']]
|
M
|
{'32476871': 1, '19249026': 1, '4836337': 1, '11796908': 1, '12583627': 1, '3944878': 1, '8417196': 1, '12897340': 1, '18496978': 1, '25512071': 1, '9797115': 1, '32743458': 1, '15589877': 1, '23956834': 2}
|
{}
|
162,675 |
3743144-1
| 24,027,699 |
noncomm/PMC003xxxxxx/PMC3743144.xml
|
Neonatal Hepatitis with Toxoplasmosis
|
A 2-month-old girl born of nonconsanguineous marriage, 2nd of twins, was referred for incidentally detected jaundice. The first twin had neonatal cholestasis with increased galactose and lactose on urine organic acids and had died subsequently. Both babies were small in size at birth as per the mother (exact birth weight is not known). The mother had no fever or rash during pregnancy and there was no exposure to animals. On examination, the child had hepatosplenomegaly with jaundice, while the other systems were normal. Investigations showed hemoglobin of 10.1 gm%, WBC count of 16,800/cumm and platelets were adequate on smear. Bilirubin was 5.1 mg/dL (normal <1.2 mg/dL), with direct bilirubin of 2.5 mg/dL, SGOT=144 IU/L (normal=5-40 IU/L), SGPT=88 IU/L (normal=5-25 IU/L), alkaline phosphatase of 3050 IU/L (normal <650 IU/L), GGTP of 27 IU/L (normal), total proteins of 7.4 gm/dL and albumin of 3.5 gm/dL. Prothrombin time and partial thromboplastin time were normal. Urine reducing substance was negative and ultrasound abdomen showed hepatosplenomegaly and presence of gall bladder. Hepatobiliary iminodiacetic acid scan (HIDA) scan was normal. Toxoplasmosis, other (syphilis), rubella, cytomegalovirus and herpes (TORCH) titres showed positive Toxoplasma IgG (40 IU/mL, negative <10 IU/mL), cytomegalovirus IgG (40 IU/mL, negative <10 IU/mL) and rubella IgG (75 IU/L, negative <10 IU/mL). On repeating the TORCH titres after 3 weeks, Toxoplasma IgG was 60 IU/mL and Toxoplasma IgM was also positive. Parents were advised regarding testing for galactosemia and PCR for Toxoplasma and CMV, but they could not afford the same. (Testing for galactosemia costs Rs 2250, PCR for Toxoplasma is not available in India and CMV PCR test costs Rs 4000.) Ultrasound of the skull showed mild prominence of both lateral ventricles. No other neuroimaging tests were done due to nonaffordability. Cerebrospinal fluid examination was not done and neurological examination was normal. The child was started on Sulphadoxine (20 mg/kg/day) and Pyrimethamine (1 mg/kg/day), and this was given for 1 year. The child had normal achievement of milestones during the year and jaundice resolved by 5 months of age. At the end of 1 year, her weight was 6.5 kg, she had mild hepatomegaly on ultrasound and examination, head circumference was 42.2 cm, length was 70 cm and hemogram and liver function tests as well as ultrasound of skull were normal. Her hearing and ophthalmology examination was also normal.
|
[[2.0, 'month']]
|
F
|
{'15602204': 1, '8638258': 1, '20278771': 1, '14552742': 1, '13041286': 1, '6517455': 1, '24027699': 2}
|
{}
|
162,676 |
3743176-1
| 23,918,583 |
noncomm/PMC003xxxxxx/PMC3743176.xml
|
IgG4-Related Sclerosing Disease Involving the Superior Vena Cava and the Atrial Septum of the Heart
|
A 55-year-old woman was admitted to our institution with recurrent episodes of syncope and dizziness. She had no underlying disease, including autoimmune diseases. The patient's past medical history was not significant for any medications or illicit drugs. The electrocardiogram on admission showed first-degree atrioventricular block with a prolonged PR interval of 240 ms (). Furthermore, the patient demonstrated atrial fibrillation () and a sinus pause of six seconds during an exercise test (). During ambulatory Holter monitoring, frequent episodes of sinus pauses and atrial fibrillation were observed.\nTransthoracic echocardiography and magnetic resonance imaging demonstrated a mass extending from the superior venacava (SVC)-right atrium (RA) junction to the right atrium posterior wall and interatrial septum (). Fluorodeoxyglucose positron emission tomography showed increased uptake in a mass involving the RA wall and interatrial septum (). No other evidence of abnormal uptake was noted. Transcutaneous cardiac biopsy was performed, however, failed to obtain enough tissue to confirm the histologic diagnosis. Therefore, the patient underwent open chest biopsy. Histologically, the lesion was composed of proliferating IgG4-positive plasma cells and lymphocytes (). The ratio of IgG4/IgG positive cells was 68% in average. And absolute number of IgG4-positive cells was approximate 146.5 per high-power field in the hottest area. These findings are consistent with IgG4-related sclerosing disease.\nThe cardiac mass involved the SVC and interatrial septum, and was inoperable. Additional chemotherapy or steroid therapy was not performed because of patient's preference. A permanent VVI-type pacemaker was implanted due to frequent sinus pauses and syncope. During a one-year follow-up, the patient had no additional episodes of syncope, and the mass showed no evidence of progression ().
|
[[55.0, 'year']]
|
F
|
{'12094395': 1, '31956206': 1, '22154614': 1, '22137380': 1, '15855821': 1, '11236777': 1, '26101684': 2, '17026742': 1, '29502226': 1, '18415756': 1, '16679702': 1, '31118383': 1, '20733352': 1, '15545176': 1, '21803920': 1, '23918583': 2}
|
{'4460202-1': 1}
|
162,677 |
3743204-1
| 23,918,585 |
noncomm/PMC003xxxxxx/PMC3743204.xml
|
Familial Occurrence of Pulmonary Embolism after Intravenous, Adipose Tissue-Derived Stem Cell Therapy
|
A forty-one year old man visited our hospital because of chest pain starting one month earlier. During the diagnostic work-up, chest CT revealed wedge-shaped consolidation at the subpleural area of the right upper lobe (). In addition, multiple emboli were found in small pulmonary artery branches of both lungs with right pleural effusion (). There was mild elevation of D-dimer (0.8 µg/mL, normal; 0-0.5 µg/mL) which suggested the diagnosis of pulmonary embolism and infarct. Full diagnostic work-up for hypercoagulability was done. Antinuclear antibody, anti-dsDNA and lupus anticoagulant were all negative. Levels of anti-cardiolipin antibody, homocysteine and anti-thrombin III and activity of protein C and S were within normal range. Factor V Leiden gene mutation was not detected. There was no evidence of deep vein thrombosis in his lower extremities by Doppler ultrasound. He was a non-smoker and did not have chronic illnesses. He did not take a medicine and had not recently taken airplane for a long period. We were puzzled about the cause of the multiple embolism and infarct. We checked his medical history more closely and he confessed to having taken autologous adipose tissue-derived stem cell therapy for cervical herniated intervertebral disc three times intravenously. The each stem cell therapy was at intervals of one month and the last treatment was finished one month before his visit. We considered the possibility of pulmonary embolism by intravenous infusion of hASC. The suspicion of IV stem cell therapy as the cause of pulmonary embolism became more solidified when we came to know that his parents had taken the same therapy for treatment of knee osteoarthritis five times. We invited them for diagnostic work up. They had no specific respiratory symptoms. His father was a current smoker (40 pack years) and his mother was a non smoker. Except for old age, they did not have risk factors for thromboembolism. His father's chest CT showed similar findings: there were multiple emboli at both pulmonary artery branches with right pleural effusion (). In addition, pulmonary infarct was noted at the periphery of right lower lobe. Serum D-dimer was also elevated (1.0 µg/mL). As for his mother, we also confirmed multiple emboli in the pulmonary artery branches in both lungs () with mild elevation of serum D-dimer (1.1 µg/mL). They had no abnormal findings in the tests for hypercoagulability either. The index patient was first treated with enoxafarin, and then overlapped and switched to warfarin. Anti-coagulant therapy was stopped after a month because of the development of hematuria. His parents were observed without anti-coagulation therapy. Follow-up chest CT taken three month later showed disappearance of pleural effusion in index patient () and in his father. Pulmonary emboli were not detected in any of them.
|
[[41.0, 'year']]
|
M
|
{'26971682': 1, '28035134': 1, '18183546': 1, '33053945': 1, '32062355': 1, '21107396': 1, '31555259': 1, '19424006': 1, '26798353': 1, '32148780': 1, '33796536': 1, '34221026': 1, '32766255': 1, '16706604': 1, '33854883': 1, '30324571': 1, '31417542': 1, '33648596': 1, '12571852': 1, '33527780': 1, '22258608': 1, '30063299': 1, '19003780': 1, '20061008': 1, '31394759': 1, '29507631': 1, '32775370': 1, '31130624': 1, '34539792': 1, '34109994': 1, '19249320': 1, '26338463': 1, '30341718': 1, '25689404': 1, '29769612': 1, '32636850': 1, '33690263': 1, '32574263': 1, '21789960': 1, '33988482': 1, '33911038': 1, '30893822': 1, '21054930': 1, '33436061': 1, '34359898': 1, '33986057': 1, '32656249': 1, '34931077': 1, '32854985': 1, '11785965': 1, '34315546': 1, '34296207': 1, '28494937': 1, '31569696': 1, '23313481': 1, '34660740': 1, '32216447': 1, '27478310': 1, '32110683': 1, '24464141': 1, '25377914': 1, '31001253': 1, '34513962': 1, '34256842': 1, '26257702': 1, '33542737': 1, '30992990': 1, '25722427': 1, '33942217': 1, '32787917': 1, '34803612': 1, '30915025': 1, '32028991': 1, '32760740': 1, '23918585': 2}
|
{}
|
162,678 |
3743206-1
| 23,918,584 |
noncomm/PMC003xxxxxx/PMC3743206.xml
|
Spurious Elevation of Glucose Concentration during Administration of High Dose of Ascorbic Acid in a Patient with Type 2 Diabetes on Hemodialysis
|
A 31-year-old female was admitted to the department of Ophthalmology for proliferative diabetic retinopathy (PDR) treatment. She had suffered from type 2 diabetes for 12 years and had been on hemodialysis due to diabetic nephropathy. She had been treated with multiple-dose insulin injection therapy using a basal-bolus regimen. On the day after the admission, she was referred to the department of Endocrinology and Metabolism for the loss of consciousness and discrepancies between capillary and venous blood glucose levels. The physical examination showed blood pressure 140/90 mm Hg, heart rate 100/min, and body temperature 36.5℃. Brain computed tomography was normal. Her glucose level measured using Breeze 2 (Bayer HealthCare LLC, Elkhart, IN, USA) was 291 mg/dL.\nHowever, the venous blood glucose concentration (Modular Analytics DP, Roche Diagnostics, Mannheim, Switzerland) of the blood sample collected simutaneously was 12 mg/dL. After an intravenous injection of 50 mL of 50% glucose solution, the patient became alert. At the time, she was on 10-day medication of high dose ascorbic acid (10 g per day). Because it has been known that glucose measurement reading in SMBG device could be interfered by ascorbic acid, the high dose ascorbic acid treatment was stopped immediately.\nshows the results of glucose concentration measured with Breeze 2, Accu-Chek Active (Roche Daignostics, GmbH, Mannheim, Germany) and corresponding venous blood glucose concentration in this patient. The glucose concentrations measured with Breeze 2 and Accu-Chek Active upon cessation of the ascorbic acid was also different from the venous glucose concentration. It may be due to the half-life or clearance of ascorbic acid in the body. The Breeze 2 and Accu-Check Acitve meet the international accuracy guideline for blood glucose monitoring systems.\nshows the glucose concentration measured with SMBG devices and venous glucose concentration in patients with type 2 diabetes mellitus on hemodialysis without ascorbic acid treatment. Overestimation in measurement using SMBG devices did not happen in these patients, suggesting that spurious elevation of glucose concentration in our patient was due to the administration of high dose ascorbic acid. Serum ascorbic acid concentration measured in the blood sample collected during the event in this patient was 1336.64 µg/mL (reference interval of our hospital: 1.90-15.00 µg/mL).
|
[[31.0, 'year']]
|
F
|
{'31788483': 1, '26915620': 1, '16362814': 1, '34602626': 1, '17076977': 1, '22399892': 1, '12969932': 1, '20351227': 1, '15920083': 1, '10631860': 1, '21129345': 1, '16873777': 1, '29862091': 2, '15333503': 1, '34307844': 2, '30661388': 1, '20144340': 1, '34020705': 2, '20550042': 1, '25519295': 1, '14578265': 1, '18465900': 1, '23918584': 2}
|
{'8139369-1': 1, '5976960-1': 1, '8282517-1': 1}
|
162,679 |
3743330-1
| 23,961,296 |
noncomm/PMC003xxxxxx/PMC3743330.xml
|
Spinal subarachnoid hemorrhage accompanied with intraventricular hemorrhage
|
In 2010 year A 66-year-old man referred to our hospital because of acute onset paraplegia and incontinency started 3 h before admission. He was referred from a town at about 300 km far from our center. He had been completely healthy until the morning of admission day else slight low back pain since 2 days before. In the morning of that day, he experienced retrosternal chest pain radiating to neck. He had been admitted in local hospital and heparin had been started with diagnosis of unstable angina besides other routine treatment. In the afternoon, back pain had increased and retrosternal stabbing pain had occurred. Some minutes later, right sided lower limb plegia had developed. The physician of the patient called us and we gave admission of the patient. On the way to our hospital, contralateral weakness and incontinency had developed. On admission in our hospital, he was conscious, alert, and oriented. The back pain had been resolved since development of paraplegia and incontinency. On initial physical examination, blood pressure was 180/90 mm/Hg. He had urinary and fecal incontinency. On neurological examination, cranial nerves were completely intact. Funduscopy was normal. On limbs, upper limbs were Medical Research Council (MRC) grade 5 bilaterally but lower limbs were MRC grade 0. Deep tendon reflexes were 2+ on upper limbs but absent on lower limbs. Plantar reflexes were mute bilaterally. There was sensory level at the level nipple (T4). He had severed cervical pain and neck stiffness on neck bending. Bulbocavernous reflex was absent. With impression of spinal hemorrhage, emergent cervicothoracic spinal MRI performed []. On MRI mixed hyper/iso intense lesion in anterior subarachnoid space from C7 to T5 and filling defect in MR myelogram [] was seen. At about 2 h later, brief episodes of apnea happened. After supportive treatment brain CT scan was performed. On brain CT scan, SAH and intraventricular hemorrhage in posterior parts of brain was seen []. SAH management started. In the next morning of the admission day generalized tonic clonic seizure occurred and the patient went to deep coma. Patient was intubated and supported under mechanical ventilation. (please write the results of different biochecmial lab tests) The patient died 10 days later (the cause of death).
|
[[66.0, 'year']]
|
M
|
{'15111997': 1, '11566245': 1, '12520314': 1, '33045880': 2, '16219857': 1, '18584394': 1, '23961296': 2}
|
{'7563852-1': 1}
|
162,680 |
3743331-1
| 23,961,297 |
noncomm/PMC003xxxxxx/PMC3743331.xml
|
Jacksonian seizure as the relapse symptom of multiple sclerosis
|
A 46-year-old woman complained of the sudden appearance of muscle twitching or contractions of the fingers of right hand, spreading to arm and face on the same side. Seizure was happened three to four times per day as reported by herself. This is sometimes felt as a tingling sensation of right lower and then upper extremity. The seizures usually lasted 30-60 s. There was no loss of awareness, alertness, or consciousness during seizures.\nIn October 2000, a previously healthy 34-year-old woman complained of the acute onset of paresthesia, numbness, and tingling of lower and upper extremities. She had unsteadiness gait with fatigability. These symptoms continued at least 2-3 months and then followed by a focal motor or sensory seizures of hands occasionally.\nOn neurologic examination right-side finger to nose dysmetria and hyper reflexia was detected. Routine laboratory tests were normal except mild anemia. Brain MRI was showed low signal nonenhancement lesions on T1-weighted and some high signal changes of white matter on T2-weighted. The possible MS was suggested and the patient followed.\nDuring 2001-2008 the patient did not complain of any symptom referable to MS and EDSS (expanded disability status scale) was zero. The patient received no treatment for MS during this period.\nThe second MS relapse occurred in May 2009 and was characterized by blurred vision and diplopia. Neurological examination disclosed a mild right internuclear ophthalmoparesis and MRI revealed the absence of new T2-w or Gd-enhancing lesions []. A course of methyl-prednisolone 1 g/day for 5 days was administered and symptoms subsided in 4 weeks. The patient was not received beta interferons because of she had past history of seizures.\nThe third MS relapse occurred 3 years later (September 2012) and was characterized by focal motor seizures of right hand, reduction of vision of both eyes, and diplopia.\nIn neurologic examination, the limitation of ocular motility with multidirectional nystagmus and mild-to-moderate optic atrophy of both eyes together with dysmetria and tandem gait ataxia is reported. In addition, memory, attention, and problem solving were mildly reduced, and EDSS score increased to 2 []. MRI activities emerged, showing new T2-W lesions in brain and Gd- enhancing T1-W brain lesions [Figures and ]. Brain MRI with T2-W and FLAIR conditions show multiple high-signal-intensity plaques in the periventricular, semi-oval, cortico-medullary junction regions [Figures and ].\nA new course of methyl-prednisolone 1 g/day for 5 days was administered and symptoms subsided in 4 weeks.\nIn October 2000, 6 months after the appearance of the sensory and visual disturbance syndrome, the patient presented a focal epileptic seizure. Interictal EEG was normal. No specific treatment for seizures was initiated. Recurrent simple partial seizures especially focal motor type was occasionally happened between 2000 and 2012; however, because of lack of abnormal EEG patterns patient did not receive any antiepileptic drug.\nIn September 2013, the third and the last attack of MS relapse presented with recurrent focal motor seizures (Jacksonian type). The stepwise focal motor seizures confirmed the Jacksonian type.
|
[[46.0, 'year']]
|
F
|
{'11006371': 1, '15804240': 1, '12644744': 1, '22258045': 1, '22938970': 1, '4215528': 1, '18336559': 1, '17712344': 1, '22262195': 1, '19521080': 1, '16302852': 1, '19739692': 1, '18495419': 1, '23961297': 2}
|
{}
|
162,681 |
3743332-1
| 23,961,298 |
noncomm/PMC003xxxxxx/PMC3743332.xml
|
Brain radiation and possible presentation of multiple sclerosis
|
A 43-year-old woman was admitted to hospital 2 years ago complaining of progressive generalized headache and bilateral blurred vision, with no history of hemiparesis or seizure. Her past medical and familial history was unremarkable for any neurological disorders or other disease. General clinical assessment was within normal limits. Laboratory exams were also found to be normal. Neurological exam, including visual field and ophthalmoscopy was within normal limits; on her magnetic resonance imaging (MRI) of brain a tumor in optic chiasm was observed.\nThe mass was restricted and surgically removed. Histological examination revealed meningothelial meningioma, and a diagnosis of meningioma was confirmed. Patient underwent 28 session of radiotherapy and 15 months after the last session of radiotherapy there was no sign of meningioma.\nNine months after the last session of radiotherapy she was referred to the clinic complaining of blurring vision in the right eye. General clinical assessment was normal. Neurological examination revealed visual acuity of 20/200 in right eye, increased deep tendon reflexes (3+) and also bilateral extensor plantar reflexes. The remaining neurological examination and fundoscopy was normal. On her MRI, radiological finding showed multiple lesions in periventricular, centrum semiovale and corpus callosum [] in which it showed compatibility with a diagnosis of MS according to 2005 MC Donald's criteria.\nDrug therapy for MS with beta-interferon 1a (Avonex) was begun.
|
[[43.0, 'year']]
|
F
|
{'22820412': 1, '32021912': 1, '34572030': 1, '15981002': 1, '12580715': 1, '11548988': 1, '5347126': 1, '77315': 1, '1078790': 1, '12021883': 1, '14219197': 1, '29867445': 1, '18641881': 1, '11105086': 1, '28970242': 1, '8858525': 1, '14672509': 1, '1564485': 1, '18342535': 1, '18209952': 1, '23961298': 2}
|
{}
|
162,682 |
3743340-1
| 23,961,460 |
noncomm/PMC003xxxxxx/PMC3743340.xml
|
Anaphylaxis due to spontaneous rupture of primary isolated splenic hydatid cyst
|
A 57-year-old woman was admitted to the emergency department for diffuse maculopapular rashes on the whole body and anaphylactic shock. She had been complaining of sudden- onset of abdominal pain, dyspnea, pruritus, and urticaria. On physical examination, it revealed tenderness, guarding, and rigidity all over the abdomen. Her blood pressure was 90/60 mmHg, heart rate 118/min, and temperature 37.0°C. Blood test analysis was normal and subsequent leucocytosis with eosinophil dominance. Hydration, hydrocortisone, and antihistamines were used to treat the possible anaphylactic reaction. The patient received oxygen as supportive treatment. The patient recovered after emergency medications and then abdominal computed tomography (CT) revealed a splenic cystic lesion measuring about 9’ 6 cm2 in diameters and containing floating membranes. The anterior wall of the cyst showed discontinuity at a point []. Diffuse pelvic and minimal perisplenic fluid were detected. Our fundamental concerns were to preserve the spleen. Then, the patient underwent a laparoscopic partial cystectomy and omentoplasty, since the spread of the disease into the peritoneal cavity of lesions was strong contraindications for a radical surgical approach. At the time of laparotomy, the cyst's outer membrane was seen ruptured []. The postoperative course was uneventful, and the patient was discharged 10 days after the surgery. We applied albendazole, 10 mg/kg/day for 6 months, and the patient was followed up with CT that displayed no recurrence of the disease during a follow-up of 6 months []. She is still symptom-free in the 12-month follow-up.
|
[[57.0, 'year']]
|
F
|
{'13120785': 1, '19272345': 1, '7893176': 1, '12637803': 1, '28458996': 1, '16847712': 1, '1913311': 1, '10741441': 1, '1389656': 1, '14923537': 1, '14534375': 1, '9143567': 1, '20101579': 1, '23961460': 2}
|
{}
|
162,683 |
3743341-1
| 23,961,461 |
noncomm/PMC003xxxxxx/PMC3743341.xml
|
Traumatic pulmonary pseudocyst
|
A 26 year old unmarried male was referred to us with history of left sided chest pain for two days. He had consulted at local hospital immediately after trauma. A skiagram chest taken there [] showed non homogenous opacity with central lucency in the region of left hilum. On examination, the patient was afebrile. Except for a few abrasions on anterior chest wall, general examination and respiratory system examination was normal.\nThe patient gave history of trauma - a tractor wheel hitting him on the anterior chest wall, while he was lying down; following which he developed the pain. There was no history of breathlessness, fever, cough, hemoptysis, cough or expectoration. There was no history suggestive of bronchial asthma or exposure to pets at home or work place. A repeat chest X ray on 31/08/2011 showed cavitations in the left hilar region. The margins of the lesion were now thinned out and smooth [].\nHis sputum for AFB was negative. Gram stain showed few gram positive cocci but was sterile on culture. A mantoux test was done and read 8 mm at end of 72 hours. Other lab investigation revealed haemoglobin 14.4, leukocyte count 7900, and differential count of 78 % polymorphs and 19% lymphocytes. His total eosinophilic count was 88/cc. His serum was non reactive for HIV antibodies. A CT scan of thorax done on 03-09-2011 showed a single smooth walled cavity abutting left chest wall with surrounding areas of ground glass haziness, probably suggestive of lung contusion [].\nFibre optic bronchoscopy was performed to achieve a microbiological diagnosis and to inspect the trachea-bronchial tree in view of previous reports being inconclusive. Bronchoscopy revealed a bleeding spot in left main bronchus, but no active bleeding was seen. Bronchial brushings taken from left upper lobe were negative for malignant cells and AFB, and the lavage fluid also was sterile. In view of the patient's history of ancedent recent trauma, negative past and present history for any infectious process, and negative microbiological reports, a diagnosis of Post traumatic pulmonary pseudo cyst (TPP) was made. The patient was reassured and advised analgesics and bed rest for 3 days. Serial follow up chest skiagram showed rapid resolution of the cavities [] without any antibiotics, thus confirming our diagnosis of TPP.
|
[[26.0, 'year']]
|
M
|
{'12493502': 1, '30112242': 2, '19668030': 1, '367546': 1, '14344349': 1, '935428': 1, '9156292': 1, '2810415': 1, '19809060': 1, '12707537': 1, '32405234': 1, '33623878': 1, '30009231': 1, '3943352': 1, '454006': 1, '16600612': 1, '7321063': 1, '18630798': 1, '16967385': 1, '10798626': 1, '19327190': 1, '2110749': 1, '33061003': 1, '23961461': 2}
|
{'6077363-1': 1}
|
162,684 |
3743342-1
| 23,961,462 |
noncomm/PMC003xxxxxx/PMC3743342.xml
|
Polyuria following an overdose
|
A 42-year-old man with a known psychiatric history was admitted in the morning to ITU for respiratory and circulatory support following a mixed overdose. He had taken 50 mg of ramipril, 150 mg of olanzapine, and 200 mg of citalopram. He had taken no alcohol, paracetamol, aspirin, or recreational drugs and had not suffered any head injury.\nOn ITU he was sedated with 120 mg/h infusion of propofol 1%.\nIn the afternoon, he was noted to be polyuric with a urine output greater than 500 ml/h and his urine was noted to be progressively more dilute [].\nUrine and serum osmolarity were measured. Urine osmolarity was 160 mosmol/L (normal range 300–1000), serum osmolarity was 304 mosmol/L (normal range 280–300), demonstrating inappropriately dilute urine production. His blood glucose level was normal.\nHe was given intravenous fluid to replace urinary losses and was monitored. The following morning, sedation was stopped and he was extubated successfully. Shortly thereafter, urine concentration returned to normal.
|
[[42.0, 'year']]
|
M
|
{'10422942': 1, '20728301': 1, '15169711': 1, '18929291': 1, '12680486': 1, '23961462': 2}
|
{}
|
162,685 |
3743379-1
| 23,961,495 |
noncomm/PMC003xxxxxx/PMC3743379.xml
|
Severe gynecomastia due to anti androgens intake: A case report and literature review
|
A man, aged 63, was referred in 2004 for gynecomastia. His childhood, puberty and sexual life were unremarkable. His medical history began in 2000. He was treated successfully for prolactinoma. At that time his endocrinologist was sure gynecomastia was absent. Bromocriptine normalized prolactin (810 vs. 2 ng/ml) and testosterone (7 ng/ml), and induced an empty sella.\nIn 2004, he was diagnosed as having a suspect lesion arguing for prostate cancer. Although that one has never been confirmed by histology, he was treated by endoscopic surgery, radiotherapy, and nonsteroid antiandrogen (Flutamide: 750 mg/day) as other products were not available. After that, he had impotency and aching progressive gynecomastia.\nClinical examination showed a stressed man wearing very loose cloths to hide his chest. Physical examination was normal except for bilateral, severe, and asymmetrical giant gynecomastia [].\nThere were no nipple discharge, mass, or axillary lymphadenopathy. His BMI was equal to 23 kg/m2, blood pressure and heart rate were normal. Body hair repartition and testicles were normal.\nMammography, ultrasounds, and breasts MRI showed dense, bilateral glandular aspect without any tumor [].\nRoutine analyses were all in normal ranges, and hormonal exploration showed sub clinical hyper gonadotrophic hypogonadism [].\nThyroid function, prostatic acid phosphates (PAP) and total HCG were normal [respectively 0.52 μU/ml for TSH (n: 0.4-4), 12 pmol/l for free T4 (n: 8-24), 0.02 ng/ml for total PAP (n: 0-4) and 5 mU/ml for HCG (n < 10)]. Liver and kidney functions were normal too.\nRadiological exploration of adrenals, kidney, liver, pancreas and chest did not show any abnormities. Body scan and testes ultrasounds did not show any tumor.\nFor different etiologies, although the iatrogenic cause was the most evident, we discussed all causes of gynecomastias in elderly. Prolactinoma was the first to be discussed, but it was ruled out as the gynecomastia appeared many years after normalization of prolactin and testosterone. Other hypothalamo-pituitary causes were improbable. Congenital etiologies such true and pseudo hermaphrodism, Klinefelter's syndrome, and other dysgenetic causes were improbable too. Adrenal feminizing tumors were excluded by adrenal biochemical and radiologic explorations. Tumors secreting HCG were eliminated too as beta HCG and ultrasounds were normal. Bilateral breast metastases of prostate cancer were excluded too.\nAccording to the context, the remaining etiologies are iatrogenic, and paraneoplastic. As metastases were absent, we kept in mind a double iatrogenic cause (radiotherapy and flutamide intake).
|
[[63.0, 'year']]
|
M
|
{'19481335': 1, '21209041': 1, '15066232': 1, '20096213': 1, '14970289': 1, '20233285': 1, '17881754': 1, '33012931': 1, '15154626': 1, '19175864': 1, '16671273': 1, '23961495': 2}
|
{}
|
162,686 |
3743380-1
| 23,961,496 |
noncomm/PMC003xxxxxx/PMC3743380.xml
|
Catecholamine induced cardiomyopathy in pheochromocytoma
|
A 42-year-old male working as a clerk, presented elsewhere with episodic palpitations, headache, and sweating of 2 years duration. The frequency of these paroxysms gradually increased over the past 6 months. On evaluation elsewhere, he was found to have hypertension, which was difficult to control with three antihypertensive drugs. He was hence evaluated for secondary hypertension.\nAn ultra sonogram of the abdomen was performed initially, as he had undergone left side nephrectomy for voluntary kidney donation 9 years ago. The ultra sonogram revealed a right adrenal mass and he had a positive metaiodobenzylguanidine scan suggesting a right adrenal pheochromocytoma. He was started on three antihypertensive agents, elsewhere.\nHe was referred to our institute for further management. A computerized tomography of the abdomen revealed a heterogeneously enhancing mass of size 4.9 × 5.3 × 5.0 cm [] in the right adrenal gland. Left adrenal appeared normal []. He was evaluated further and was found to have elevated 24-h urinary metanephrin and normetanephrin levels {2050 μg (normal <350 μg/24 h) and 6240 μg (normal <600 μg/24 h) respectively}. He was admitted to the ward at 8.30 PM. At admission his heart rate was 120/min and blood pressure was 160/100 mmHg in the right upper limb in the supine position with no significant postural drop. Cardiovascular examination was unremarkable; few basal crackles were heard on auscultation of chest. Central nervous system examination including optic fundii did not show any significant abnormality. Examination of the abdomen was unremarkable except for a 12 cm nephrectomy scar on the left side.\nHe did not have any features suggestive of syndromic association including multiple endocrine neoplasiae, Von Hippel Lindau syndrome, or neurofibromatosis.\nAn electrocardiogram done at admission was within normal limits.\nIn view of pheochromocytoma, he was started on an alpha blocker. Forty five minutes after administering 2.5 mg of Prazosin, he developed giddiness and had a fall. His systolic blood pressure at that point of time was 60 mm of Hg. First dose effect of alpha blocker was thought of at that point of time. However, the bibasal crepitations, which he already had, worsened progressively. An electrocardiogram done revealed a new onset left anterior fascicular block. Cardiac enzymes were grossly elevated creatinine kinase-muscle brain faction {CKMB: 35 ng/ml (normal <6.7 ng/ml); Troponin T: 1234 pg/ml (normal <14 pg/ml)}. The possibility of a myocardial injury was considered and cardiology opinion was sought.\nAn emergency echocardiogram was performed. This revealed global hypokinesia with no regional wall motion abnormality. Left ventricular ejection fraction was 31%. This was not consistent with an acute coronary syndrome. The patient was shifted to coronary care unit for further management. Cardiac enzymes were repeated after 4 h. This did not show an elevation.\nGiven the absence of regional wall motion abnormality on echocardiogram and lack of serial rise of cardiac enzymes, the possibility of catecholamine induced cardiomyopathy was considered to be more likely than an acute coronary event.\nPatient was started on Milrinone (a phosphodiesterase 3 inhibitor) infusion along with a loop diuretic. He improved gradually, blood pressure stabilized over the next 48 h. He was restarted on beta blockers and continued on alpha blocker prazosin and was shifted out of cardiac intensive care unit (CCU). Phenoxybenzamine was also started within the next 24 h, which he tolerated well.\nHe was prepared for surgery and underwent the same uneventfully after 2 weeks. During laparoscopic adrenalectomy, a 6 × 5 cm vascular tumor arising in right adrenal gland was found and excised. Immediate postoperative period was managed in surgical intensive care unit as he had a hypertensive surge. After control of blood pressure, he was shifted to ward on the second postoperative day. His blood pressure stabilized and remained within normal limits there after without any antihypertensives.\nHis cardiac function improved and he did not have any features of failure thereafter.
|
[[42.0, 'year']]
|
M
|
{'11451258': 1, '6195467': 1, '1467043': 1, '6195468': 1, '7995660': 1, '21860721': 2, '33066731': 2, '2634991': 1, '33575936': 2, '30991354': 1, '30959487': 1, '33714404': 1, '23961496': 2}
|
{'8110488-1': 1, '8110488-2': 1, '3150700-1': 1, '3150700-2': 1, '3150700-3': 1, '7566064-1': 1}
|
162,687 |
3743381-1
| 23,961,497 |
noncomm/PMC003xxxxxx/PMC3743381.xml
|
Hashimoto's thyroiditis associated Evans syndrome: A rare case report on the clustered autoimmune disease triad
|
A 34-year-old female, who is a known case of Hashimoto's thyroiditis, on synthetic thyroid hormone intake (50 μg/day) since five years, presented with high-grade intermittent fever associated with chills and rigors, headache, and breathlessness. There was no significant family history of thyroid disease and she was on no other medication except for the thyroxine intake. On examination, the patient was disoriented, looked pale with anemic conjunctiva, and icteric sclera. Her blood pressure was 110/90 mm of Hg, body temperature was 101°F, and pulse rate was 120 per minute. She had minimal, firm thyromegaly, tenderness in the right hypochondrium, and mild splenomegaly, on an ultrasound scan of the abdomen. There were neither enlarged peripheral lymph nodes nor any enlargement of them on the abdominal ultrasound scan. There were no signs or symptoms of overt hypothyroidism. Further investigations were negative for malaria, hepatitis B surface (HBs) antigen, hepatitis C virus (HCV) antibody, Dengue, HIV, Syphilis, and Leptospirosis. Antinuclear antigen (ANA) and “Anti-ds DNA” were negative. She had low hemoglobin, hematocrit, red blood cells (RBC), and platelet count along with high mean corpuscular volume (MCV). Peripheral blood smear examination showed a marked anisocytosis comprising of macrocytes, polychromatic cells, and microspherocytes. A high percentage of nucleated RBC and thrombocytopenia were also seen []. There were no hemoparasites or abnormal cells.\nBone marrow aspiration was done to rule out any underlying lymphoproliferative conditions and the slides showed only hypercellular marrow with erythroid hyperplasia and increased megakaryopoiesis []. The overall impression on hematological examination was hemolytic anemia with thrombocytopenia and reactive marrow hyperplasia. We performed a further workup and the results are shown in . To summarize, the patient had a positive direct antiglobulin test, evidence of hemolysis in the form of reticulocytosis, elevated indirect bilurubin, and serum lactate dehydrogenase (LDH). She also had increased anti-thyroid peroxidase antibody levels. The constellation of the clinical and laboratory data suggested that the patient was a case of Hashimoto's thyroiditis complicated by Evans syndrome. The patient was put on corticosteroids and she showed a significant improvement. She was now on a followup for six months. Her present hemoglobin is 13.2 grams% and total serum bilirubin is 0.8 mg/dl.
|
[[34.0, 'year']]
|
F
|
{'19395674': 1, '22259635': 2, '15270837': 1, '11921020': 1, '1488666': 1, '16807996': 2, '19918501': 2, '19638626': 1, '565282': 1, '15762980': 1, '12126638': 1, '12466323': 1, '14782741': 1, '11484692': 1, '23961497': 2}
|
{'2688166-1': 1, '2769331-1': 1, '3259521-1': 1}
|
162,688 |
3743382-1
| 23,961,498 |
noncomm/PMC003xxxxxx/PMC3743382.xml
|
Mazabraud syndrome
|
25 year old lady presented with swelling and pain of left thigh of seven years duration. This gradually increased in size without weight loss or proximal muscle weakness. She did not have difficulty in walking and her activities of daily living were not affected by the pain. Examination of the left thigh revealed bowing of the left femur and a soft tissue swelling not attached to the bone. The size of the swelling was 2 × 3 cm, mobile and mildly tender to palpation.\nShe had attained menarche at the age of 13 years and had normal menstrual cycles. She was married for the past one and a half years and had not conceived yet. Her body mass index was 25.1 kg/m2 with height of 150 cm. She did not have any bony deformity or café au lait spots. On biochemical evaluation she had normal alkaline phosphatase, normal serum calcium, phosphorous and 24 hrs urine calcium, phosphorous and creatinine. She had a low level of 25 hydroxy vitamin D of 4.85 ng/ml (20.0-32.0 ng/ml) X-rays of pelvis and hip showed expansile bony swelling with cortical thinning of both tibia []. She underwent a bone scan which showed abnormal, irregularly increased tracer activity in left scapula, left tibia, left femur, pubis and left sacroiliac joints, L5 vertebra, left distal humerus and multiple ribs [], suggestive of polyostotic fibrous dysplasia. MRI of the left thigh showed well defined intramuscular mass lesions []. These lesions were hypointense on T1 weighted image and hyperintense on T2W. They were partly exophytic and measured: 28 × 41 mm in the anteromedial aspect of right adductor longus, 16 × 23 mm in the right adductor magnus at the level of mid-thigh and 9 × 10 mm in the gluteus maximus A bone biopsy [] from the left femur revealed fibrous dysplasia and a biopsy of the soft tissue mass from left thigh was confirmed as intramuscular myxoma [].
|
[[25.0, 'year']]
|
F
|
{'15188030': 1, '9719504': 1, '28224215': 1, '10525796': 1, '31559221': 2, '26722294': 1, '23961498': 2}
|
{'6742871-1': 1}
|
162,689 |
3743383-1
| 23,961,499 |
noncomm/PMC003xxxxxx/PMC3743383.xml
|
Rapid development of thymic neuroendocrine carcinoma despite transcervical thymectomy in a patient with multiple endocrine neoplasia type 1
|
A 56-year-old non-smoker male presented with generalized bodyaches, low back pain, and proximal myopathy of 1-year duration without any fragility fractures. Examination revealed bony tenderness over the sternum and proximal muscle weakness of the lower limbs. Laboratory evaluation revealed hypercalcemia (serum total calcium 12.8 mg/dl, normal 8.5-10.5 mg/dl), hypophosphatemia (serum phosphorus 2.1 mg/dl, normal 2.5-4.5 mg/dl), normal serum albumin (3.8 g/dl), normal serum alkaline phosphatase (136 IU/L, normal 50-150 IU/L), vitamin D sufficiency (serum 25OH vitamin D 31 ng/ml), and normal renal function (serum creatinine 1.2 mg/dl). Hypercalcemia was PTH dependent (serum calcium 12.8 mg/dl with high serum intact PTH 215 pg/ml, normal 15-70 pg/ml). His hemogram and ESR were unremarkable (Hb 13.4 g/dl, TLC 6700/mm3, platelet count 2.8 lakhs/mm3, and peripheral smear showed normocytic, normochromic RBCs, ESR 20 mm at end of the first hour). A diagnosis of sporadic PHPT was made. Bone mineral density by dual energy X-ray absorptiometry showed osteoporosis (T-score −2.7 at lumbar spine, −2.0 at total hip, and −3.4 at distal forearm). Ultrasound neck revealed multiglandular parathyroid enlargement, while a 99mTc tetrofosmin parathyroid scan showed a right inferior parathyroid tumor. The patient was advised surgery as he had serum calcium >12 mg/dl and osteoporosis. The patient was subjected to bilateral neck exploration, where asymmetrical parathyroid hyperplasia was found. Subtotal parathyroidectomy (3.5 gland) with TCT was performed. TCT was performed to identify any supernumerary parathyroid glands. No supernumerary parathyroid glands were identified, and the excised thymus was unremarkable. The patient had an uneventful postoperative recovery. Histopathology showed multiglandular parathyroid hyperplasia and a normal thymus.\nOn follow-up, 8 months after parathyroidectomy, he presented with heaviness in the left side of the chest, dry cough, and exertional dyspnea of 3 months duration. Chest radiograph revealed mediastinal widening with an oval well-circumscribed homogenous opacity (-dark arrow) in left hemi-thorax. Contrast-enhanced computed tomography (CT) of thorax showed a 10 × 6.7 cm inhomogenously enhancing anterior mediastinal soft tissue mass in the prevascular space on the left side, in close proximity to the ascending aorta and arch of aorta []. Chest radiograph done 9 months earlier [] did not show any mediastinal widening.\n99mTc Methylene diphosphonate (MDP) whole-body skeletal scan showed increased tracer uptake at thoraco-lumbar vertebrae and multiple ribs suggestive of skeletal metastases. A CT-guided biopsy from D11 and L3 vertebrae showed metastatic NE carcinoma.\nThe anterior mediastinal mass was excised in toto via trans-sternal approach. On surgery, the tumor was not found to invade any of the adjacent structures. The excised tumor measured 12 × 7 × 5 cm and weighed 264 g []. On microscopy [ and ], the tumor was partially encapsulated, and was composed of rosettes of tumor cells traversed by thin fibro-vascular septae. The tumor cells displayed round to oval nuclei, granular chromatin, occasional nucleoli, and moderate amount of granular to pale cytoplasm with areas of punctate necrosis and lympho-vascular emboli suggestive of thymic NE carcinoma. Immuno-histochemical studies were suggestive of positive staining for chromogranin and synaptophysin, but absence of staining for NSE and vimentin [ and ], consistent with thymic NE carcinoma.\nWith strong suspicion of sporadic MEN-1, in view of coexistence of PHPT with metastatic thymic NE carcinoma, work up for MEN-1 was done, which revealed raised fasting serum gastrin (18,000 pg/ml, normal <200) suggestive of gastrinoma. His serum prolactin (12 ng/ml, normal 2.1-17.7 ng/ml) and serum IGF-1 (131 ng/ml) were within normal range, thereby ruling out any functioning pituitary tumors. There was no family history of disorders suggestive of MEN-1 (family pedigree chart, ). Biochemical screening of family members for MEN-1 was also negative. Somatostatin-receptor scintigraphy with 68Ga-DOTANOC PET/CT revealed somatostatin receptor expressing tumors involving second part of duodenum, head, body, and tail of pancreas, suggestive of gastrinomas. There was no evidence of somatostatin receptor expression in the mediastinum or vertebrae, suggesting that the vertebral metastasis were from the thymic NE carcinoma and not from the gastrinomas.\nThe diagnosis of sporadic MEN-1, with two major endocrine gland involvement (PHPT due to parathyroid hyperplasia and gastrinomas) along with a rare occurrence of thymic NE carcinoma was apparent. The thymic NE carcinoma had evolved rapidly within a span of 8 months after parathyroidectomy and TCT, and presented with bony metastases. With wide-spread metastatic disease, the patient was managed palliatively (pantoprazole, zoledronic acid 4 mg intravenous infusion 4 weekly and Lanreotide 20 mg intramuscular 4 weekly). The patient has been followed up with serum alkaline phosphatase, calcium, chromogranin and gastrin estimations; and 68Ga-DOTANOC PET/CT and 99mTc MDP bone scans at 6 monthly intervals, and other appropriate imaging such as abdomnal and thoracic CE-CT scans. He has been treated with external beam radiotherapy as well as 153Sm Samarium therapy for palliation of painful spinal lesions. Thirty months in follow-up, biological therapy in form of Tab. Sunitinib maleate- a multi-target tyrosine kinase inhibitor- 37.5 mg per orally, once daily was initiated in view of progressive metastatic disease, including liver, lungs and skeletal metastases, which he has received for 18 months with effective symptom palliation, and manageable toxicity. He suffered osteo-necrosis of the jaw- a known complication of long-term zoledronic acid usage, which has been managed by discontinuation of Inj Zoledronic acid and other supportive care. Four years since being operated upon for the thymic N-E carcinoma, the patient is alive, ambulatory, is reasonably symptom free with good quality of life, and is normocalcemic, with no loco-regional recurrence of the thymic tumor.
|
[[56.0, 'year']]
|
M
|
{'12629087': 1, '9671073': 1, '19040992': 1, '19081021': 1, '9735087': 1, '15713725': 1, '26905068': 1, '22723327': 1, '11894982': 1, '34413971': 1, '19949948': 1, '23961499': 2}
|
{}
|
162,690 |
3743385-1
| 23,961,501 |
noncomm/PMC003xxxxxx/PMC3743385.xml
|
Simultaneous presentation of giant pheochromocytoma, primary hyperparathyroidism, and mixed-medullary–papillary thyroid cancer in MEN 2A
|
A 40-year-old, married man, having five children, fifth of eight siblings, was referred to our tertiary care referral centre, with the complains of persistent headache and palpitations (at rest), that had increased since the last 2 months, on the background of hypertension (14 years) and a single episode of renal calculi 7 years ago. His treating physician admitted him at a local hospital for difficult-to-control severe hypertension and undertook a computed tomography (CT) scan of the abdomen, which revealed a mass in the abdomen. He was then subsequently referred to the surgical department with the aim of removing the mass. The surgeons on suspecting an underlying catecholamine secreting adrenal mass, referred the patient to our endocrine team for further evaluation. Family history suggested hypertension in three of his siblings. His parents expired at a young age. He was a nonsmoker, nonethanolic, on the following antihypertensive medication (calcium-channel blocker, angiotensin converting enzyme inhibitor, and beta-blocker).\nExamination revealed a young man with weight of 70 kg, body mass index 23.5 kg/m2, pulse 100 beats/minute and a blood pressure 160/100 mm of mercury pressure supine, without any postural fall. Systemic examination revealed a mass in the region of the left thyroid gland that was firm without obvious lymphadenoapthy. There was no other significant finding of note.\nWe considered workup for a possible catecholamine secreting pathology associated with a thyroid mass in a young patient.\nBiochemistry revealed normal blood counts, blood film, liver function tests (albumin 4.5 g%); impaired renal function (creatinine 1.71 mg%, urine routine + protein); hyperuricemia (uric acid 10.2 mg%), hypomagnesemia (1.4 mg%); impaired fasting glucose (oral glucose tolerance test 75 g: 0 hours 108 mg% 1 hour 201 mg% 2 hours 138 mg%) and parathormone-dependent hypercalcemia [calcium 13.8 mg/dl, corrected calcium 13.4 mg/dl, inorganic phosphorous 1.7 mg/dl, alkaline phosphatase 140 IU/l (50-136), parathormone 326 pg/ml (10-69), vitamin D3 11.2 nmol/l (11-42)].\nThe patient was euthyroid [Ft4 1.1 ng/dl (0.9-1.7) Ft3 2.8 ng/dl TSH 0.76 mIU/ml (0.4-5)] with 9 am adrenocorticotrophic hormone (ACTH) 31 pg/ml (0-46 pg/ml), 9 am cortisol 23 mcg/dl; midnight cortisol 1.6 mcg/dl (collected within 10 minutes of awakening) and normal overnight dexamethasone suppression test (9 am cortisol 0.9 mcg/dl).\nTumor markers, thyroglobulin 1980 ng/ml (<33), calcitonin 590 pg/ml (<18.2) and carcinoembryonic antigen 15.31 ng/ml (<5) were elevated suggesting possible medullary carcinoma of thyroid. Twenty-four-hour urinary metanephrines 4810 mcg/day (0-350 mcg/day) and normetanephrines 3660 mcg/day (0-650 μg/day) were significantly elevated suggesting catecholamine secreting tumor.\nAn echocardiogram showed a reduced left ventricular ejection fraction of 40%.\nCT scan whole body: [] revealed a 16.4 cm × 14 cm mass with multiple hypodense areas of necrosis in the left para and suprarenal area, compressing and displacing the left kidney []; multiple bilateral renal calculi (largest 2.4 cm × 1.3 cm in the left kidney); mild left-sided hydronephrosis and a 3.4 cms mass in the left lobe of the thyroid.\nDoppler ultrasound of neck: [] showed a 4 × 3.7 × 3 cm mass in the left lobe of thyroid.\nTc thyroid uptake scan: Enlarged left lobe of thyroid with cold nodule in the left lobe and isthmus.\nSESTAMIBI: Localized to the thyroid mass with a brisk wash out, ruling out a parathyroid lesion. This however was on the background of a parathormone-dependent hypercalcemia.\nThe imaging confirmed a thyroid mass, but localizing studies for a parathyroid adenoma or hyperplasia was unrewarding.\nThe patient's calcium was corrected using fluid resuscitation with diuretic cover and pamidronate. Calcitonin was used in a single dose before we realized that the patient had a possible medullary thyroid carcinoma. Fortunately the blood for serum calcitonin was analyzed in a sample that was collected prior to administering calcitonin. He was rendered normocalcemia prior to pheochromocytoma surgery.\nHe was alfa blocked using intravenous phenoxybenzamine for 3 days and volume resuscitated before surgery. An adrenal mass weighing 1.8 kg was removed. The postoperative course was complicated by acute tubular necrosis. During this time he was conservatively managed while keeping a close eye on his serum calcium. His blood pressure had normalized and was off all antihypertensives. Histopathology confirmed pheochromocytoma [].\nHistopathology of adrenal mass showed alarge circumscribed tan tumor weighing 1.836 kg []. Cut surface was fleshy, friable, tan-coloured with cystic spaces containing foci of hemorrhage consistent with pheochromocytoma. The immunohistochemistry profile was strongly positive for synaptophysin, chromogranin A, and S-100.\nOn the eighth postoperative day, surgery addressing of the parathyroids and thyroid was planned. The surgeon undertook a total thyroidectomy and removed all the parathyroid glands. Frozen section confirmed by histopathology revealed parathyroid hyperplasia [] and medullary carcinoma of the thyroid [].\nHistopathology of the thyroid showed a 4 × 3.7 × 3 cm gray white firm tumor [] replacing most of the thyroid parenchyma. Microscopy was consistent with medullary thyroid carcinoma mixed with papillary thyroid carcinoma [, ].\nPostoperatively the patient became hypocalcemic requiring 2 days of intravenous calcium therapy. A repeat calcitonin done on the seventh postoperative day was 17.8 pg/ml, ensuring adequacy of surgery. The patient was finally discharged with a follow-up to discuss genetic counseling; however he denied any further assistance and was lost to follow-up.
|
[[40.0, 'year']]
|
M
|
{'10369850': 1, '20447064': 1, '8153413': 1, '21447639': 1, '21552134': 1, '2914297': 1, '19260112': 1, '23958408': 1, '15606377': 1, '20463576': 1, '20833330': 1, '3614355': 1, '23961501': 2}
|
{}
|
162,691 |
3743386-1
| 23,961,502 |
noncomm/PMC003xxxxxx/PMC3743386.xml
|
A case of hemiagenesis of thyroid with double ectopic thyroid tissue
|
An 18-year-old male presented with gradual onset swelling in front of the neck for 4 years. It was painless and was not associated with dysphagia, dysphonia, or dyspnea. There was no history of tremors, palpitations, or change in weight or bowel habits. There was no history of neck surgery or irradiation. Clinical examination of the neck revealed a soft swelling in the region of the left lobe of thyroid which moved freely with deglutition. There was no cervical lymphadenopathy and no eye or skin changes suggestive of autoimmune thyroid disease. Systemic examination was normal with no dextrocardia. Investigations revealed the following: (i) Thyroid function test was suggestive of subclinical hypothyroidism [free T4 1.1 ng/ml (normal 0.8-1.7), TSH 8.8 mIU/L (normal 0.4-4.2)]; (ii) antithyroperoxidase antibody was negative; (iii) ultrasound neck showed absent isthmus and right lobe with normal echogenecity and vascularity of the left lobe suggestive of hemiagenesis of thyroid; and (iv) technetium uptake nuclear scan of the thyroid gland revealed hemiagenesis of right lobe of the thyroid gland and also showed uptake in the suprahyoid and infrahyoid position suggestive of double ectopic thyroid gland [].
|
[[18.0, 'year']]
|
M
|
{'29732163': 1, '15466939': 1, '7388347': 1, '11353296': 1, '14599114': 1, '7111107': 1, '18577277': 1, '5508735': 1, '33026543': 2, '2699300': 1, '15009918': 1, '6869855': 1, '10867854': 1, '10403172': 1, '29692520': 2, '8770681': 1, '3934219': 1, '29279781': 2, '12679435': 1, '8973289': 1, '10595455': 1, '7793746': 1, '23961502': 2}
|
{'7593389-1': 1, '5723948-1': 1, '5894311-1': 1}
|
162,692 |
3743387-1
| 23,961,503 |
noncomm/PMC003xxxxxx/PMC3743387.xml
|
Pituitary oncocytoma presenting as Cushing's disease
|
A 19-year-old girl presented with complaints of weight gain, hypertrichosis, menstrual irregularities of 2 years and hypertension of 4 months duration. She also gave history of easy bruisability, broad voilaceous striae over abdomen and thighs, recurrent vaginal candidiasis. Her height was 154 cm, weight 77 kg, BMI of 32 kg/m2, and waist hip ratio 0.95 on examination. She was normotensive on antihypertensive medications. There was thinning of scalp hairs, mooning of face, facial plethora, hypertrichosis over face, increased supraclavicular and dorsocervical fat pad thickness, voilaceous abdominal striae, thinning of skin over dorsum of hands, and proximal muscle weakness. There was no neurological deficit including visual fields. OGTT detected IFG (fasting plasma glucose 102 mg/dl) and IGT (postglucose load 156 mg/ dl). Her bone mineral density estimation by DXA revealed osteopenia. Her hormonal evaluation revealed normal basal ACTH levels (38.7 pg/ml) in the presence of basal cortisol levels of 21.3 μg/dl (8 am) and evening cortisol of 23 μg/ dl (4 pm). Serum cortisol levels remained unsuppressed following overnight (18.6 μg/dl) and low dose (15.7 μg/dl) dexamethasone suppression test. However, it decreased by 73% on high dose dexamethasone suppression test (5.8 μg/ dl). MRI brain did not reveal any pituitary abnormality. Since neurosurgeons were reluctant to operate without localization and also to find source of ACTH, bilateral inferior petrosal sinus sampling (BIPSS) was planned with vasopressin stimulation due to nonavailability of CRH and desmopressin. The central to peripheral ACTH ratio on the right side was 28/1 and 32/1 in basal and postvasopressin respectively (normal <2 and <3 respectively). The interpetrosal sinus gradient was also significant (right IPS/left IPS = 13; normal <1.5) suggesting pituitary microadenoma on the right side of adenohypophysis. The patient was diagnosed as having Cushing's disease caused by an ACTH-secreting pituitary adenoma, which was extirpated (adenomectomy) by transphenoidal surgery. The sixth postoperative day basal Cortisol level was 0.33 μg/dl, suggestive of possible remission of disease. She was discharged on replacement doses of hydrocortisone with advice on stress dosing and she is planned for gradual tapering of hydrocortisone doses.\nHistopathological examination on light microscopy showed more than 95% of cells arranged in a large sheet of polyhedral cells with eccentric nuclei and moderate amount of bright eosinophilic, granular cytoplasm consistent with oncocytes, which confirmed the diagnosis of oncocytoma []. These cells were arranged in diffuse, solid, and sinusoidal pattern []. These cells were strongly positive for ACTH []; prolactin; GH; S100; neuron specific enolase; chromatogranin A; and synaptophysin on immunohistochemical staining and displayed a bright brown positivity universally. Phosphotungstic acid hematoxylin (PTAH) staining revealed dark blue oncocytic cytoplasm [].
|
[[19.0, 'year']]
|
F
|
{'1928557': 1, '9224529': 1, '3303231': 1, '4191778': 1, '709533': 1, '7191348': 1, '7479351': 1, '8410141': 1, '4121198': 1, '4377574': 1, '10452574': 1, '15214824': 1, '4350182': 1, '7456308': 1, '11482580': 1, '6362613': 1, '30945144': 1, '1941118': 1, '2769482': 1, '23961503': 2}
|
{}
|
162,693 |
3743519-1
| 23,966,796 |
noncomm/PMC003xxxxxx/PMC3743519.xml
|
Streptococcus group C meningitis with cavernous sinus thrombosis
|
An eighteen year old African American male presented to the emergency room with a 1-week history of sore throat, muscle aches, fever, headache, and photophobia. He also complained of nausea, one episode of vomiting, and abdominal pain. He was a college student and lived in a dormitory. He denied any recent travel or contact with ill people. Past medical history was significant for sickle cell trait and Osgood Schlatter’s disease. He was up to date on vaccinations.\nPhysical examination revealed a tall, thinly built young man, in mild pain with an oral temperature of 97.5°F, blood pressure of 114/69 mmHg, heart rate of 89 beats per minute (BPM) and respirations of 18/minute. He had injected conjunctiva of the right eye, and pharyngeal and tonsillar exudates. The examination of the central nervous system revealed neck stiffness; Kernig’s and Brudzinski’s signs were not elicited. Cranial nerves were intact. The power and deep tendon reflexes were essentially normal. The rest of the systemic examinations were unremarkable.\nHemoglobin was 17.5 g/dL, hematocrit 50.8 g/dL, and white count 20.3 × 109/L with 89% granulocytosis, and platelet count of 35 × 109/L. Basic metabolic profile was within normal limits, except for a potassium level of 3.2 meq/L, blood urea nitrogen of 44.9 mg/dL, and creatinine of 2.3 mg/dL. Chest X-ray revealed bilateral infiltrates in the middle and lower lung fields. Computed tomography (CT) of the head was unremarkable. The patient declined lumbar puncture. The blood culture grew penicillin sensitive Group C Streptococcus (GCS) within 24 hours of incubation. A few hours into the admission, he developed third and sixth nerve palsy. Further work-up revealed right cavernous and ophthalmic vein thrombosis on magnetic resonance imaging ( and ). Multiple patchy cavitary lesions on both lungs were seen in the chest CT. There was no vegetation on transesophageal echocardiogram. The oculomotor and abducens palsies resolved after medical management for 16 days.
|
[[18.0, 'year']]
|
M
|
{'8463391': 1, '20492747': 1, '18925443': 1, '23105024': 1, '34306778': 2, '28694832': 1, '26231260': 1, '20632899': 1, '8968872': 1, '27928417': 1, '25247162': 2, '22416199': 1, '7559958': 1, '30761237': 2, '20514161': 1, '32509525': 1, '23966796': 2}
|
{'6367117-1': 1, '8272663-1': 1, '4170087-1': 1}
|
162,694 |
3743520-1
| 23,966,763 |
noncomm/PMC003xxxxxx/PMC3743520.xml
|
Color vision abnormality as an initial presentation of the complete type of congenital stationary night blindness
|
A 17-year-old male who was in a technical school of the transportation industry showed abnormalities in the color perception test for employment, and was referred to our hospital for a detailed examination. While he was in the elementary school, he received a color perception test during a health check. There were no abnormalities on the examination. He had no family history of color vision deficiency, and had no other symptoms. During the initial examination, his best-corrected visual acuity was 1.2, with no refractive error in either eye. The referral doctor, who specialized in color vision, investigated his color vision. Testing with Ishihara pseudoisochromatic plates, the patient could read only the first plate, and was diagnosed to have a color vision defect. However, he passed the panel D-15 dichotomous test with no errors. The patient’s color vision defect was mild, with no definite axis of error according to the 100-hue test performed at the referral hospital, and he showed normal match with an anomaloscope color blindness test.\nThe referring doctor also performed Standard Pseudoisochromatic Plates, part 2 to assess the type of color defect. The patient made two mistakes for blue–yellow differentiation and five mistakes for red–green differentiation in the right eye; and two mistakes for blue–yellow differentiation and four mistakes for red–green differentiation in the left eye, suggesting that the color vision defect had no definite axis.\nDuring the initial examination, his fundus showed no abnormalities except for a somewhat yellowish reflex in the fovea of both eyes. Fundus autofluorescence, optical coherence tomography, and multifocal ERG were normal (). Fluorescein fundus angiography also revealed no abnormalities (). Color vision deficiency with no apparent retinal abnormalities is sometimes associated with retinal diseases. Thus, these findings prompted us to obtain an ERG. Both the cone ERG and 30 Hz flicker ERG (recorded by International Society for Clinical Electrophysiology Vision [ISCEV] standard protocol ERG [using Tomei LE3000, Tomei, Tokyo, Japan]) showed a good response; however, the cone ERG showed wide a-wave trough. Bright flash, mixed rod and cone ERG showed a negative type with a reduced b-wave and a disappearance of oscillatory potential. No response was recorded in the rod ERG, either (). Based on the ERG findings, the patient was diagnosed with complete CSNB. Observation was recommended; he has been monitored for 5 years, and remains asymptomatic with no changes in visual acuity and fundus appearance since the first visit.
|
[[17.0, 'year']]
|
M
|
{'20300565': 1, '12610835': 1, '8795377': 1, '18227204': 1, '22190596': 1, '3488053': 1, '6601088': 1, '23714322': 1, '23966763': 2}
|
{}
|
162,695 |
3743521-1
| 23,966,762 |
noncomm/PMC003xxxxxx/PMC3743521.xml
|
Obvious optic disc swelling in a patient with cryopyrin-associated periodic syndrome
|
In 2009, a 35-year-old Japanese male visited the dermatology clinic of our hospital presenting with urticarial-like rash from infancy, periodic fever, and arthralgia. He also presented with deafness, repeated eye redness, ocular pain, headache, and general fatigue from the time he was a child. He had a previous history of meningitis at the age of 20 years. At first, Behçet’s disease was suspected based on his symptoms. Consequently, he was seen for diagnosis in the ophthalmology clinic at our hospital in September 2009. His best-corrected visual acuity was 1.0 OD and 0.9 OS and his manifest refraction was uncorrected OU. Intraocular pressure was 9 mmHg OD and 7 mmHg OS. Slit-lamp examination showed conjunctival and episcleral injection in both eyes, clear and smooth corneas, and infiltration of inflammatory cells without posterior synechia in the anterior chamber. Gonioscopy did not reveal hypopyon, nodules, or peripheral anterior synechia. Ophthalmoscopy and fundus photography examination revealed obvious bilateral optic disc swelling and retinal vascular sheathing around the optic discs, with absence of dilated capillaries on the optic discs, vitreous opacifications, and retinal exudates (). Critical flicker frequency was normal (43.8 Hz OD and 47.2 Hz OS). Goldmann perimetry showed only enlarged blind spots in both eyes. The patient had no ocular findings of Behçet’s disease. Hematologic examination showed increased inflammatory markers, a white blood cell count of 18,700 cells/μL (neutrophil count 75.5%, lymphocyte count 20.5%), C-reactive protein of 2.94 mg/dL, and an erythrocyte sedimentation rate of 44 mm. Magnetic resonance imaging showed no intracranial space-occupying lesion.\nThe anterior uveitis was treated with steroid and nonsteroidal anti-inflammatory eye drops. The patient was also treated at the department of rheumatology and clinical immunology with immunosuppressive agents (methotrexate, tacrolimus, azathioprine, cyclophosphamide) and antirheumatic agents (salazosulfapyridine, leflunomide) to reverse systemic symptoms. However, conjunctival and episcleral injection and systemic symptoms played a limited role in these treatments. Three years later, his best-corrected visual acuity was 1.2 OD and 1.2 OS. His conjunctival and episcleral injection remained unchanged (). The optic discs became white in color () and fluorescein angiography demonstrated strong staining and weak late phase leakage from the optic disc (). Spectral domain optical coherence tomography (Spectralis, Heidelberg Engineering, Heidelberg, Germany) revealed obvious optic disc swelling ().\nIn 2012, his mother was genetically diagnosed with CAPS. Therefore, the patient underwent genetic testing for the diagnosis of CAPS at Kyoto University Graduate School of Medicine after informed consent was obtained, according to the tenets of the Declaration of Helsinki. Genetic tests detected heterozygous mutations in c.907G>A [p.Asp303Asn (D303N)], a previously reported mutation responsible for CAPS. Thus, he received a definitive diagnosis of CAPS.
|
[[35.0, 'year']]
|
M
|
{'25963520': 1, '18668535': 1, '33401496': 1, '21104172': 1, '19302049': 1, '11992256': 1, '15541451': 1, '21538043': 1, '11590390': 1, '11030821': 1, '16899778': 1, '19494217': 1, '32019187': 1, '25833143': 1, '14630794': 1, '20425006': 1, '21484180': 2, '34947964': 2, '23966762': 2}
|
{'8709039-1': 1, '8709039-2': 1, '8709039-3': 1, '3170123-1': 1}
|
162,696 |
3743637-1
| 23,966,803 |
noncomm/PMC003xxxxxx/PMC3743637.xml
|
Resolution of exudative retinal detachment and regression of retinal macrocyst post-laser in Coats disease
|
A 15-year-old boy presented with painless progressive blurring of vision in the right eye for one year in duration. It was not associated with floaters or fashes of light and there was no history of trauma. He was born full term via spontaneous vaginal delivery and had no past ocular history or medical illness.\nVisual acuity in his right eye was hand movement and his left visual acuity was 6/6. Anterior segment examination was normal with a normal pupillary reaction in both eyes. The right fundus showed the presence of extensive subretinal exudates at the posterior pole (macular area) extending to the superotemporal arcade (). There was also the presence of a retinal macrocyst at the temporal periphery of the retina (). This was associated with exudative retinal detachment at the inferior periphery of the retina with no foveal involvement. There was the presence of telangiectatic retinal vessels at the superotemporal retina. The left fundus was normal with an absence of subretinal exudates or any abnormal retinal vessels. B-scan ultrasound showed the presence of inferior retinal detachment with no mass lesion or calcification. Fundus angiography revealed telangiectatic retinal vessels at the superotemporal retina.\nBased on clinical and angiographic findings, a diagnosis of Coats disease in the right eye was made. The patient was classified as having Coats disease stage 3A based on the presence of exudative retinal detachment with no foveal involvement. He was treated with retinal laser photocoagulation at the area of telangiectatic vessels aiming to cause regression of these vessels. The laser therapy was given in four sessions within 3 months.\nAt 3-month follow-up after initial presentation, the exudative retinal detachment was resolved with minimal reduction of subretinal exudates. Review at 14 months post-retinal laser photocoagulation showed a reduction of the subretinal exudates at the posterior pole (). There was regression of the size of the retinal macrocyst with reduction of subretinal exudates surrounding the retinal macrocyst at 2 years post-retinal laser photocoagulation (). His right visual acuity was improved to 1/60, with no further improvement due to persistent dense and calcified subretinal exudates at the fovea.
|
[[15.0, 'year']]
|
M
|
{'22205832': 1, '11336930': 1, '11336931': 1, '20029154': 2, '23269680': 1, '22792170': 1, '6685529': 1, '23481001': 1, '20029156': 2, '20195034': 1, '22774595': 1, '23221067': 1, '23966803': 2}
|
{'2841384-1': 1, '2841382-1': 1, '2841382-2': 1, '2841382-3': 1}
|
162,697 |
3744716-1
| 23,960,455 |
noncomm/PMC003xxxxxx/PMC3744716.xml
|
Effectiveness of Mechanical Embolectomy for Septic Embolus in the Cerebral Artery Complicated with Infective Endocarditis
|
A 39-yr-old woman without any underlying medical conditions including heart problems visited the emergency department with ten minutes of right hemiparesis and aphasia on April 23, 2012. Her National Institutes of Health stroke scale (NIHSS) score was 16.\nOn presentation, she has been often febrile for 1 month. Her pulse was regular, blood pressure was 124/67 mm Hg and temperature was 37.1℃. Laboratory tests upon admission disclosed mild normocytic anemia (hemoglobin, 11 g/dL), a normal leukocyte count (8,600/mL), and a platelet count of 193,000/µL. The serum C-reactive protein level was 3.48 mg/dL and an erythrocyte sedimentation rate was 53 mm/h. The initial electrocardiogram showed a right bundle branch block. Results of other routine laboratory tests were within normal limits. A chest film was normal.\nThe brain computed tomography (CT) showed no abnormal findings. The diffusion-weighted magnetic resonance (MR) images and corresponding apparent diffusion coefficient maps revealed hyperacute infarction of left insula cortex, corona radiata, centrum semiovale and posterior inferior cerebellar artery territory of right side cerebellum. The MR angiography showed left MCA proximal segment (M1) occlusion. The diffusion-perfusion mismatch was found in the mean transit time & time to peak perfusion maps. (, ) She was not given an intravenous tissue plasminogen activator because of the unclear onset time of the neurological deficits. Considering the time window, diffusion-perfusion mismatch and the patient's young age, we decided to perform intra-arterial thrombolysis. The patient received urokinase 150,000 units and tirofiban (Aggrastat; Merck) 100 micrograms intra-arterially. However, there was no flow restoration of the left MCA. After the second trial of mechanical thrombectomy with retrievable stent Solitaire AB 4×15 mm (ev3/Covidien Vascular Therapies, Mansfield, Massachusetts, USA), the MCA was recanalized to the thromobolysis in cerebral infarction (TICI) grade 2b (). (, ) After 36-hr procedure, her right side motor power was almost fully recovered. The patient improved greatly and had only right hemifacial palsy and aphasia, which also improved gradually. A postoperative CT scan obtained 24 hr later showed no evidence of infarct or hemorrhage.\nUnfortunately, we had not detected early on, but a cardiac examination revealed a regular heart beat with pansystolic murmur on apex. A transthoracic echocardiogram showed a mass like-lesion on the anterior mitral valve (1.07×0.59 cm) and moderate mitral regurgitation without any functional problems and the evidence of heart failure. Ceftriaxone and gentamicin treatment for IE started immediately. On the third day, Streptococcus gordonii was subsequently grown from the initial blood culture sets. With the patient fulfilled clinical Duke criteria for definite IE (), she was treated with parenteral penicillin and gentamicin. The patient's NIHSS score was 7 at this time. We underwent a sequential echocardiography once a week during hospitalization. The volume of mitral regurgitation and the size of vegetation on echocardiography did not increase. After two weeks, the size of vegetation on echocardiography was decreased to about 0.7×0.5 cm. During the four weeks of her antibiotics course, the patient's hemiparesis and aphasia improved (NIHSS score of 3). She has had no recurrent infarction and congestive heart failure and has been recovering well at home.
|
[[39.0, 'year']]
|
F
|
{'15956145': 1, '27815693': 1, '32700224': 2, '25705308': 1, '19688612': 1, '23983869': 1, '25410029': 1, '29948467': 1, '22120371': 1, '8366515': 1, '29768962': 1, '22296678': 1, '8607669': 1, '34084613': 2, '12869717': 1, '21546485': 1, '16794213': 1, '25426306': 2, '22738096': 1, '16214341': 1, '22626714': 1, '11025788': 1, '23960455': 2}
|
{'8168679-1': 1, '4239408-1': 1, '7655561-1': 1, '7655561-2': 1, '7655561-3': 1}
|
162,698 |
3744717-1
| 23,960,456 |
noncomm/PMC003xxxxxx/PMC3744717.xml
|
Imatinib Plasma Monitoring-Guided Dose Modification for Managing Imatinib-Related Toxicities in Gastrointestinal Stromal Tumor Patients
|
A 67-yr-old Asian man who presented with intermittent melena and significant weight loss was diagnosed with small bowel GIST with multiple liver metastases and peritoneal seeding on May 25, 2010. He underwent jejunal resection and anastomosis with palliative intent. The excised jejunal GIST measured 7 × 5 × 5 cm and had a c-KIT exon 9 mutation (1,510-1,515 duplication). After surgery, the patient was treated with 400 mg/day imatinib. He had no concomitant medications or co-morbid diseases.\nTwo months later, the patient developed grade 3 edema, grade 3 ascites, and grade 2 vomiting, with chest radiography revealing layering of a moderate amount of pleural fluid. Because the patient had peritoneal seeding, it was hard to determine whether his ascites and pleural effusion were due to imatinib toxicity or the progression of GIST. Although the follow-up abdomino-pelvic computed tomography (CT) scan showed that the patient's liver metastases had not changed significantly, disease progression was suspected, which prompted a cessation in imatinib treatment and a commencement of sunitinib treatment. The patient was transferred to our hospital for a second opinion after he had been taking sunitinib for approximately 2 months. A thorough review of his previous serial CT scans showed no definitive evidence of disease progression whilst he was on imatinib treatment. We therefore decided to resume 400 mg/day imatinib and use 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET)/CT for accurate assessment of response to imatinib treatment.\nOne month after the patient restarted imatinib, a PET/CT scan revealed a significant decrease in maximum standardized uptake value from 4.2 to 2.9 in one of his liver metastases (), suggesting the tumor was responding to imatinib. However, the patient required paracentesis once weekly to control his ascites, and he complained of peripheral edema and dyspnea. Because imatinib blood level testing revealed that the patient had very high imatinib trough plasma exposure, 4,120 ng/mL and 4,600 ng/mL on two different days (), we decreased his dose to 300 mg/day, which resulted in a steady-state imatinib plasma trough concentration of 3,220 ng/mL (). However, the patient still had grade 2 edema, ascites, and dyspnea on exertion due to pleural effusion. As his imatinib trough plasma exposure was sufficiently high to achieve an adequate tumor response (), we further reduced his dose to 200 mg/day. At this dose, his fluid retention, including ascites, edema, and pleural effusion, was greatly improved, and he had no difficulties in daily life; in addition, his liver metastases remained stable ().\nFive months later, the patient expressed concerns that 200 mg/day of imatinib may be insufficient to control his tumor, as studies have shown that GIST patients with the c-KIT exon 9 mutation may benefit from higher than normal exposure to imatinib (, , ). We therefore increased his dose to 300 mg/day. He was able to tolerate ascites and dyspnea with the use of regular diuretics but had some limitation of activities. Follow-up CT scans to date showed the patient's disease remained stable ().
|
[[67.0, 'year']]
|
M
|
{'27384163': 1, '19451435': 1, '30693663': 1, '8424704': 1, '27446421': 1, '14990650': 1, '21140148': 1, '20124181': 1, '26184165': 1, '16624552': 1, '18256322': 1, '12181401': 1, '16418188': 1, '20177019': 1, '16122278': 1, '18475296': 1, '19307738': 1, '23960456': 2}
|
{'3744717-2': 2}
|
162,699 |
3744717-2
| 23,960,456 |
noncomm/PMC003xxxxxx/PMC3744717.xml
|
Imatinib Plasma Monitoring-Guided Dose Modification for Managing Imatinib-Related Toxicities in Gastrointestinal Stromal Tumor Patients
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A 69-yr-old Asian man presenting with melena was diagnosed with duodenal GIST and underwent Whipple's operation on May 6, 2004. The excised mass measured 5.5 × 4.5 × 2.0 cm and had a low mitotic rate (< 5 mitoses per 50 high-powered fields). Mutation analysis showed that the tumor had a KIT exon 11 deletion at amino acid 552. Twenty-two months after surgery, a liver metastasis was detected on follow-up CT scans. The patient was started on imatinib 400 mg/day. The treatment was effective, with a partial response noted after 3 months (); the treatment was also tolerable, with grade 2 edema the only adverse event experienced by the patient.\nAt 26 months following the commencement of imatinib treatment, the patient developed several small, round, mesenteric lymph node enlargements, which were regarded as a sign of disease progression even though the metastatic lesions in his liver remained stable. Imatinib dose was increased to 800 mg/day. After 7 months at this dosage, the patient experienced grade 3 dyspnea and grade 3 pericardial effusion. He was transferred to our clinic for the treatment of these adverse events. However, an in-depth review of his previous serial CT scans by an experienced gastrointestinal radiologist revealed that the morphology of these enlarged mesenteric lymph nodes suggested reactive changes, instead of lymph node metastases, which are rare in GIST (). The patient was therefore restarted on treatment with 400 mg/day of imatinib. CT scans 10 months later showed that the patient's liver metastasis were stable (). Although his ascites and pleural effusion gradually improved, the patient complained of dyspnea, and diuretics were required for the control of grade 2 generalized edema. Because imatinib plasma monitoring revealed that the patient had high imatinib plasma trough concentrations (3,850 ng/mL and 4,280 ng/mL on two different days; ), we reduced his dose to 300 mg/day, which resulted in imatinib plasma trough concentrations of 2,670 ng/mL and 2,880 ng/mL (). However, pericardial effusion was persistently observed, even after his imatinib dose was further decreased to 200 mg/day, which resulted in steady-state imatinib plasma trough concentrations of 3,070 ng/mL and 2,710 ng/mL (). As the patient's imatinib trough plasma exposure was still sufficiently high () and the follow-up CT scan showed that his liver metastasis remained stable (), we further decreased his dose to 100 mg/day, which resulted in imatinib plasma trough concentrations of 1,660 ng/mL and 1,480 ng/mL (). To date, the patient has been taking 100 mg/day of imatinib for approximately 1 yr. His fluid retention has improved, with durable partial response in his liver metastasis.
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[[69.0, 'year']]
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M
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{'27384163': 1, '19451435': 1, '30693663': 1, '8424704': 1, '27446421': 1, '14990650': 1, '21140148': 1, '20124181': 1, '26184165': 1, '16624552': 1, '18256322': 1, '12181401': 1, '16418188': 1, '20177019': 1, '16122278': 1, '18475296': 1, '19307738': 1, '23960456': 2}
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{'3744717-1': 2}
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