Datasets:

zhengyun21

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PMC-Patients

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3988602-1

noncomm/PMC003xxxxxx/PMC3988602.xml

Pulmonary Hyalinizing Granuloma Associated with Idiopathic Thrombocytopenic Purpura

The present case report is about a 39-year-old woman who presented with pulmonary nodules incidentally detected on abdominal computed tomography (CT) performed for renal calculi []. Further work-up revealed a 2-year history of minimally progressive, non-specific symptoms, which included fatigue, generalized weakness, dyspnea on exertion, and occasional cough associated with recumbent positioning. The patient denied fever, weight loss, chest pain, hemoptysis, or tobacco use. The patient's past medical history was significant for idiopathic thrombocytopenic purpura (ITP) for at least 4 years prior to presentation, for which she had never received any treatment. Additional history indicated chronic sinusitis and medical marijuana use for intractable pain and presumed ilioinguinal neuralgia that followed robotic hysterectomy. The patient also had a left oophrectomy for dysmenorhea 3 years prior to presentation. A chronic organizing abdominal wall hematoma resulting from an intraoperative inferior epigastric vessel injury probably also contributed to her chronic abdominal pain. A family history of malignancy included leukemia, lymphoma, and renal and prostate cancers.\nAdditional immune, infectious, and malignancy test results were negative. Specifically, fungal serologies, transglutanin antibody, phospholipid antibody, rapid plasma reagin, antinuclear antibody, anti-mitochondrial antibody, double-stranded deoxyribonucleic acid antibody, anti-Ro (SS-A/B) antibodies, anti-smith antibody, ribonucleoprotein antibody, striated muscle antibody, anti-smooth muscle antibody, anti-collapsin response mediator antibody, voltage-gated potassium channel antibody, N-type calcium channel antibody, and angiotensin-converting enzyme testing were within normal limits. A chest radiograph demonstrated bilateral rounded pulmonary opacities of various sizes []. A contrast enhanced chest CT showed multiple rounded, discrete pulmonary nodules bilaterally with relative lower lobe and peripheral predominance, which is a common presentation for metastases []. The largest nodule was 2 cm in diameter. Neither enlarged mediastinal or hilar nodes, nor pleural effusions were demonstrated. Positron emission tomography (PET) CT scan was negative []. CT-guided left lower lobe nodule biopsy yielded non-specific lymphoplasmacytic infiltrate, areas of fresh alveolar hemorrhage and no evidence of well-formed granuloma or malignancy. Transbronchial left lower lobe nodule biopsy 6 months later demonstrated fragments of normal lung parenchyma without evidence of a well-formed granuloma or malignancy.\nFollow-up CT scans performed 8- and 16-months after the initial abdominal CT demonstrated stability of the existing nodules and no new nodules. However, continued diagnostic uncertainty led to a thoracoscopic wedge resection of nodules in the superior segment of the left lower lobe and anterior segment of the left upper lobe. Microscopic analysis of each of the two resected round, well-circumscribed, indurated, tan nodules demonstrated some defining features for hyalinizing granuloma, including layers of collagen concentrically arranged in a whorled fashion around small blood vessels []. Inflammatory infiltrate both within and around the nodules consisted primarily of lymphocytes and plasma cells with a few neutrophils and histiocytes. No treatment has been initiated at this point in view of the documented stability of the lung lesions and a lack of significant evidence to suggest that the nodules were responsible for the patient's reported clinical symptoms. Steroids have been reported to be successful for symptom relief and nodule regression in patients with PHG.

[[39.0, 'year']]

F

{'15219012': 1, '7849383': 1, '16155671': 1, '22498827': 1, '17599621': 1, '21085833': 1, '20592998': 2, '1713275': 1, '33572722': 2, '31538016': 1, '27561787': 1, '1714226': 1, '262110': 1, '30363224': 2, '24744965': 2}

{'6159233-1': 1, '7931080-1': 1, '2892707-1': 1}

3988605-1

noncomm/PMC003xxxxxx/PMC3988605.xml

Large ovarian leiomyoma in young woman

A 22-year-old woman was referred to our hospital for abdominal pain and palpable mass at lower abdominal region. Biochemistry laboratory results were not contributory. On computed tomography scan a large mass was revealed close to uterine. The patient was undergone surgical treatment and the large well circumscribed ovarian mass was excited. The left ovary was occupied by this mass without any attachment to other organs.\nOn gross examination, the mass was grayish white and measured about 14.5 × 11.5 × 10 cm. the mass had whorling pattern in cut surface. There was no any hemorrhage or necrosis [].\nOn microscopic examination, the tumor show interlacing bundles of spindle cells with some area of hyalinization. There were no mitosis, necrosis, and atypia [].\nFor confirming the initial diagnosis of ovarian leiomyoma and rule out other ovarian sex cord-stromal tumor, immunohistochemical staining for actin, desmin, and inhibin was performed. The cells showed positive staining for actin and desmin but not for inhibin, so the diagnosis of ovarian leiomyoma was confirmed.

[[22.0, 'year']]

F

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{'2724421-1': 1}

3988606-1

noncomm/PMC003xxxxxx/PMC3988606.xml

Endovascular Coil Occlusion of Traumatic Intradural Aneurysm with Presentation as Carotid Cavernous Fistula

A 40-year-old man presented to the emergency room following a road traffic accident. Computed tomography scan of the brain (plain) revealed frontal hematoma, intraventricular hemorrhage, and subarachnoid hemorrhage with depressed skull fracture. Emergency craniotomy with decompression was performed. On the 4th day of hospitalization, he developed increasing proptosis and conjunctival congestion []. Magnetic resonance (MR) imaging showed hyperintense signals in the basal cisterns suggestive of subarachnoid hemorrhage on T1-weighted sequence. Time of flight MR angiogram maximum intensity projection image showed abnormal communication between internal carotid artery and cavernous sinus. However, the precise location of the rent was not identified [Figure and ]. Digital subtraction angiogram of the left internal carotid artery showed intradural aneurysm (caused by the trauma), which was seen communicating inferiorly with cavernous sinus, basillar plexus, and petrosal sinus [Figure and ]. There was severe vasospasm seen in all the cerebral vessels. Endovascular treatment was planned in order to occlude the aneurysm and the fistulous communication. Balloon occlusion test was not tolerated and hence we chose to occlude the aneurysm and the fistulous communication (preserving the parent artery) over parent vessel occlusion.\nUnder general anesthesia, 6 French guiding catheter was placed in the left internal carotid artery. Echelon micro catheter with traxcess microwire was inserted into the aneurysm. A gentle steam shaping of the micro catheter tip was done to facilitate the navigation of the distal end of the micro catheter into the sinus []. Selective micro-catheter angiogram showed high flow through the aneurysm into the cavernous sinus and inferior petrosal sinus. After achieving stable position of the micro-catheter distally, multiple platinum detachable coils were placed occluding the flow into the sinus. Thereafter, the aneurysm was completely packed with multiple coils and complete occlusion was achieved with no flow into the fistulous communication. Post-coiling angiogram showed complete obliteration of the fistula and exclusion of the aneurysm from the circulation [Figure –]. Patient's proptosis and congestion dramatically decreased over the next few days. Long-term follow-up to assess the coil compaction and recanalization is waiting to be done.

[[40.0, 'year']]

M

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{'6208227-1': 1}

3988609-1

noncomm/PMC003xxxxxx/PMC3988609.xml

Hyperdense Endobronchial Mass - A Rare Manifestation of Metastatic Melanoma

A 57-year-old man with a history of right lower extremity cutaneous melanoma, who had undergone first and second toe amputation 3-years prior, presented with dyspnea and black-colored sputum. Chest radiograph revealed a collapsed left lung, pathologic fracture of the left sixth rib, and a destructive mass involving the right posterior fifth rib []. Non-Enhanced CT (NECT) of the chest showed a hyperdense mass with a mean density of 56 Hounsfield units within the left main bronchus, resulting in postobstructive left lower lobe collapse [Figure and ]. In addition, there were two hyperdense left lower lobe intraparenchymal masses, one of which was lobulated []. There were also lytic bone lesions in the right scapula (not shown) and thoracic vertebrae []. Contrast-enhanced CT (CECT) through the lower chest demonstrated heterogeneous enhancement of the left lower lobe masses []. Bronchoscopy revealed a black-colored hemorrhagic endobronchial mass that was confirmed on histopathology to be an endobronchial metastasis from melanoma []. The patient was treated with imatinib (Gleevec) (Novartis Pharmaceuticals, East Hanover, NJ, USA).

[[57.0, 'year']]

M

{'480395': 1, '34900220': 1, '7828696': 1, '11452056': 1, '18175356': 1, '2556362': 1, '18614346': 1, '6779562': 1, '21295201': 1, '16135176': 1, '27085884': 1, '1138668': 1, '24744964': 2}

{}

3988610-1

noncomm/PMC003xxxxxx/PMC3988610.xml

A Rare Case of Oropharyngeal Teratoma Diagnosed Antenatally with MRI

A 25-year-old female (gravida 2 para 1) was seen by a radiologist for evaluation of polyhydraminos. Her previous anomaly scan reports were normal. Ultrasound evaluation of the fetus revealed no significant abnormalities []. Fetal spine and facial structure were normal. Fetal stomach bubble was seen and was found to be relatively small in size. Placenta was normal. Amniotic fluid volume was greater than normal, amniotic fluid index (AFI) measured 45 cm. Some problem in fetal swallowing due to small stomach and polyhydraminos was suspected. A fetal magnetic resonance imaging (MRI) was done to evaluate cause of acute polyhydramnios and relatively small size of the stomach.\nFetal MRI done on 1.5 T Philips Achieva magnet with T2W turbo spin echo sequences and balanced turbo field echo sequences. Sagittal [] and axial [] images show well-defined mixed intensity lesion with cystic component measuring about 4.5 × 3.5 cm in the oropharyngeal region. No obvious sign of invasion of hard palate or nasopharynx was noted []. No other significant abnormality was noted in the fetus. No destruction of facial structure was found. Large amount of amniotic fluid was seen []. The lower and mid regions of the trachea were well visualized. The mandible appeared normal [].\nBecause of polyhydramnios and severe maternal discomfort, cesarean section was done at 35 weeks. After birth, the baby was found to be hypoxic with difficulty in breathing. Baby was intubated and airway was maintained. Surgery for tumor removal was planned and done on the fourth day after birth. At surgery, well-defined lobulated tumor measuring about 4.5 × 3.4 cm arising from palate was resected [] and sent for histopathology examination. Post surgery, baby recovered well. Histopathology report proved it as immature teratoma [Figures and ]. After 4 weeks, the baby's serum alfa-feto-proteins were found to be elevated to 600 ng/ml. Parents were advised to consult a medical oncologist, who advised follow-up after 6 months. After 6 months, positron emission tomography - computed tomography [] was done to rule any recurrence. The scan showed no signs of any recurrence or metastasis. Serum alpha-feto-protein was repeated and found to be 180 ng/ml. Medical oncologist advised chemotherapy and radiation but the parents did not agree to this treatment. Presently, the boy is 27 months old and doing well without any clinical symptoms.

[[25.0, 'year']]

F

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{'6958897-1': 1, '4700629-1': 1, '6258982-1': 1}

3988631-1

noncomm/PMC003xxxxxx/PMC3988631.xml

Bilateral multiple recession coverage with platelet-rich fibrin in comparison with amniotic membrane

A 40 year-old male patient reported to the Department of Periodontology with a complaint of hypersensitivity to chilled drinks, in relation to the upper left and right back teeth region. He had no significant medical history. The patient gives a two-year prior orthodontic history. On clinical examination, multiple adjacent recessions were identified on the right and left posterior maxillary teeth. The bilateral recession defects, Miller Class I, were measured by calculating the distance between the cementoenamel junction (CEJ) and the gingival margin. It was recorded as the second premolar of 3 mm and first molar of 3 mm. A hard tissue abrasion defect was also present on these teeth and was measured to be less than 0.5 mm in dimension. Phase 1 therapy was completed with oral hygiene instruction reinforced. The surgical procedure was explained to the patient and informed consent was obtained. The use of an additive membrane was assigned by toss of a coin.\nThe operative site, that is, 15 and 16 was anesthetized using 2% Xylocaine with adrenaline (1:200,000). A coronally positioned flap technique was performed at the surgical site in relation to 15 and 16 []. This was performed by making two horizontal incisions with respect to the distal and mesial interdental papillae of 16 and 15, followed by a crevicular incision, two vertical releasing incisions at the mesial and distal aspects of 16 and 15. A full thickness flap followed by a partial thickness one was reflected []. A horizontal releasing incision was made in the periosteum, at the base of the flap, to facilitate tension-free coronal displacement. The exposed root surfaces were scaled and root planed. Following this, the cervical step at the CEJ was eliminated using an aerator and a diamond bur.\nAfter the recipient site preparation was completed, 5 ml of venous blood was drawn in test tubes without an anticoagulant, and centrifuged immediately. It was centrifuged for 12 minutes at 2700 rpm. The resultant product consisted of the following three layers: The topmost layer consisted of acellular Platelet-Poor Plasma (PPP), a PrF clot in the middle, and red blood cells (RBCs) at the bottom. After centrifugation, the PrF clot was obtained, separated from the RBC base using scissors, and placed in a sterile dappen dish. The PrF membrane was prepared by placing it into a petri dish. At the recipient site, the PRF clot was placed over the denuded root surfaces []. The flap was coronally advanced to cover the membrane as well as the defect and sutured []. A tin foil and periodontal dressing were placed over the surgical area.\nThe patient was advised to use 0.2% chlorhexidine digluconate mouth rinse, twice daily. Systemic analgesics were prescribed and he was advised to follow the routine postoperative instructions. The dressing and sutures were removed 10 days after surgery.\nFollow-up of seven months [].\nA similar surgical procedure was followed for the receipt bed preparation along with reduction of the cervical step in relation to 25and 26, similar to that for the PrF membrane [Figures –]. The commercially available amniotic membrane# was cut into the desired shape and length with scissors and placed onto the recession site []. The flap was coronally advanced and sutured []. A tin foil and periodontal dressing were placed over the surgical area.\nSimilar postoperative instructions were advocated as those for CAF with PrF.\nFollow-up of seven months [].\nPostoperative examination was done for one, three, six, and seven months. At the end of the seventh month, both the treatment procedures showed 100% root coverage and increased gingival biotype. However, the amniotic membrane-treated sites showed more stable results than the PrF-treated sites at the end of the seventh month.

[[40.0, 'year']]

M

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{'6009162-1': 1, '6875521-1': 1}

3988652-1

noncomm/PMC003xxxxxx/PMC3988652.xml

Odontogenic fibroma WHO-type simulating periodontal disease: Report of a case

A 54-year-old Caucasian woman was referred to the clinic of Periodontology at the School of Dentistry of the University of Sγo Paulo, complaining of mobility of tooth 25. Oral examination showed the overlying mucosa and gingiva to be with normal color and texture, with no swelling, accentuated mobility of tooth 25, and no other symptoms or history of pain. Percussion and palpation tests showed normal response. There was generalized advanced periodontal disease compromising the other teeth.\nThe radiographic examination showed the presence of a unilocular radiolucent area between the left superior lateral incisor and the first left molar []. Computed tomography (CT) showed bone wall reabsorption between the right first premolar and first molar, compromising of the maxillary sinus floor.\nAn incisional biopsy was performed; removing all the granulomatous tissue present in the area and tooth 25 was removed, as it was decayed []. The specimen was sent for histopathological analysis []. The microscopic examination revealed a cellular connective tissue with multiple islands and strands of odontogenic epithelium covered by stratified squamous epithelium []. Immunohistochemical reactions for AE1/AE3 showed positive staining for an odontogenic epithelium, confirming the central odontogenic fibroma WHO-type diagnosis [].\nThe lesion was surgically removed along with other teeth extractions, as the bone support was lost. The patient showed no signs of recidivism after the six-month follow up.

[[54.0, 'year']]

F

{'8340628': 1, '17327815': 1, '16879337': 1, '15356466': 1, '26457211': 2, '15995576': 1, '7898916': 1, '16618998': 1, '26125006': 2, '24744552': 2}

{'4592713-1': 1, '4483617-1': 1}

3988653-1

noncomm/PMC003xxxxxx/PMC3988653.xml

Peripheral ossifying fibroma, some rare findings

A 27-year-old male patient reported to the department of periodontology and oral implantology, with the chief complaint of a growth of gum tissue in between the upper front teeth []. The lesion had been present for approximately one year. There was no contributory past medical history. Past dental history revealed that patient had a similar growth, which was excised ten years back. He also gave the history of wearing a removable partial denture for a brief period two years back, but he stopped wearing the same as the partial denture broke.\nIntra-oral examination revealed a sessile growth (1 cm × 0.7 cm × 0.5 cm) in between the upper central incisors on marginal and attached gingival. The lesion was firm and erythematous having a smooth, non-ulcerated surface. On occlusal examination, the patient had a traumatic deep bite where the lower central incisors interfered with the lesion during biting []. However, the lesion was asymptomatic, with no sign of pain. Upon swallowing, the patient exhibited a habit of tongue thrusting with midline diastema.\nAn intra-oral periapical radiograph was obtained. The radiographic examination revealed the superficial erosion of the bone [], which was later reconfirmed during surgical excision.\nDifferential diagnosis: Irritation fibroma, pyogenic granuloma, and peripheral giant cell granuloma (PGCG) were considered.\nFull mouth scaling was done to remove local irritants []. Occlusal correction was also done at this stage []. Excision and microscopic examination were planned, and patient's consent for the same was taken.\nA full thickness flap was elevated facial to tooth 11, 21 using crevicular incision []. The lesion was excised completely using a 15 no. B.P blade []. The flap was repositioned over the exposed teeth of 11, 21 and stabilized with 3-0 silk sutures under local anesthesia []. During reflection of flap, the superficial erosion of bone was seen []. The excised tissue measured 1 cm × 0.7 cm × 0.5 cm []. The tissue was submitted to the oral pathology division for histopathological examination.\n“H and E-stained soft tissue section shown fibrous connective tissue, which is composed of varying degree of cellularity, which includes plumb hyperchromatic, fibroblasts, calcification (Bone like), dense bundles of collagen fiber, chronic inflammatory cells comprising mostly of lymphocytes, and blood vessels [].\nOverlying epithelium is parakeratinized stratified squamous epithelium, which shows long and narrow rete ridge."\nThe histopathological findings confirmed the lesion as POF.\nThe patient presented for follow-up examination 7 days, 15 days, and 45 days postoperatively []. The surgical site appeared to be healing well. There was no evidence of recurrence of the lesion, and the patient had no complaints pertaining to the lesion.

[[27.0, 'year']]

M

{'26556782': 1, '19414975': 1, '5223950': 1, '4626993': 1, '3472146': 1, '11447957': 1, '17220623': 1, '5248843': 1, '7776054': 1, '6750498': 1, '3479457': 1, '24744553': 2}

{}

3988655-1

noncomm/PMC003xxxxxx/PMC3988655.xml

Inflammatory hyperplasia: From diagnosis to treatment

A female patient aged 38 years reported with a chief complaint of swelling in the left front region of the gums.\nThe lesion was nodular, circumscribed polypoid lesion measuring about 1.5 cm × 1.2 cm, pinkish to reddish in color, which bled easily, and was painless. This lesion involved the marginal and interdental gingiva on the facial surface of the maxillary left canine and 1st premolar. Local factors plaque and calculus were present [].\nOral hygiene instructions were given and scaling and polishing were done on the first visit. Then, the patient was recalled for surgical excision of the lesion. After excision, residual calculus was removed and root planing was performed [Figures and ]. The excised lesion was sent to the Department of Oral Pathology for histopathological examination. The patient was motivated to maintain oral hygiene and was asked to rinse her mouth with 0.2% chlorehexidene mouthwash twice daily for 1 week. The patient was kept under observation through recall checkups.\nMicroscopic examination revealed hyper-parakeratinized stratified squamous epithelium with ulceration and acanthosis of the stratum spinosum. The underlying dense fibrous connective tissue stroma showed severe chronic inflammatory cell infiltrate consisting of lymphocytes and plasma cells and a moderate number of endothelial-lined blood vessels suggestive of chronic inflammatory fibrous hyperplasia [].\nFigures and show the post-operative photograph of the same lesion after 1 and 3 weeks, respectively.

[[38.0, 'year']]

F

{'21968923': 1, '17097201': 1, '27761588': 1, '2120653': 1, '29751776': 1, '21528029': 1, '26818898': 1, '24744554': 2}

{}

3988656-1

noncomm/PMC003xxxxxx/PMC3988656.xml

An undiagnosed case of acute myeloid leukemia

A 43-year-old female patient reported to the Department of Periodontology, with the chief complaint of generalized bleeding gums, and gingival swelling from last 2 months. Patient gave no history of fever, malaise, weight loss in the recent past. Patient was not under any medication for chronic illness. Extra oral examination reveals bilateral submandibular and deep cervical lymphadenopathy; lymph nodes were indurated and tender on palpation. Systemic examination reveals mild hepatomegaly and splenomegaly.\nIntraoral examination revealed generalized enlargement of the maxillary and mandibular gingiva involving the buccal, lingual, and palatal aspects [Figure –]. The gingiva was swollen, inflamed, erythematous, and devoid of stippling. On palpation gingiva was firm and edematous, tender and bleeding on slight provocation. There was a fair amount of plaque and calculus, but did not justify the amount of enlargement. Orthopantomogram did not reveal any significant findings.\nThe following differential diagnoses were considered: Inflammatory enlargement, conditioned enlargement, systemic enlargement, and neoplastic enlargement.\nComplete blood count [] revealed marked increase in white blood cells, decrease in red blood cells with decrease in hemoglobin levels, and low platelets count; indicative of leukocytosis, anemia, and thrombocytopenia.\nPeripheral smear depicted numerous blast cells, mainly immature leukocytes with few erythrocytes and thrombocytes [].\nThese results confirmed the final diagnosis of acute myeloid leukemia. Oral hygiene instruction was given to the patient. Patient was instructed to use soft bristle toothbrush, as gingiva was inflamed, friable and edematous use of hard or regular brush is not recommended. Thrice a day Chlorhexidine (0.2%) was prescribed as oral rinse.[] Scaling and root planning was postponed since the treatment needs a minimum platelet count of 60 000 in this condition. Patient was immediately referred to the oncology centre for further management, where bone marrow biopsy confirms acute myeloid leukemia M5 and chemotherapy started. Patient did not respond well to chemotherapy and succumbed to the disease within 10 days of admission.

[[43.0, 'year']]

F

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{}

3988657-1

noncomm/PMC003xxxxxx/PMC3988657.xml

Labial-cervical-vertical groove: A silent killer-Treatment of an intrabony defect due to it with platelet rich fibrin

A 47-year-old male patient reported to the Department of Periodontology, with a chief complaint of pus discharge from maxillary left central incisors with dull intermittent pain. There was no relevant medical history. The patient was a non-smoker. On clinical examination, a localized gingival inflammation was present with soft edematous tissue with the accumulation of plaque and calculus with #11 and #21. Periodontal examination depicts a pocket depth of 11 mm on mesial aspect and 8 mm on midbuccal aspect of #21 [] with no mobility. Fremitus was found to be negative precluding the possibility of trauma from occlusion and tooth was found to be vital electric and thermal pulp testing. On radiographic examination, a tear-shaped radiolucency was present with localized bone loss in #21 []. On careful examination, LCVG was found on #21 which was extending into gingival sulcus.\nThe patient was subjected to complete scaling and thorough root planning. The patient was given oral hygiene instructions. The patient was reviewed after 2 weeks. Clinical symptoms subsided, but the deep pocket was still present and hence a periodontal surgery was carried out to eradicate the underlying problem. The procedure was explained to the patient and the consent was obtained for the same. Routine blood investigations were done.\nAfter assuring surgical asepsis, a pre-procedural rinse with 0.2% chlorhexidine gluconate was accomplished. After administration of local anesthetic (2% lignocaine with 1:80000 adrenalin), the papilla preservation flap (Takei et al.) was adopted since there was sufficient space between the maxillary central incisors. A full-thickness flap was reflected on both facial and palatal surfaces. The exposed root surfaces were thoroughly scaled and root planed and bone defect carefully curetted. LCVG noted on #21 [], terminated in the cervical third of root surface was sealed with glass ionomer cement (Fuji II; GC Corporation, Tokyo, Japan) [].\nThe PRF was prepared following the protocol developed by Choukroun et al. Briefly, the procedure of PRF preparation: 10 ml intravenous blood was collected by venepuncture at the antecubital fossa. This was transferred into 10 ml sterile tube without anticoagulant and immediately centrifuged at 3000 rpm for 10 min. Fibrin clot formed in between the acellular plasma on top and the red blood cells at the bottom were separated using sterile tweezers and scissors [].\nPRF was placed in the intrabony defect with #21 []. Suturing was done using 3-0 black silk. Then periodontal dressing was given.\nThe patient received post-operative instructions and was prescribed post-operative antibiotic – amoxicillin 500 mg thrice for 7 days and analgesic – aceclofenac 100 mg twice for 3 days.\nThen, 1 week postoperatively, the dressing was removed and saline irrigation was done. The patient was monitored at regular intervals and was under maintenance therapy. At the end of 3 months and 6 months, clinical examination and intraoral periapical radiographs of the treated area were taken. The clinical measurements were repeated and compared to the baseline values.\nOn examination during subsequent follow-ups, treated area showed satisfactory healing without any post-operative complications. LCVG was completely sealed off. The pocket depth was 2 mm on mesial and 1 mm on midbuccal aspect at 6 months []. Periodontal health was stable and bone regeneration was noticed in radiograph []. The patient was satisfied with the result.

[[47.0, 'year']]

M

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{}

3989827-1

noncomm/PMC003xxxxxx/PMC3989827.xml

Virilizing lipoadenoma of the adrenal gland in a pre-pubertal girl: A rare case

A 12-year-old girl presented to our hospital with a history of abnormal menstruation and progressive hirsutism. She had a normal childhood until 2 years back when she started noticing appearance of hair on her face, body, extremities and pubic region. Her height, weight and body mass index were within the normal limits. Blood pressure was 104/64 mm Hg and pulse rate was 92 beats/min. There was thick black hair on the face, arms, chest, back, legs and over the pubic region. Her breasts were pre-pubertal. Pelvic examination showed enlargement of the clitoris. Results of routine lab studies including serum electrolytes were normal.\nAbdominal and pelvic ultrasonography showed the presence of 10 cm × 8 cm sized well- defined, primarily hyperechoic mass lesion seen in the right adrenal region with indentation of the adjacent surface of liver and kidney. The uterus appeared small in size. Multi-detector computed tomography (MDCT) of abdomen, plain and contrast, showed a large well-defined heterogeneously enhancing predominantly fat attenuating lesion measuring 9.5 cm × 8.7 cm × 8.0 cm involving the right adrenal gland. The lesion demonstrated multifocal area of nodular calcification with enhancing solid component and was seen compressing the superolateral aspect of the right kidney with the minimal inferomedial displacement [Figure and ]. Blood tests were carried out for functional assessment of the right adrenal tumor. Serum testosterone level was raised to 2.24 ng/ml. Serum adrenocorticotrophic hormone, 17 hydroxyprogesterone, progesterone and cortisol levels as well as urinary 17 keto steroids, 17 hydroxy corticosteriods and vanilylmandelic acid levels were normal. A clinical diagnosis of adrenal myelolipoma was made and right adrenalectomy was performed. The specimen showed an encapsulated tumor measuring 10 cm × 8 cm × 7 cm []. Microscopic examination showed compressed adrenal tissue with foci of hemorrhage within the well- encapsulated tumor. The tumor nodules were primarily composed of eosinophilic lipid poor cells resembling zona reticularis. Mitotic rate was <5/50 hpf. No atypical mitosis was seen. The tumor nodules were separated by bands of hyalinized fibrous tissue containing proliferating thick walled vessels, hemorrhagic foci and sparse lymphocytic infiltrate. Islands of abundant mature adipose tissue were also seen. Scattered foci containing lipofuscin pigment were seen and no vascular/capsular invasion or necrosis was seen [].\nBased on the size, weight of tumor, microscopic features and Weiss criteria a final diagnosis of lipoadenoma, a morphological variant of adenoma was made.\nPost-operatively serum testosterone level returned to 0.158 ng/ml, which was within the normal limits. Patient's menstrual cycles regularized and features of hirsutism decreased [].

[[12.0, 'year']]

F

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{}

3989828-1

noncomm/PMC003xxxxxx/PMC3989828.xml

Ureteral spread of a primary cutaneous diffuse large B-cell lymphoma, leg type

A 76-year-old male patient presented with 2 months history of progressing, non-specific, right flank pain without any other accompanying symptoms. He had no history of urolithiasis, but he had presented 1 year earlier with a mass of the right knee measuring 5 cm in its greatest diameter. Histological examination showed lymphoid diffuse large cells proliferation, which stained diffusely with anti CD20, anti Bcl2 but was CD10 negative in the immunohistochemical study. A diagnosis of primary cutaneous diffuse large B-cell lymphoma, leg type (PCDLBCL-LT) was then made. No others lymphomas were found at the time of diagnosis. The patient had no others skin conditions, especially no history of infections.\nFor the current symptoms, he underwent ultrasonography of the abdomen which revealed right hydronephrosis. Abdomino-pelvic computed tomography scan showed pyelo-calyceal dilatation with continuous obstruction, 8 cm in length, of the distal portion of the right ureter []. No retroperitoneal or mesenteric lymphadenopathy was found. The diagnosis of ureteral tumor of urothelial origin was then suspected and the patient underwent a right radical nephroureterectomy.\nMacroscopic examination showed a kidney measuring 10 × 6 × 3 with a ureter measuring 12 cm of length. On sectioning the ureter, a white, firm, concentric thickness of the pelvic portion of the right ureteral wall was found. The abdominal portion of the ureter as well as the pelvi-calyceal swystem was dilated.\nHistological examination showed infiltration of the ureteral wall by a lymphoid diffuse large cells proliferation that spared the urothelium []. The tumoral cells were medium to large size centrocytes with a variable proportion of centroblasts and immunoblasts mixed with small reactive lymphocytes []. On immunohistochemical study, the large cells stained diffusely and intensely with anti CD20, anti Bcl2 and were CD10 and Bcl6 negatives [Figure –].\nThe diagnosis of ureteral spread of the cutaneous diffuse large B-cell lymphoma, leg type was then made.

[[76.0, 'year']]

M

{'17875875': 1, '15692063': 1, '28225499': 2, '21109511': 1, '16492713': 1, '494460': 1, '27313721': 1, '27588189': 1, '18567836': 1, '8431700': 1, '31099459': 1, '17862436': 1, '24744525': 2}

{'5569421-1': 1}

3989829-1

noncomm/PMC003xxxxxx/PMC3989829.xml

Mesenchymal chondrosarcoma of kidney

A 22-years-old female complained of hematuria, high grade fever, heaviness, and pain in right flank for 2 months. Contrast enhanced computed tomography (CECT) revealed a complex hypodense mass with variegated attenuation measuring 6 × 6 × 5.6 cm in mid-polar region of right kidney, involving the inferior vena cava. No calcification or fat was noted within the mass. No perirenal infiltration or lymphadenopathy was observed. Magnetic resonance imaging (MRI) revealed a large lobular mass measuring 6.5 × 6.2 × 5.6 cm in the right kidney with mixed hyperintense and hypointense signals on T2 weighted imaging. Positron emission tomography showed some subcentimetric non-FDG avid lung nodules which were suspected to be metastatic deposits. A clinical diagnosis of right sided renal cell carcinoma (T3bN0Mx) with invasion into inferior vena cava and metastasis to lungs was made. Right radical nephrectomy with IVC thrombectomy and lymph node dissection was performed. Per-operatively, the tumor involved the medullary region of right kidney. The IVC thrombus was infiltrating its wall and extended upto the level of caudate lobe of liver.\nPathology - Grossly, the right nephrectomy specimen measured 9 × 6 × 4 cm and showed a friable tumor measuring 4 × 4 × 3 cm in the medullary region, invading the renal parenchyma and compressing the pelvicalyceal system, but not involving the latter []. The tumor was fleshy in appearance and there were no glistening areas visible within the tumor grossly. The renal vein showed a tumor thrombus. IVC thrombus, sent separately, measured 5 × 2 × 2 cm. Attached ureter measured 2 cm and was grossly free of tumor. Histopathology showed a well circumscribed tumor comprising of an unusually large component of well differentiated cartilage alternating with stromal component which comprised of small sized, oval to spindle shaped cells with moderate nuclear pleomorphism, hyperchromatic nuclei, inconspicuous nucleoli, and moderate cytoplasm [Figure and ]. The spindle shaped cells displayed a hemangiopericytoma like pattern of arrangement []. Numerous atypical mitotic figures were noted along with focal areas of myxoid change and necrosis. The tumor was not involving the pelvicalyceal lining, which showed normal morphology and displayed no features of dysplasia/carcinoma in situ. On immunohistochemistry (IHC), the spindle cells were positive for vimentin and the cartilaginous component was strongly positive for S-100 []. The tumor was involving the inferior vena cava. However, the ureter and the lymph nodes (29 in number) were free of tumor. Based on these findings, a diagnosis of extra skeletal mesenchymal chondrosarcoma of kidney was made.\nTreatment - The patient was planned for close follow up at monthly intervals. Within 3 weeks of surgery, she presented with dyspnoea and chest pain of acute onset. CT pulmonary angiography was suggestive of pulmonary thromboembolism with partial IVC thrombosis. She was started on systemic chemotherapy with intravenous Cisplatin (90 mg/m2) and Epirubicin (75 mg/m2) on Day 1 at 3 weekly intervals. After six cycles of chemotherapy, the patient showed marked clinical improvement with significant regression in lung nodules [].

[[22.0, 'year']]

F

{'16643625': 1, '30909775': 2, '34976575': 2, '14416919': 1, '32782706': 1, '31897203': 1, '26622628': 1, '14161087': 1, '6861090': 1, '15661546': 1, '3697943': 1, '24744526': 2}

{'8571990-1': 1, '6442158-1': 1}

3989830-1

noncomm/PMC003xxxxxx/PMC3989830.xml

Appendicocalicostomy: A case of mistaken identity

A 32-year-old female patient presented with right flank pain of 3 weeks duration. She had undergone right open pyelolithotomy 6 weeks ago at the private hospital. Intraoperatively, a double J (DJ) stent was placed, which was removed 3 weeks later. Following stent removal she had progressively increasing flank pain. Examination showed a well healed scar of pyelolithotomy and tenderness in the right flank. Her hematological and biochemical investigations were normal. Ultrasonography showed normal left kidney with hydronephrotic right kidney (parenchymal thickness of 7 mm) and 400 ml perinephric collection. A perinephric drain and right percutaneous nephrostomy (PCN) tubes were placed. A total volume of 300 ml of turbid perinephric fluid was drained stat. PCN output was ≈ 1.5 L/day. Drain was removed after 7 days. A right nephrostogram with the right retrograde ureteropyelogram (RGP) was done, which showed complete cut-off at the pelvi-ureteric junction with small intrarenal pelvis and ureter showed complete cut-off at L2 vertebral level [Figure and ]. Length of defect was ≈ 3 cm. After 1 month, right ureterocalicostomy was done. Intraoperatively, there were dense perinephric adhesions. Lower pole of the kidney could be mobilized only in the subcapsular plane and the PCN came out during the mobilization. Ureter was dissected inferomedial to the lower pole of the kidney. Lower polar parenchyma was amputated and ureter was spatulated. Ureterocalicostomy was done over DJ stent. Stent could be placed easily. However, urinary bladder was not distended prior to stent placement; hence, no attempt was made to see retrograde efflux of urine from side holes of cranial end of the stent. Post-operative X-ray showed a malpositioned lower end of stent []. Right RGP showed stent lying outside the ureter []. PCN was placed and nephrostogram was done, which showed that the contrast going into the cecum thereby establishing that the lower pole of the kidney was inadvertently anastomosed to tip of the appendix. Patient was re-explored. Ureter was identified medial to the appendix []. Ureterocalicostomy and appendicectomy was done []. Post-operatively patient made smooth recovery. PCN and DJ stent were removed after 1 week and 6 weeks respectively. Intravenous urography done 6 weeks following stent removal showed patent ureterocalyceal anastomosis with prompt drainage of contrast. Patient is asymptomatic at 1 year follow-up.

[[32.0, 'year']]

F

{'24744527': 2}

{}

3989831-1

noncomm/PMC003xxxxxx/PMC3989831.xml

Keratinizing squamous metaplasia of the upper urinary tract in a child with a solitary kidney

A 3-year and 6-month-old male child presented to us with complaints of intermittent fever for 1 month. The parents complained of refusal for feeds and lethargy. He had a history of polydipsia and polyuria. Antenatal ultrasound scans had identified an absent right kidney with hydronephrosis of the left kidney. His parents had been advised surgery for left pelviureteric junction obstruction at the age of 2 months, but they had refused.\nAt presentation to us, the child had chronic renal failure with severe metabolic acidosis. A large renal lump was palpable in the left flank. Blood investigations revealed Hb of 6 gm%, total leukocyte count of 15,900/cumm, serum sodium of 116 mmol/L, serum potassium of 2.1 mmol/L, serum creatinine of 2.8 mg/dL and blood urea nitrogen of 97 mg/dL. Urine examination revealed pyuria with significant growth of Escherichia coli. Ultrasound of the kidney revealed absent right kidney with gross hydronephrosis and parenchymal thinning on the left side. Debris was noted in the dilated pelvicalyceal system.\nThe child was stabilized in pediatric intensive care for fluid and electrolyte imbalance and was administered culture specific antibiotics.\nThe DTPA scan revealed non-visualization of the right kidney with severely diminished parenchymal uptake on the left side without any excretion over 24 hours.\nAfter stabilization, he was taken for open left pyeloplasty. The kidney was grossly dilated with thinned-out parenchyma. The dilated pelvicalyceal system was full of an unusual, white creamy material with thin flakes, not resembling pus []. The system was also lined by the same material. The flakes were gently aspirated out and sent for culture and histopathology. Anderson-Hyne's dismembered pyeloplasty was performed with a nephrostomy tube. The post-operative course was uneventful. Hisopathology revealed focal areas of mature squamous epithelium with keratinization. The flakes were suggestive of an acellular keratin-forming membranous sheath [].\nAt a follow-up of 1 year, the child is asymptomatic with normal renal function.

[[3.0, 'year'], [6.0, 'month']]

M

{'5776550': 1, '27433075': 1, '7069821': 1, '27635299': 1, '6724826': 1, '22606632': 2, '3798607': 1, '5052238': 1, '33487948': 2, '1159901': 1, '9730474': 1, '24744528': 2}

{'3350100-1': 1, '7815026-1': 1}

3989832-1

noncomm/PMC003xxxxxx/PMC3989832.xml

Supernumerary testis: Imaging appearance of a rare entity

A 52-year-old gentleman, suffering from chronic kidney disease presented to our hospital with the complaint of abdominal distension. During the course of clinical examination, a painless extratesticular solid lump was detected. The patient was aware of this lump since childhood but had not sought medical advice since it was small, painless and not growing. Scrotal sonography revealed presence of two testis like structures in the left hemiscrotum and a normal testis on the right side []. Each of the left testes was smaller than the right sided normal testis and showed normal echotexture and vascularity. The rete testis of one of these testes was prominent []. Each of these left sided testis had an independent epididymis and a common vas deferens draining both the testes. Gross scrotal wall edema was also present, secondary to chronic kidney disease along with gross ascites, which was responsible for abdominal distension.\nMagnetic resonance imaging (MRI) of the scrotum confirmed the presence of two testis-like structures in the left half of scrotum with signal intensities identical to the right testis []. Both these structures showed a surrounding tunica albuginea, existence of independent epididymis and a common vas deferens in agreement with the ultrasound findings. Presence of prominent rete testis in one of the testicle and scrotal wall edema was confirmed.\nAfter confirmation of the diagnosis of supernumerary testis without evidence of any complication, no treatment was offered.

[[52.0, 'year']]

M

{'3046267': 1, '1988735': 1, '17559037': 1, '19765760': 1, '28479781': 1, '24744529': 2}

{}

3990079-1

noncomm/PMC003xxxxxx/PMC3990079.xml

Ibuprofen Associated Acute Vanishing Bile Duct Syndrome and Toxic Epidermal Necrolysis in an Infant

A 7-month-old girl was hospitalized with complaints of fever and erythematous rashes on body. Two days earlier, she had fever and received ibuprofen at conventional pediatric doses (maximum of 30 mg/kg/day). She had no history of allergic disease. Three months ago, she had been treated with one-dose of ibuprofen (10 mg/kg) for sporadic fever. There was no family history of atopic disease, immunodeficiency or hepatobiliary disease. On admission, physical examination revealed macular erythematous eruption on her face, trunk, and arms, which progressed within 8 hours into the bullae around the arms, and involved the face and trunk. Skin lesion covered more than 30 percent of her body surface area. There were no lesions in the lips or in the eyes. A diagnosis of toxic epidermal necrolysis was made.\nThe initial peripheral white cell count was 5910/mm3 with 69.7% neutrophils, 20.3% lymphocytes, and 3% eosinophils. Hemoglobin level was 12.2 g/dL, platelets count 250000/mm3, erythrocyte sedimentation rate of 120 mm/h, and C-reactive protein 9 mg/dL. Aspartate aminotransferase (AST) level was 716 IU/L, alanine aminotransferase (ALT) 523 IU/L, alkaline phosphatase (ALP) 500 IU/L, total bilirubin (TB) 0.52 mg/dL and direct bilirubin (DB) 0.15 mg/dL. Serological test for hepatitis A, B, and C, Epstein Barr virus, parvovirus B19, herpes virus, adenovirus, cytomegalovirus, human immunodeficiency virus, leptospira, and mycoplasma were negative.\nAt hospital day 6, fever and cutaneous lesion resolved after supportive care but cholestatic picture was presented. AST level was 879 IU/L, ALT 723 IU/L, ALP 890 IU/L, TB 8.5 mg/dL, DB 5.7 mg/dL, gamma-glutamyl transferase 270 IU/L, and total cholesterol 760 mg/dL. The following laboratory findings were normal: amylase, lipase, prothrombin and partial thromboplastin time, α1-antitrypsin, immunoglobulins, complement levels, antinuclear antibody, anti-DNA antibody, anti-smooth muscle antibody, antimitochondrial antibody, anti-liver/kidney microsomal, anti-cytosol antibody, and antineutrophil cytoplasmic antibody. Abdominal ultrasound showed that the liver had homogeneous texture with normal bile ducts and gallbladder. Ursodeoxycholic acid treatment (15 mg/kg per day) was administered.\nAt hospital day 20, skin lesion recovered, but the TB and DB levels were still high (TB 9.5 mg/dL, DB 7.7 mg/dL). Liver biopsy was performed 20 days after admission. It showed lymphocyte infiltrations, marked degeneration of the interlobular bile duct epithelium, and the destructive narrowing of the ductules in the portal tracts and no intralobar bile ducts in at least 10 portal areas on H&E stain, suggesting VBDS (). Neither an organism nor viral cytopathic effect was identified. There was no significant hepatocellular damage and no evidence of sclerosing cholangitis or autoimmune hepatitis.\nThe diagnosis of VBDS associated with TEN was made. During a follow-up period of 3 months, clinical symptoms and biochemical data had shown tendency for resolution. The ursodeoxycholic acid treatment was discontinued. During the next three years, she has a normal physical status with normal liver synthetic functions.

[[7.0, 'month']]

F

{'30268094': 2, '33251781': 2, '15289784': 1, '17168994': 1, '8759674': 1, '276660': 1, '1735527': 1, '11837721': 1, '9721172': 1, '28597358': 1, '18698687': 1, '26581761': 1, '11713940': 1, '21510822': 1, '18377375': 1, '16807519': 1, '24719156': 2}

{'6162916-1': 1, '7700876-1': 1}

3990081-1

noncomm/PMC003xxxxxx/PMC3990081.xml

Aggravation of Hypertriglyceridemia and Acute Pancreatitis in a Bipolar Patient Treated with Quetiapine

A 51-year-old woman with a history of bipolar affective disorder was presented to our hospital with an 8-h history of nausea and epigastric pain radiating caudally. Three months prior to admission, an elevated serum triglyceride level (408 mg/dL) was noted, but the patient didn't receive any lipid-lowering agents. Two months before presentation, she was treated for bipolar effective disorder with valproic acid 500 mg twice daily, quetiapine 600 mg at bedtime, and flurazepam 30 mg at bedtime. One month prior to admission, valproic acid was tapered and stopped, and quetiapine dose had been increased to 800 mg at bedtime. At current presentation, she was taking both quetiapine 800 mg and flurazepam 30 mg at bedtime. There was no history of alcohol abuse, recent abdominal trauma or surgery, preceding viral syndromes, or cholelithiasis, and no other concomitant medications were being used.\nThe initial physical examination indicated a diffuse abdominal tenderness without muscle guarding or rebound tenderness, and hypoactive bowel sounds were auscultated. Laboratory studies showed a leukocyte count of 9.9×109/L, with a differential count of 68% neutrophils and 24% lymphocytes. Serum electrolytes and liver function tests were within normal limits. Other pertinent laboratory values included a serum amylase of 352 IU/L (normal, 30-110 IU/L), serum lipase of 1210 IU/L (normal, 23-300 IU/L), triglyceride of 1508 mg/dL (normal, 35-150 mg/dL), and a total cholesterol level of 450 mg/dL (normal, 130-200 mg/dL). Abdominal ultrasound showed no evidence of gallbladder disease or dilatation of the bile ducts. Abdominal computed tomography showed a blurring contour from pancreatic head to tail, with minimal fluid collection at the pancreatic head region. A diagnosis of acute pancreatitis was made.\nThen the patient was treated symptomatically with volume repletion and meperidine for pain relief. Quetiapine was suspected as the cause of severe hypertriglyceridemia, and was immediately withdrawn. In addition, treatment with oral fenofibrate 160 mg daily was commenced for reducing serum triglycerides. Ten days later, the patient was free of abdominal pain, the serum amylase and lipase values were normal, and the triglyceride level was reduced to 337 mg/dL. The patient was discharged on the following medications: aripiprazole 5 mg at bedtime, flurazepam 60 mg at bedtime, and fenofibrate 160 mg once daily. The patient was discharged with appointments for follow-up with the endocrinology and psychiatry services. She was asymptomatic at the 3-month follow-up.

[[51.0, 'year']]

F

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{'7805503-1': 1}

3990116-1

noncomm/PMC003xxxxxx/PMC3990116.xml

An 18-Year-Old Man With Hepatitis B Virus Infection and Hepatoblastoma

An 18-year-old man referred due to right upper quadrant (RUQ) pain since two months prior to admission in this hospital. The RUQ pain, which was constant has had radiation to his back, and gradually was worsened. He gradually developed yellowish discoloration of the sclera and skin and abdominal distention. He had complaints of low back pain, that aggravated by movement since one month prior to admission. The patient had anorexia with a 15 kg weight loss during these two months with no history of fever, chills, vomiting, diarrhea, change in bowel habits or tarry stools.\nIn physical examination he was icteric and wasted. The abdomen was protruded, flanks were bulged and shifting dullness was positive. Few collateral vessels were present in abdominal surface. The liver was enlarged with firm two nodular consistency, and spleen was palpable by ballottement maneuver. Examination of genitalia and testes were normal. Laboratory results were as follows: hemoglobin (9.1 g/dl), platelets (257000/mm3), Homocysteine: 20.5 μmol/L (normal 5-15), anti-cardiolipinIgM 2.9 MPL (normal <15), anti-phospholipid IgG: 1.8 (normal <10), protein C: 127% (normal 70-130), protein S: 51% (normal 65-140), lupus anticoagulant: negative, alanine aminotransferase: 113 IU/L, aspartate aminotransferase: 495 IU/L, alkaline phosphatase: 1253 IU/L, total bilirubin: 12.6 mg/dl, direct bilirubin: 12 mg/dl and LDH: 789 U/L, serum HBs Ag was positive and HBV DNA serum level was 247 IU/ml. Total protein, albumin, and coagulation indexes were within normal ranges. Paracentesis of ascitic fluid showed clear color with high serum ascites albumin gradient, without findings of peritonitis.\nUltrasonography of abdomen showed a coarse liver parenchyma, without mass or space occupying lesion. The portal vein diameter was 11 mm. The spleen was 201x55 mm with a homogeneous echo pattern. Moderate ascites was also noted.\nEndoscopy was notable for the presence of F1 esophageal varices, and fundal varices (without active bleeding or stigmata of recent hemorrhage), and a kissing type duodenal ulcer disease.\nColor Doppler Ultrasonography of abdomen showed splenic and portal vein thrombosis, but the hepatic artery and inferior vena cava were normal. The initial serum alpha-fetoprotein level was 300 ng/ml (normal 0-8.5) that after ten days increased to 112000 ng/ml. Spiral triphasic CT scan () and MRI () revealed atrophic right lobe with mild enlargement of left lobe.\nThe caudate lobe was heterogeneous and severely enlarged. There was thrombosis in the main portal vein with extension to the intra-hepatic branches, and splenic vein. Moderate ascites was also seen. The patient underwent a liver biopsy under sonography guide.\nLiver biopsy ( and ) contained normal as well as neoplastic tissues. In the non-neoplastic tissues, there was no evidence of cirrhosis. The tumor component was composed of small and large nests of small hepatocyte-like cells. The nests were separated by very delicate fibrovascular fascicles. The individual cells were round to polygonal shaped with amphophilic to somewhat eosinophilic cytoplasm and round to oval hyperchromatic nuclei with occasional nucleoli. Intranuclear optically clear inclusions were occasionally seen. Intracytoplasmic micro- as well as macro-vesicular fat accumulation was prominent. There were also scattered and large aggregates of polygonal cells with abundant fat accumulation in the cytoplasm (). Immunohistochemistry (IHC) was positive for Hepar1 (focal), vimentin, CK, AFP, pCEA and AFP (diffuse), and alfa-1 anti-trypsin. IHC was negative for CD34, synaptophysin, NSE, TTF-1, desmin, chromogranin, placental alkaline phosphatase, CD99, CD10, albumin, and S100. According to the histopathology features and IHC profile, the diagnosis was reported as fetal type hepatoblastoma.

[[18.0, 'year']]

M

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{'2990241-1': 1}

3990119-1

noncomm/PMC003xxxxxx/PMC3990119.xml

Castleman’s Disease of the Porta Hepatis

A 41-year-old female presented with easy fatigability. Physical examination was normal and there was no significant finding noted in her medical history. Hematologic studies revealed normal complete blood count (CBC) and a high erythrocyte sedimentation rate (ESR) of 110 mm/h. Biochemical analysis showed: total protein of 10.3 gr/dl, albumin of 3.6 gr/dl, and globulin of 6.7 gr/dl. Liver function tests, including alanine aminotransferase (ALT) and aspartate aminotransferase (AST), were normal. Serum protein electrophoresis showed hypergammaglobulinemia (5.7 gr/dl). Immunoelectrophoresis showed an IgG level of 4750 gr/dl; other fractions were decreased. Urine Bence-Jones protein was negative. Bone marrow aspiration and biopsy were also unremarkable. Abdominal CT scan showed several lymphadenopathies (LAP) in the hilum of the liver. The patient underwent exploratory laparotomy to find out the cause of the LAP. Very enlarged lymph nodes were noted in the porta hepatis (each almost 3 cm). Frozen section showed reactive lymph nodes. Therefore, all lymph nodes were excised and sent for pathologic studies.\nMicroscopic examination of the lymph nodes showed lymphoid follicles with small germinal centers bearing resemblance to Hassall’s corpuscles of the thymus. Hyaline deposits were present within the germinal centers (). With the diagnosis of Castleman’s disease (hyaline vascular type), the patient was discharged from the hospital and followed with laboratory tests. After less than a month, she was completely free of symptoms; ESR and serum protein levels returned to normal. She remained well for 2 years when her symptoms of easy fatigability and loss of well-being returned. Physical examination was unremarkable with no LAP. Laboratory findings showed hypergammaglobulinemia and high ESR, but this time liver enzymes that included ALT (40 IU/L) and AST (36 IU/L) were also mildly elevated (normal <28 IU/L). Imaging studies were unremarkable and no sign of LAP was detected in the thorax and abdomen. All autoimmune and viral markers were negative. The decision was made to perform a liver biopsy. The microscopic section of the liver was unremarkable except for 2 to 3 scattered large lymphoid follicles with germinal center(s) (). No evidence of hepatocellular injury or bile duct epithelial damage was noted. Serial cut sections were performed to determine characteristic findings of Castleman’s disease, but the histologic picture was the same. Immunohistochemical studies of the liver showed follicles with CD20+ centrocytes and some centroblastic lymphocytes. Interfolliclular areas showed CD3+ T cells admixed with CD20+ B cells. No hyaline deposit or any angiofollicular hyperplasia was noted. With the diagnosis of giant reactive lymphoid nodular hyperplasia (LNH), possibly secondary to recurrence of Castleman’s disease, the patient was treated with steroids. She showed dramatic response to treatment, and after less than 2 weeks, had relief from all physical signs and symptoms. After 2 months, the patient is currently on steroids (5 mg/day) and to be followed by imaging and laboratory tests.

[[41.0, 'year']]

F

{'19202935': 1, '32922772': 1, '17616028': 1, '15202159': 1, '16802013': 1, '34109527': 1, '18639706': 1, '16415667': 1, '29561464': 1, '20193070': 2, '8916149': 1, '13111435': 1, '9543591': 1, '24829655': 2}

{'2845114-1': 1}

3990122-1

noncomm/PMC003xxxxxx/PMC3990122.xml

Laparoscopic Repair of Morgagni Hernia Using Polyvinylidene Fluoride (PVDF) Mesh

A 75-year-old woman with vague epigastric pain from one year prior was admitted to the Emam Khomeyni hospital. Her epigastric pain worsened with large meals and was associated with nausea, vomiting, and constipation. Symptoms were exacerbated since one month prior to admission. No sweating, palpitation, dyspnea, anorexia, early satiety, weight loss, dysphagia, and odynophagia were detected. The patient had a history of hypertension and hyperlipidemia for which she was under treatment with antihypertensive drugs and lipid lowering agents. A chest X-ray (CXR) revealed the presence of a hypodense mass in the proximity of the right lung base. Consequently, thoracic CT scan was performed. After complete clinical and imaging evaluations, the patient was sent for surgical repair of the Morgagni hernia. Preoperative risk assessments that included an ECG, echocardiography, cardiologist consult, routine laboratory analyses, ABG, PFT, and anesthesiologist consult were performed. She had an Left Ventricular Ejection Fraction(LVEF) of 55% and mild Mitral Regurgitation(MR).\nThe second patient was an 80-year-old woman who suffered from dyspnea at rest and orthopnea since two weeks before admission that was associated with vomiting after heavy meals, generalized vague abdominal pain, dysphagia, regurgitation, epigastric fullness, constipation, sweating, and cough. Clinical and diagnostic imaging that included CXR and a spiral thoraco-abdominal CT scan was indicative of a Morgagni hernia.\nFor the laparoscopies, both patients were placed in the supine position with their arms at their sides. A Foley catheter was inserted under general anesthesia. CO2 insufflations were performed by Veress needle. One, 10-mm trocar port was inserted above the umbilicus and a camera (30o angulated optic) was introduced into the abdominal cavity through this port. After primary evaluation in both patients, the Morgagni hernia was located and a segment of transverse colon and omentum was seen in the hernia sac. After insertion of two 10-mm and 5-mm trocar ports from the right and left upper abdominal quadrants (RUQ, LUQ), respectively, the colon and omentum were reduced back into the abdominal cavity. Subsequently, patients’ positions were changed to perform a reverse Trendelenburg; the anesthesiologist manually inflated the lungs to ensure positive pressure in order to facilitate the reduction of the sac contents. The hernia sac was excised( ) and the falciform ligament was divided by LigaSure. The size of the defect was 6 x 7 cm in the first patient and 5 x 6 cm in the second patient.\nDual-sided mesh (15 x 20 cm) was inserted into the abdominal cavity through the 10 mm port in the LUQ. Mesh was expanded over the defect( ) and fixed to the anterior abdominal wall and edge of the diaphragmatic defect in the posterior part with spiral tacks (Protack®, Covidien, Mansfield, MA, USA)\n( ).\nApplication of spiral tacks at the diaphragm carries the risk of life-threatening complications such as cardiac tamponade.\nAfter removal of the trocars under direct visualization, the fascia at the 10 mm trocar sites were closed and incisions repaired. Patients were admitted to the SICU for the first postoperative day and discharged 72 hours after surgery. Both were discharged ambulatory and were on soft diets.\nThere was no complication or recurrence during 18 months of follow up for either patient.

[[75.0, 'year']]

F

{'9876719': 1, '17943226': 1, '26126719': 2, '12099293': 1, '29556855': 1, '26155537': 1, '18572736': 1, '17149554': 1, '14634839': 1, '18853228': 1, '15640427': 1, '27677114': 1, '18435400': 1, '27957378': 2, '18437474': 1, '25973243': 1, '25437681': 1, '19694239': 1, '24829663': 2}

{'5121438-1': 1, '5121438-2': 1, '5121438-3': 1, '4487111-1': 1}

3990127-1

noncomm/PMC003xxxxxx/PMC3990127.xml

Hepatocellular Carcinoma in Pregnancy withUnusual Presentations

A 41-year-old pregnant woman referred to our hospital in the 22nd week of gestational age with right upper abdominal pain and jaundice. She had mild abdominal pain six weeks before presentation which was aggravated one week before admission. Abdominal pain was not related to food intake and referred to her right shoulder. Four days before admission, she had icter, tea colored urine and edema in her lower extremities. She had nausea and vomiting but no headache, blurred vision or bleeding was mentioned. She mentioned fatigue and hypertension from the eighth week of pregnancy. A past history was remarkable for two abortions and one live birth prior to this pregnancy. She took only ferrous sulfate and aspirin in this pregnancy and no other drugs, herbal medicines or oral contraceptives (OCPs).\nThere was no history of blood transfusion, hepatitis or exposure to aflatoxin in her past history however her father died from HCC due to hepatitis B virus (HBV). Laboratory investigations showed features of microangiopathic hemolytic anemia that included schistocytes, elevated prothrombin time and erythrocyte sedimentation rate (ESR), and negative viral markers(negative HBsAg and HBcAb). Differential diagnoses of HELLP syndrome, thrombotic thrombocytopenic purpura (TTP) or acute fatty liver of pregnancy (AFLP) were made for further evaluation and management.\nShe seemed ill and icteric at admission but not toxic. Her blood pressure was 110/70 mmHg with a pulse rate of 110 beats/min, respiratory rate about 18/min and oral temperature of 370C. Conjuctivae was pale and sclera was icteric. Jugular venous pressure was normal. Pulmonary sounds were diminished in the basal parts but cardiac examination showed no abnormalities. Her abdomen was tender, particularly in the right upper quadrant, but without rebound and guarding. Lower extremities had 3+ pitting edema and there were ecchymotic lesions at previous injection sites.\nLaboratory examination showed leukocytosis, anemia and lower limit platelet counts. Blood electrolytes were normal but there was direct hyperbilirubinemia and liver enzymes showed a cholestatic pattern. Lactate dehydrogenase (LDH) was elevated and haptoglobin was low. Peripheral blood smear showed features of microangiopathic hemolytic anemia that included target cells, tear drop and nucleated RBCs, and numerous schistocytes. Urine analysis was positive for microscopic hematuria and proteinuria.A 24-hour urine collection showed 226 milligrams of protein.\nViral markers of HBV and HCV, autoantibodies and Adisintegrin-like and metalloproteinase with thrombospondin type 1 motif (Adamts)-13 antigen and antibody (markers for Thrombotic Thrombocytopenic pupura=TTP) were all negative. AFP level was 90.7 and cancer antigen 125 (CA125) titer was >1000.\nTransabdominalsonography showed a normal fetus with a gestational age of about 23 weeks and normal amniotic fluid in the breech position. The liver showed a coarse echopattern with a diameter of 20 cm. The biliary ducts were normal and the gallbladder was contracted. No lesion was noted in the portal vein, which had a diameter of 10 mm. The inferior vena cava and suprahepatic vessels were normal. The pancreas, spleen and kidneys were all normal. There were no ascites, however bilateral pleural effusion was detected.\nA possible diagnosis of HELLP was made and supportive care for correction of coagulation disorder with fresh frozen plasma (FFP) and corticosteroids were administrated. Because of deterioration in her mental state in conjunction with an increased bilirubin level and international normalized ratio (INR), the pregnancy was terminated. Vaginal delivery was not possible because of the patient’s decreased mental state so a cesarean section was performed. The fetus was delivered and transferred to NICU but expired because of immaturity. At laparotomy, approximately one liter of ascitic fluid was noted in the abdomen and the liver had multiple malignant appearing mass lesions, which were biopsied with wedge resection. Pathologic evaluation showed sheaths of malignant hepatocytes typical of HCC ( ).\nAfter delivery the patient experienced progressive loss of conscious along with multi-organ failure and unfortunately died after a few days.

[[41.0, 'year']]

F

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{'7524929-1': 1, '5931943-1': 1}

3990132-1

noncomm/PMC003xxxxxx/PMC3990132.xml

Acute Bleeding In Duodenal Gastrointestinal Stromal Tumor

A 24-year-old male had no history of previous medical problem , but complained of acute upper gastrointestinal bleeding (hematemesis). A submucosal tumor located about 3 cm distal to the papilla of Vater was found by endoscopy. The lesion bulged beneath the mucosa with a central depressed ulceration, which was the origin of the massive bleeding. Following blood transfusion the bleeding spontaneously stopped ().\nMagnetic resonance imaging (MRI) was remarkable for a homogenous tumor of the duodenum (). MRI and CT scans showed no metastases. The patient experienced another episode of bleeding for which a blood transfusion was performed due to a decreased hemoglobin level to 4g/dl. Fortunately the bleeding stopped again. Endoscopic ultrasonography showed a 12 x 10mm hypoechoic lesion that originated from the muscularis layer without any regional lymphadenopathy. The patient was diagnosed to have a duodenal GIST ( ).Surgery was recommended and a laparotomy was done. The submucosal tumor was located in the distal third portion of the duodenum, about 3 cm distal to the ampulla of Vater. No penetration of the pancreas or other adjacent organs was detected and there were no suspicious lymph nodes. The tumor was managed by a partial resection of the distal third and fourth portion of the duodenum with a 1cm safe margin on each side and an end-to-end anastomosis. His postoperative course passed without any problem and the patient was discharged on the fifth day after the operation. The diameter of the operated tumor was 3 cm (). Histopathology showed a GIST with a typical spindle tumor cell structure (). The overlying duodenal mucosa was ulcerated. The tumor had a thin fibrous capsule that reached the muscularis mucosae, but did not penetrate it. The tumor had a moderately malignant potential according to tumor grading and the excised margin was tumor-free. Immunohistochemistry was strongly positive for C- KIT and CD34 and DOG-1 and KI67(the pathologic tumor mitotic labeling index which expression has positive correlation to tumor size) =8% , while desmin, smooth muscle, HH8, EMA and beta-catenin were negative. Mitotic activity was less than 5 mitoses/10 high power fields (). No formal lymph node dissection was done, and as it was expected no lymph nodes were noticed in the resected specimen. The tumor diameter and low proliferative activity revealed a low risk for malignancy.

[[24.0, 'year']]

M

{'16121353': 1, '34616250': 2, '16249977': 1, '30959366': 1, '20200041': 1, '19434705': 1, '15781488': 1, '15761716': 1, '20140534': 1, '15928335': 1, '16772777': 1, '22878613': 1, '30363779': 1, '29971179': 2, '18026747': 1, '15648083': 1, '18163461': 1, '29764388': 1, '12181401': 1, '16369707': 1, '34434434': 2, '12717247': 1, '12835984': 1, '18826622': 2, '17391535': 2, '16414236': 1, '17624289': 1, '24829670': 2}

{'1851968-1': 1, '6008800-1': 1, '2567321-1': 1, '8454229-1': 1, '8383613-1': 1}

3990136-1

noncomm/PMC003xxxxxx/PMC3990136.xml

A Rare Presentation of Ménétrier’s Disease as Gastroduodenal Intussusception

The patient was a 26-year-old female with a chief complaint of epigastric pain since one year previous. Anorexia, heartburn, sensation of postparandial fullness, nausea-vomiting, early satiety and a 10 kg weight loss were among the other signs and symptoms experienced over the previous year. She was prescribed omeprazol and clidinium C with no significant improvement. The patient was admitted to the hospital for further evaluation of worsening symptoms. On physical examination, the vital signs were stable, with no abnormal findings observed in the lungs, heart and extremities. The epigastric area was tender without guarding or detection of a mass. During her hospital course, the patient had two episodes of melena. Laboratory data were remarkable for the following results ().\nThe patient underwent an endoscopic evaluation. The results indicated a large friable mass with tumoral features in the body, antrum, and prepyloric areas of the stomach which was invaginated into the bulb and the second portion of the duodenum (). The endoscopist recommended a barium meal and/or abdominal contrast CT scan. The barium study was remarkable for enlarged gastric folds and varying sizes of multiple filling defects in the distal stomach that continued into the whole parts of the duodenum (). In order to relieve the obstruction, surgical interventions were planned. During the surgery, the surgeon observed large polypoid lesions in the stomach that lead to gastroduodenal intussusception. A distal partial gastrectomy and intussusception release was performed.\nThe gross appearance of stomach wall resembled cerebral convolutions and there was diffuse involvement of the stomach (). The major histopathologic findings in the gastric specimen included foveolar cell hyperplasia, cystic gland changes, and glands that penetrated into the muscularis mucosa. There were significantly diminished parietal cells noted on histologic examination (). No evidence of malignancy was found in multiple histologic sections. These in addition to other clinical and paraclinical findings were all suggestive for diffuse type Ménétrier’s disease.

[[26.0, 'year']]

F

{'8019343': 1, '17200708': 1, '11777307': 1, '31187012': 2, '5656222': 1, '5314392': 1, '1248687': 1, '4918665': 1, '31976093': 2, '3264139': 1, '640345': 1, '5905821': 1, '16415785': 1, '199063': 1, '24829671': 2}

{'6955129-1': 1, '6541164-1': 1}

3990139-1

noncomm/PMC003xxxxxx/PMC3990139.xml

A Rare Cause of Dysphagia in a Pregnant Woman:Herpes Simplex Esophagitis

A healthy 36-year-old (gravida 3, para 3) female presented to the Infectious Diseases Department at 27 weeks gestation with a six day history of fever, epigastric pain and dysphagia. She had difficulty swallowing liquids, solids, and her own saliva. There was no history of medication use or corrosive ingestion. Her temperature was 38.5°C; other vital signs were normal. Physical examination revealed gingivostomatitis, ulcerations and erythema of the gingiva, buccal mucosa and tongue. Laboratory analyses showed a white blood cell count of 15000/mm3 with 73% neutrophils. Her C-reactive protein was 78 mg/dL. The liver function was normal and HIV serology was negative. Upper endoscopy revealed several white patches and exudates throughout the esophagus with an edematous friable mucosa suggestive of severe candidal esophagitis. Except for mild gastric mucosal erythema, the endoscopy was otherwise normal. Histological examination of the esophageal biopsies revealed multinucleated giant cells with intranuclear inclusion bodies, typical for HSE (). No genital lesions were seen during gynecological examination. Her symptoms resolved completely within five days following the administration of intravenous hydration and a high dose proton-pump inhibitor. She did not receive any antiviral medications. One month later, the patient had no difficulty with swallowing. An esophagogastroduodenoscopy showed a complete resolution of the lesions. At 41 weeks gestation she delivered a healthy daughter that weighed 3100 g, whose Apgar scores were 9 (one minute) and 10 (five minutes). After 14 months of follow-up, the patient and her baby remained in good health.

[[36.0, 'year']]

F

{'14675270': 1, '1756917': 1, '9820405': 1, '631511': 1, '1576285': 1, '2984077': 1, '21991950': 1, '1363215': 1, '8686361': 1, '19750238': 2, '4364256': 1, '11864149': 1, '20616659': 1, '16197537': 1, '21411844': 1, '20736469': 1, '6706085': 1, '21912064': 2, '2854849': 1, '8783688': 1, '7778827': 1, '16580943': 1, '17614059': 1, '24829678': 2}

{'2740326-1': 1, '3178925-1': 1, '3178925-2': 1}

3990143-1

noncomm/PMC003xxxxxx/PMC3990143.xml

Lower Gastrointestinal Bleeding due to Non-Steroid Anti-Inflammatory Drug-Induced Colopathy Case Report and Literature Review

A 43-year-old female, known to have lumbar disc herniation and severe low back pain, was admitted to the hospital because of painless hematochezia, since one day prior to admission. She had no history of abdominal pain, altered bowel habits, fever, anorexia, weight loss or previous gastrointestinal (GI) bleeding.\nCurrent medications were: extended release Alfen-X (oral diclofenac, 100 mg bid), Gabapentine (300 mg qd), Baclofen (10 mg qd) and intermittent usage of ibuprofen and indomethacin, for four months, due to chronic low back pain. On physical exam, the vital signs was stable and she was afebrile. Abdomen was soft, non-tender,and with normal bowel sound.\nLab tests showed white blood cells count of 9.8 x 103/μL, hemoglobin of 9.5 g/dL, and MCV of 79fL,a normochrom-normocytic anemia which was probably due to acute blood loss. ESR, CRP, LFT, Bun and Cr were within normal limits. Colonoscopy revealed multiple ulcers with clot and fibrin exudates on it in the ascending colon, cecum and terminal ileum respectively (,,), and a few small superficial ulcerations in the transverse, descending colon.\nBiopsies from ascending colon, cecum and terminal ileum showed edema, an intense inflammatory cells (lymphocyte and neutrophils) infiltration between glands and ulceration and without evidence of granuloma, fibrosis, crypt abscess, dysplasia and malignancy.(,,)\nBleeding stopped spontaneously one day after admission, and she was discharged four days later without any complications. Additional lab tests were negative for anti-saccharomyces cerevisiae antibody, and anti-neutrophil cytoplasmic antibodies; the stool culture was also negative. According to clinical, endoscopic, pathologic and laboratory data in addition to her history of excessive NSAIDs use, the preferred diagnosis was NSAID-induced colopathy. Alfen-x, ibuprofen and indomethacin were stopped and the patient was followed with a planned colonoscopy, 6-8 weeks later. Two months after discontinuation of NSAIDs, the second colonoscopy showed normal appearing colonic mucosa up to the level of the cecum.(,,). The patient had no GI complaint in serial follow-up.

[[43.0, 'year']]

F

{'9563932': 1, '10385740': 1, '20361083': 1, '12439124': 1, '16203193': 1, '19937416': 1, '8617127': 1, '10502183': 1, '11142931': 1, '28878772': 1, '11907361': 1, '1973396': 1, '18995219': 1, '1427372': 1, '7851196': 1, '10321754': 1, '10882981': 1, '11232693': 1, '3265394': 1, '33976617': 2, '11231941': 1, '1546927': 1, '20027808': 1, '8421154': 1, '12945011': 1, '24829679': 2}

{'8077422-1': 1}

3990149-1

noncomm/PMC003xxxxxx/PMC3990149.xml

Ulcerative Colitis Associated with Aplastic Anemia; A Case Report

A 45-year-old man a known case of ulcerative colitis since 7 years ago was admitted to the hematology wardof our hospital with fatigue and high fever.\nAt the first (7 years ago) he presented with bloody diarrhea (up to 10 urgent trips to bathroom per day), tenesmus, emergency sensation, fever, abdominal pain, and weight loss (about 5-lb) to the emergency department for 7 days. He denied emesis or extra intestinal manifestations. Laboratory evaluation and abdominal radiographs were significant only for a hemoglobin level of 10.8 g/dl. He has had no history of medical illness or surgeries, recent antibiotic or nonsteroidal anti-inflammatory drug use, and no known sick contacts or exposure to tainted foods. He has had experienced increased emotional stress for several weeks due to tumultuous personal relationship. He is a lifelong nonsmoker.\nThe patient was admitted in the hospital and treated for presumed infectious enterocolitis for intravenous hydration, and empirical ciprofloxacin. Stool culture was negative for infection, but fecal leukocytes were present. After 48 hours with minimal response to therapy, he underwent a flexible sigmoidoscopy and biopsies were taken. Sigmoidoscopy (,), showed friable and erythematous mucosa in a diffuse circumferential distribution from the anal verge to the splenic flexure with petechial hemorrhage, shallow ulcerations surrounded by injected mucosa, and an abnormal vessel pattern in the sigmoid to descending colon. The changes involved a length of 50 cm from anal verge. There were no pseudomembranes. Histologic evaluation showed acute and chronic inflammation with crypt branching and irregularity of size and shape, with an increase in chronic inflammatory cells in the lamina propria (,,).\nUltimately the patient was diagnosed as a case of left sided UC. The bloody diarrhea resolved after 2 weeks of treatment with mesalazine (4g/day) and hydrocortisone intravenously (300mg/day). The steroid dose was reduced and eventually discontinued after 5 months of treatment.\nTwo years ago referred with relapse of UC, and was treated with mesalazine (4g/day) and prednisolone (30mg/day) for the exacerbation of UC. Despite his relief of his ulcerative colitis, the patient’s laboratory data showed a worsening of the pancytopenia without any gastrointestinal symptoms. His Laboratory findings revealed a hematocrit of 14.5%, and hemoglobin 11.9 g/dl with normocytic appearance (MCV; 94.1 fl & reticulocytes 9×109/liter), white blood cell count (WBC) of 2 ×109/liter, an absolute neutrophilcount (ANC) of 0.3× 109/liter, and a platelet count of 80 × 109/liter. Bone marrow biopsy was consistent with a diagnosis of aplastic anemia (AA). The patient’s medical history was negative for exposure to a myelotoxic agent, a recent infection, blood transfusion, sexual promiscuity, or acute hepatitis. The patient’s serum IgG and IgA concentrations and C3 complement were normal. Serum anti-nuclear antibody and anti-DNA antibody were also negative.\nIn the hospital course his hemoglobin level dropped to 5.9g/dl; WBC count was 3.1×109/liter; and platelets counts were dropped to 68×109/liter. A bone marrow aspirate and biopsy was done for patient that showed trilineage hypoplasia, and a diagnosis of aplastic anemia was made. Two units of blood were transfused, and treatment with Danazol was initiated. The dose of Danazol was adjusted between 250-300 mg/day. Three month after termination of Danazol, pancytopenia was relapsed and the treatment with cyclosporine (CyA; 300mg/day) was initiated. The dose of CyA was adjusted to maintain a trough concentration between 200~250ng/ml in the whole blood. The patient’s hemoglobin level had increased to 10.2g/dl, his WBC count raised to 5.4×109/liter, and his platelet count to 132×109/liter. The ulcerative colitis has remained in remission, and the patient’s blood counts remained stable in his follow up.

[[45.0, 'year']]

M

{'3463495': 1, '8244153': 1, '8250009': 1, '7909039': 1, '6947923': 1, '1345871': 1, '10338378': 1, '7522519': 1, '7868909': 1, '1530197': 1, '9182881': 1, '3458502': 1, '7576567': 1, '8043874': 1, '1553933': 1, '8562389': 1, '7720475': 1, '28286502': 1, '8096500': 1, '9447839': 1, '7942717': 1, '2105500': 1, '24829696': 2}

{}

3990150-1

noncomm/PMC003xxxxxx/PMC3990150.xml

Blue Rubber Bleb Nevus Syndrome as a rare Cause of Iron Deficiency Anemia: a Case Report and Review of Literature

A 22 years old man was referred to the GI clinic of Afzalpour Hospital for evaluation of IDA. There was no history of frank bleeding including melena, hematemesis or rectal bleeding. History of abdominal pain, prolonged diarrhea and/or constipation, vomiting, flatulence and prolonged fever were negative. Drug history was negative including for non–steroidal anti- inflammatory agents. He has been receiving occasionally intravenous iron during the last three years. He suffered from a vascular mass on right supraclavicular region at birth with gradual enlargement. At the childhood, surgical resection of the mass was performed and histology showed irregular cavernous channels in both cutaneous and subcutaneous tissue compatible with venous malformation. At the age of 15, oral iron intake was started because of IDA. At about the same time, multiple bluish colored nodular lesions appeared on his lower extremities. Familial history was negative for vascular lesions resembling BRBNS and any other remarkable diseases. He was not drug abuser and drug history included only oral and intravenous iron supplementation since 7 years ago. In physical examination he appeared well nourished but pale. Multiple compressible bluish nodules on lower extremities were seen (). These nodules measured from 0.5 to 1.5 cm and tended to refill after compression. Scar of a previous incision was present on the right supraclavicular region (). Otherwise, the physical examination was unremarkable.\nLaboratory findings revealed a hemoglobin level of 10.5 g/dL. Other lab results are shown in . The results of routine laboratory tests were within normal limits. Upper and lower gastrointestinal endoscopy along with duodenal biopsy had been performed 4 years ago and was normal.Serum immunoglobulin A(Ig A) and anti-tissue transglutaminase antibody (TTG) -Ig A levels were also normal.\nIn our center the patient underwent upper and lower GI endoscopy for second time. In upper endoscopy, a bluish vascular lesion with 10 mm diameter and wrinkled surface was seen in proximal part of duodenum ().Colonoscopy also revealed a similar lesion in the descending part of colon (). The patient refused assessment of the small intestine tract.

[[22.0, 'year']]

M

{'8677949': 1, '12297791': 1, '15670176': 1, '18629772': 1, '15556778': 1, '34177541': 2, '11568521': 1, '15729077': 1, '12024162': 1, '19691801': 1, '9714907': 1, '26393188': 1, '10383782': 1, '32933636': 1, '1612387': 1, '10881076': 1, '17934757': 1, '7783168': 1, '2721277': 1, '29515720': 1, '27365887': 1, '10751092': 1, '24829697': 2}

{'8215979-1': 1}

3990175-1

noncomm/PMC003xxxxxx/PMC3990175.xml

Fulminant Hepatic Failure due to Primary Hepatic Lymphoma: a Case Report

A 47-year old man was referred with a history of fever and jaundice for two months. The fever (oral temperature = 38.5°C without chills) and jaundice persisted despite the fact that two weeks ago, he had undergone cholecystectomy in another center for cholelithiasis. The patient was admitted to our center and a full work-up for sepsis was performed, including blood and urine cultures and chest radiography. Laboratory studies revealed abnormal liver enzymes (ALT=80; AST=60; ALP=1,100) and abnormal liver function tests (PT=18”; aPTT=40”; Hb=11; MCV=90; WBC=12,000; Plt=121,000). Serologic evaluations for brucellosis, leishmaniasis, borreliosis, and bone marrow aspiration and biopsy all returned normal. Chest and abdominal CT scans were normal (no mass lesion or lymphadenopathy), except for mild hepatomegaly (). Magnetic resonance cholangiopancreatography was also performed, yielding a normal result. A liver biopsy, performed after correction of prothrombin time with fresh frozen plasma, revealed diffuse large B-cell lymphoma (). Immunohistochemical assessments indicated the expression of CD20 and Bcl2 on blast, while CD10 was negative. The cells were negative for TdT, excluding a precursor lymphoid neoplasm. Few T-cells (CD5) were intermingled. There was no EBV-association (EBER in-situ hybridization). The proliferative capacity (Ki67) reached 60-70%.\nIn the meantime, the patient expired as a result of fulminant hepatic failure.

[[47.0, 'year']]

M

{'12873593': 1, '16249751': 1, '8620406': 1, '8270296': 1, '28584842': 1, '8480749': 1, '28596829': 2, '18710584': 2, '9246036': 1, '16810767': 1, '32762403': 2, '24829689': 2}

{'5448865-1': 1, '7416148-1': 1, '2542397-1': 1}

3990177-1

noncomm/PMC003xxxxxx/PMC3990177.xml

Diffuse Large B Cell Lymphoma of the Rectosigmoid Junction: Case Report and Literature Review

A 67-year-old male patient with a one month history of abdominal pain was referred to the surgery ward of Shariati Hospital in Tehran, Iran. There had been a gradual onset of pain over the peri-umbilical and hypogastric region and the patient reported a loss of appetite and 10 kg weight loss within the past three months. The pain did not change with respect to the patient’s position or with eating. He also complained of nausea and vomiting that began one week earlier which had progressed to a partial obstruction as evidenced by the lack of defecation for three days. In addition, there was urinary frequency and urgency associated with this presentation; however, there was no incontinency or hematuria. The patient’s medical history was unremarkable except for a history of smoking (15 pack–years). Physical examination revealed an ill-defined mass in the lower hypogastrium, moderate abdominal distention, and tenderness in the hypogastric region. The remainder of the examination was unremarkable. Laboratory analyses were normal except for a Hb of 9.6 g /dl.\nThe imaging studies performed showed a normal chest X-ray, but the abdominal imaging study revealed the presence of air-fluid levels suggestive of obstruction. Abdominopelvic CT scan showed a bulky soft-tissue density mural mass in the distal sigmoid that extended to the proximal rectum within the anterior wall with accompanying enlargement of regional lymph nodes (). There were no other cervical, thoracic, or pelvic lesions. Pelvic MRI confirmed the abdominopelvic CT scan findings as a large homogeneous T1 hypointense and mildly T2 hyperintense mural mass in the rectosigmoid junction with moderate contrast enhancement (and).\nA colonoscopy was performed which showed normal mucosa with an extra-luminal mass effect noted in the upper rectum. Endorectal ultrasonography (EUS) showed a hypoechoic mass in the extraluminal superior part of the rectal area. EUS-guided needle biopsy was performed and the histological examination suggested a malignant transformation with no definite diagnosis(,).\nThe patient underwent surgical resection due to tumor location (no distant involvement) and evidence of worsening symptoms (abdominal pain and change in bowel habits). Intra-operative findings included dilation of the small and large bowel along with the presence of a pelvic mass that extended to the retroperitoneal region, a loop of ileum, and bladder. The mass was predominantly located in the distal sigmoid and superior rectum. Intra-operative biopsy and subsequent frozen section study were all suspicious for malignancy but not conclusive for the tumor type. The mass was debulked by resection of the upper rectum, sigmoid and parts of the ileum. The small bowel was repaired by primary hand-sewn anastomosis. End-to-end anastomosis of the left colon to the rectum was not possible due to involvement of the rectal margin and necessitation of a complete en-block resection. The bladder was also resected to some extent in the involved sections. An end colostomy was performed and the Hartman pouch was left open to allow for drainage by a Pezzer drain through the abdomen. The patient had an uneventful postoperative recovery and was discharged after five days from the surgical ward after which he referred to the oncology clinic for additional evaluation and adjuvant chemotherapy.\nPathologic assessment was done using immunohistochemistry (IHC) staining (positive for CD20 and Ki67) which showed diffuse infiltration of cleaved and non-cleaved cells within the intestinal wall that involved the submucosa and muscularis layers, and the serosa. Diffuse large B cell lymphoma was the confirmed diagnosis with invasion to the intestinal wall and induced ulceration in the sigmoid colon, small intestine and rectum.\nFollowing surgery and recovery, the patient underwent CHOP chemotherapy. After 18 months of follow-up the patient remains disease-free according to paraclinical and radiologic studies. He suffers only from a limited incisional hernia which has been managed non-operatively with an elastic abdominal corset. No attempt has been made to establish intestinal continuity because of an unsuitable rectal pouch and the patient’s general condition.

[[67.0, 'year']]

M

{'11115928': 1, '21267399': 1, '21912877': 1, '18024019': 1, '11559725': 1, '8071513': 1, '13884035': 1, '18723150': 1, '3096828': 1, '21647770': 1, '16919111': 1, '24829688': 2}

{}

3990464-1

noncomm/PMC003xxxxxx/PMC3990464.xml

Sequential bilateral retinal artery occlusion

An 86-year-old woman presented at the emergency room with sudden painless loss of visual field in her right eye (oculus dexter [OD]). Past medical history included primary systemic hypertension and hypercholesterolemia. She had undergone cataract surgery in both eyes (oculi uterque [OU]) 2 years previously. The patient had also experienced previous episodes of transient vision loss in her left eye (oculus sinister [OS]). Best-corrected visual acuity (BCVA) was 20/25 in OU. A confrontation test proved lower visual field defect in the OD. Intraocular pressure was normal, and anterior segment examination just revealed bilateral mild posterior capsular opacification. Fundoscopy disclosed superior BRAO in the OD, with a Hollenhorst plaque at the first bifurcation of the superior temporal arterial branch, attenuation, and “boxcarring” of the blood column in the involved region (). Small and medium-sized hard drusen were observed in OU. Oral antiplatelet therapy and rigorous follow-up of hypertension and hypercholesterolemia were recommended. Fourteen hours after discharge, the patient came back to the emergency room with sudden complete visual loss in the OS that had started 4 hours earlier. BCVA was 20/25 in the OD and hand motion in the OS, and there was a relative afferent pupillary defect in the OS. Fundus examination disclosed CRAO with cilioretinal artery sparing in the OS (). A cherry-red spot was observed in the macula. Fundoscopy of the OD showed previous BRAO with a small embolus after the second bifurcation of the superior temporal retinal vessel (). Spectral domain optical coherence tomography of the macula () showed a hyperreflective image in the OS, suggesting swelling of internal layers of the retina, and revealed 366±38 μm of foveal thickness (more prominent in the nasal quadrants). Fluorescein angiography showed impaired filling of the superior temporal arterial branch and branches of the central retinal artery (CRA) in the right and left eyes, respectively ().\nDespite some conservative maneuvers performed (paracentesis, ocular massage, intraocular hypotensive agents), there was no improvement of VA in the OS. Electrocardiogram results, erythrocyte-sedimentation rate, and serum C-reactive protein were completely normal in the acute phase. There was no evidence of systemic symptoms related to Horton’s disease. Systemic workup was completed by internal medicine and a cardiologist.\nSupra-aortic Doppler ultrasonography revealed mild right internal carotid artery stenosis (between 0% and 15%) ipsilateral to the eye with BRAO. There was moderate left internal carotid artery stenosis (between 15% and 50%), with a small, smooth, homogeneous plaque in the side of the CRAO. Transthoracic echocardiography revealed a severe calcification of the mitral valve with a mild–moderate rim of stenosis. The patient was informed about these findings and the high risk for cardiovascular disease, myocardial infarction and stroke.\nConsidering exploration and complementary studies, our patient experienced a sequential bilateral atherogenic embolic event (BRAO in the OD and nonarteritic CRAO with cilioretinal artery sparing in the OS). The patient was evaluated every month to monitor progression. Three months after BRAO, visual function remained stable, and both optic disks appeared pale ( and ).

[[86.0, 'year']]

F

{'23045923': 1, '19577305': 1, '12011681': 1, '9606570': 1, '21794842': 1, '18301027': 1, '16138997': 1, '32632617': 1, '30148234': 1, '17460582': 1, '10612510': 1, '20609991': 1, '15808241': 1, '16854826': 1, '11490104': 1, '7162779': 1, '21620994': 1, '15486774': 1, '24176901': 1, '15106952': 1, '30021732': 1, '23217587': 1, '27313672': 1, '33117913': 1, '7814205': 1, '4334005': 1, '19376586': 1, '20697039': 1, '10768337': 1, '24748768': 2}

{}

3990784-1

noncomm/PMC003xxxxxx/PMC3990784.xml

Gastrointestinal Tract Involvement of Gorham's Disease with Expression of D2-40 in Duodenum

A 13-year-old boy presented with melena for 1 month. He had experienced intermittent abdominal pain and lower backache for 2 years. He defecated black-colored loose stools measuring about 50-100 mL once every 1-2 days. Abdominal pain was localized in the epigastric and periumbilical areas with no radiating pain, developed before and after eating, was reported as a mild to moderate dull pain, and lasted for about 30 min. Lower back pain worsened when sitting for long periods or reclining. He had no nausea, vomiting, diarrhea, pain on defecation, night symptoms, fever, weight loss, or other GI symptoms. His family history was non-contributory.\nOn physical examination, bowel sounds were normoactive and there was no tenderness, hepatosplenomegaly, or edema. His body weight was 38.1 kg (10-25th percentile), height 150.7 cm (25-50th percentile), body temperature 36.5℃, heart rate 90 beats/min, respiratory rate 25 breaths/min, and blood pressure 100/50 mmHg.\nLaboratory data were as follows: hemoglobin 11.6 g/dL (normal: 13-17 g/dL), hematocrit 34% (normal: 37-47%), transferrin saturation 8% (normal: 15-50%), ferritin 11.9 ng/mL (normal: 7-140 ng/mL), serum total protein 4.6 g/dL (normal: 6.5-8.3 g/dL), and albumin 2.9 g/dL (normal: 4.0-5.3 g/dL). Serum electrolytes, blood urea nitrogen, creatinine, liver enzymes, and total cholesterol were unremarkable. The results of fecal occult blood testing were positive.\nInitial radiographic examination revealed a lytic lesion eroding the L1-3 and T8-11 vertebrae. Magnetic resonance imaging (MRI) showed the osteolytic lesion to involve L1-3, T8-11, and both femur and soft tissue mass surrounding the left paraspinal space (). These osseous and soft tissue lesions were hypointense on T1-weighted images and hyperintense on T2-weighted images. The patient underwent computed tomography (CT)-guided biopsy of the paravertebral mass at the level of the L2 vertebra. Histological study showed that the mass was consistent with vascular proliferation and telangiectasia with hemosiderin deposition, which stained positively with D2-40 (). Gorham's disease was diagnosed after evaluation of the radiologic, pathologic, and clinical features.\nEsophagogastroduodenoscopy, colonoscopy, and a Meckel's scan did not reveal any abnormal lesions. However, duodenal biopsy showed marked dilation of lymphatics in the mucosa and submucosa, which stained positively with D2-40 (). Some vessels showed ectatic change and stained positively with CD-31, which are characteristic of lymphatic or lymphovenous malformation. Double-balloon endoscopy revealed lesions of multiple red spots that caused bleeding in the terminal ileum and were managed by electrocoagulation.\nDuring examination, the patient presented with dyspnea. A chest x-ray showed a left pleural effusion and a tube was inserted on the left side of the chest for drainage. The pleural fluid was chylous and drained at a rate of 0.9-1.2 L per day. Pleural biopsy revealed thin-walled vessels of various shapes and sizes lined by a single layer of endothelial cells, which stained positively with a D2-40 immunohistochemical stain (). Radioisotope lymphangiography was used to detect any abnormalities of the lymphatic system and thoracic duct, but no abnormal lesions were found.\nAfter diagnosis of Gorham's disease, he was given symptomatic treatment: tube drainage for chylothorax and electrocoagulation for GI bleeding. His symptoms fluctuated. Abdominal pain and backache were milder than at initial evaluation but developed intermittently. The frequency of melena reduced to once every 2-4 weeks, persisting for 1 year. Both anemia and fecal occult blood continued for 3 years, after which his GI symptoms and anemia improved and his growth accelerated to a normal rate: height in the 50-75th percentile and weight in the 25-50th percentile.

[[13.0, 'year']]

M

{'6574409': 1, '21110275': 1, '16012123': 1, '12735603': 1, '12078801': 1, '15810951': 1, '14528108': 1, '9476159': 1, '13263344': 1, '8275732': 1, '11745700': 1, '8626854': 1, '24749089': 2}

{}

3990785-1

noncomm/PMC003xxxxxx/PMC3990785.xml

Epstein-Barr Virus Infection with Acute Acalculous Cholecystitis

A 10-year-old female was admitted to Seoul National University Bundang Hospital, Korea, with a 3-day history of nausea, right upper quadrant (RUQ) abdominal pain, and a 1-day history of high fever. Before visiting our hospital, she had visited a local clinic, and abdominal ultrasonography revealed diffuse edematous wall thickening of the gallbladder. She was transferred to Seoul National University Bundang Hospital with a provisional diagnosis of acute cholecystitis and acute hepatitis. She had no history of abdominal trauma or surgery. She did not report any familial history of hepatitis or cholecystitis. On physical examination, she appeared ill. Scleral icterus was not present. The pharynx was not injected and both tonsils were not hypertrophic. The right cervical lymph node was palpable and measured approximately 2×3 cm in diameter. The abdomen was soft, not distended. Bowel sounds were normoactive. The right side of the abdomen was tender with painful fullness in the right hypochondrium, indicating a positive Murphy's sign. A 8×3 cm mass-like lesion was palpable on the RUQ of the abdomen with reddish discoloration in this area. No hepatosplenomegaly or evidence of free fluid in the abdomen was noted.\nLaboratory investigations revealed a hemoglobin level of 13.7 g/dL, hematocrit value of 39.7%, platelet count of 234,000/mm3, and white blood cell count of 8,280/mm3 (neutrophils 30%, monocytes 12%, lymphocytes 56%). Atypical lymphocytes were present (1%) on peripheral blood smear. Blood chemistry revealed aspartate aminotransferase of 311 U/L, alanine aminotransferase of 489 U/L, and total/direct bilirubin level of 1.0/0.6 mg/dL. The gamma-glutamyltransferase level was raised to 308 U/L (). Other laboratory data showed a prothrombin time/international normalized ratio of 1.19, serum total protein level of 6.9 g/dL, serum albumin level of 4.5 g/dL, blood urea nitrogen level of 7 mg/dL, creatinine level of 0.54 mg/dL, and C-reactive protein level of 0.40 mg/dL.\nPlain radiographys of the abdomen revealed no abnormality. Abdominal ultrasonography showed diffuse edematous wall thickening of the gallbladder (6 mm thickness) with increased vascularity. Sonographic Murphy's sign was positive. Definite echogenic calculi was not visible. Biliary ductal dilatation was not present ().\nThe following EBV panel results were indicative of acute primary infection; IgM of the viral capsid antigen (VCA) was positive (1.59, negative≤0.90, positive≥1.10). And the VCA-IgG was equivocal (0.92); the early antigen (EA) IgM was negative (5.26); and EBV EA IgG was negative (1.15). EBV EBNA IgG was negative (4.89). Other tests were performed to exclude other infectious causes of acalculous cholecystitis, the results of viral hepatitis profiles, including HBsAg, anti-hepatitis A virus IgM, anti-hepatitis C virus, and cytomegalovirus IgM were all negative.\nOnce the diagnosis of primary EBV infection had been confirmed, the patient was treated with empirical antibiotics, and conservative management with fasting and total parenteral nutrition. Gastrointestinal symptoms such as abdominal pain and nausea then began to improve, thus she started a regular diet on the third day of admission. She continued to have episodes of fever for approximately 5 days, but her appetite gradually improved. She eventually became afebrile for 48 hours and was discharged on the seventh day of admission. During the 2-month follow-up examination at the outpatient clinic, she was in good condition without any sign of relapse of cholecystitis.

[[10.0, 'year']]

F

{'26753086': 2, '27200203': 2, '17401719': 1, '33562159': 2, '1455890': 1, '30487697': 1, '18206441': 1, '27904251': 1, '12864960': 1, '27550491': 1, '4701413': 1, '18083615': 1, '20356920': 1, '24419637': 1, '27630008': 1, '3535451': 1, '18845463': 1, '11781983': 1, '26166109': 1, '17208530': 1, '34322642': 1, '21832944': 1, '19008138': 1, '26640715': 1, '12614729': 1, '34950552': 2, '7258543': 1, '17548424': 1, '17875099': 1, '8632265': 1, '24749090': 2}

{'4693334-1': 1, '7931023-1': 1, '4855020-1': 1, '8687799-1': 1}

3990827-1

noncomm/PMC003xxxxxx/PMC3990827.xml

Glomus Tumor Causing Anterior Thigh Pain: A Case Report

A 65-year-old male patient was referred to our pain clinic due to pain in the left anterior thigh. The pain had begun 15 years earlier and had worsened following fine needle biopsy for the evaluation of a painful mass five years later. The nature of the pain was severe (score of 8 out of 10 on the visual analogue scale [VAS]) with constant dullness and paroxysmal lancinating pain. Clinical examination revealed severe tenderness at the biopsy site (VAS score 10 out of 10) and mild skin color change, loss of hair, decreased sweating, and static and dynamic allodynia and hyperalgesia in the left anterior thigh. The patient had been receiving treatment at another hospital where electromyogram, biopsy, and MRI results had been non-specific. Based on the clinical signs and symptoms, the patient had been diagnosed with complex regional pain syndrome (CRPS) type 1 and neuropathic pain. Previous treatments had included administration of non-steroidal anti-inflammatory drugs (NSAIDs), gabapentin, nortriptyline, opioids, and also several nerve blocks with little success. After arriving at our hospital, the patient received diverse interventional therapies during the next three months without significant results. Selective transforaminal epidural block (L1, L2 levels) and sympathetic ganglion block (L2 level) were effective in reducing pain 30% to 50% for only a day or two. Pulsed radiofrequency treatment of the L1 dorsal root ganglion also showed limited results. Although intravenous infusion of ketamine reduced pain for five days, the pain relief was only felt in the anterior thigh, while the tenderness in the biopsy site was not reduced.\nFurther examination with ultrasonography at the biopsy site confirmed a round 0.8 × 0.6 cm2 sized hypoechoic cyst in the subcutaneous fat tissue (). The patient first received injection of 3 ml of 0.75% levobupivacaine around the cyst under ultrasonography guidance, but this did not provide any pain relief. One week later, 2 ml of 0.75% levobupivacaine was injected directly into the cyst. Although the patient complained of severe pain during penetration of the cyst, the pain was then almost completely reduced for 24 hours. Tenderness on the biopsy site was also reduced to a VAS score of 5 out of 10 (from 10 out of 10). The patient was transferred to the surgery department and was diagnosed with glomus tumor following excisional biopsy (). The pain was immediately reduced postoperatively and the patient has been pain free for six months.

[[65.0, 'year']]

M

{'23862005': 2, '18788860': 1, '2411282': 1, '21104079': 1, '6303040': 1, '21371130': 1, '22514779': 2, '30329513': 1, '7985967': 1, '17036559': 1, '28491188': 1, '32498489': 2, '29063006': 1, '11145243': 1, '18446863': 1, '21520136': 1, '22729971': 1, '8732413': 1, '12832884': 1, '16877938': 1, '33313205': 1, '24748947': 2}

{'3324735-1': 1, '7862943-1': 1, '3710945-1': 1}

3990828-1

noncomm/PMC003xxxxxx/PMC3990828.xml

A Novel Balloon-Inflatable Catheter for Percutaneous Epidural Adhesiolysis and Decompression

A 75-year-old man presented to our clinic with pain in his back, both thighs, and calves that had persisted for seven months. He had a medical history of well-controlled hypertension and a depressive disorder. When he walked for 10 minutes, his pain was aggravated and accompanied by dysesthesia of the feet, and these symptoms were relieved by bending over. His pain score was 8 on the 11-point Numeric Rating Scale (NRS; 0 = no pain, 10 = worst pain imaginable), and his Oswestry Disability Index (ODI; ranging from 0-100; 0 = no disability) score was 56. No abnormal signs were seen on physical examination. Magnetic resonance imaging (MRI) of his lumbar spine revealed central stenosis at the L4-5 level due to a bulging disc, facet arthrosis, and thickening of the ligamentum flavum (). For two years, he had been treated with oral medication, a fentanyl patch, and five sets of epidural steroid injections. In addition, PEA had been performed three times (once with the NaviCath and twice with the Racz catheter). However, the therapeutic effect of these procedures did not last for more than three weeks, and the duration of pain relief was further shortened after a series of procedures. His functional status was worsening, and his ODI score increased to 72.\nAfter obtaining the patient's written informed consent, we performed PEA and decompression with the inflatable balloon neuroplasty catheter to reduce his pain and extend the duration of pain relief. The patient was placed in the prone position with a pillow under his abdomen to minimize lumbar lordosis. After sterile preparation for the procedure, a 10 G guide needle, which was specially designed to prevent cutting and skiving of the catheter, was inserted into the epidural space through the sacral hiatus. The epidural space was identified by injection of contrast medium (Omnipaque, Nycomed Imaging AS, Oslo, Norway) under fluoroscopy. A caudal epidurogram, checked before planning the PEA, showed a filling defect from the central epidural space at the L5-S1 level to both L5 intervertebral foramina (). We performed mechanical adhesiolysis and decompression of the intervertebral foramina with the inflatable balloon neuroplasty catheter in order of precedence (i.e., central anterior epidural space, lateral recess area, and each intervertebral foramen). PEA and decompression were conducted by gentle side-to-side movement of the catheter with ballooning. The balloon was filled with 0.13 ml of contrast agent, and each ballooning process was limited to 5 seconds () []. The extent of balloon inflation was adjusted by the degree of pain; if moderate to severe pain was noted during balloon inflation, no further attempt at treatment was made for safety reasons. The catheter moved only in the deflated state. After PEA and decompression, the contrast agent in the anterior epidural space spread upward above the level of L5-S1, suggesting that successful adhesiolysis had been achieved (). Before removal of the catheter, 6 ml of a mixture of 1% preservative-free lidocaine, 20 mg triamcinolone, and 1,500 IU hyaluronidase was administered via the catheter. There were no complications during the procedure such as bleeding or damage to the dura. On follow-up monitoring after one month, the patient's pain had been reduced from an NRS of 8 to 4. The patient could walk without pain for more than 20 minutes, and his ODI score had decreased to 36. The effect has been sustained for more than 14 months, and the patient is currently being monitored on follow-up.

[[75.0, 'year']]

M

{'27631213': 1, '31058860': 1, '27826538': 1, '16906184': 1, '30313103': 1, '21273107': 1, '15262072': 1, '16094269': 1, '22270752': 1, '33633419': 1, '32244742': 1, '16906207': 1, '22622905': 1, '23615883': 1, '28246488': 1, '10338168': 1, '17339579': 1, '23703408': 1, '22259719': 2, '22828693': 1, '28163566': 1, '30985668': 1, '31257823': 1, '33940768': 2, '27574583': 1, '23615889': 1, '7604329': 1, '16906205': 1, '15658126': 1, '24748948': 2}

{'3990828-2': 2, '3990828-3': 2, '3990828-4': 2, '3259140-1': 1, '3259140-2': 1, '3259140-3': 1, '8107254-1': 1}

3990828-2

noncomm/PMC003xxxxxx/PMC3990828.xml

A Novel Balloon-Inflatable Catheter for Percutaneous Epidural Adhesiolysis and Decompression

A 37-year-old man presented to our office with right buttock pain radiating to the leg. There was no weakness or sensory changes, and his lumbar MRI revealed a huge central disc extrusion and sequestration at central L4-5 region (). The patient was first treated with five epidural steroid injections (two by an interlaminar approach and the others by a transforaminal approach). Although this improved his pain level, the effect did not last for more than three weeks; the patient continued to complain of pain with a score of 7 on the NRS, and he could not walk for more than three minutes. His functional score on the ODI was 38.\nPEA and decompression with the inflatable balloon neuroplasty catheter were planned and prepared as described above. A caudal epidurogram, performed before the insertion of the inflatable balloon neuroplasty catheter, showed a filling defect in the anterior epidural space above the level of L5. When the inflatable balloon neuroplasty catheter was inserted and advanced to the level of L5, some resistance against the catheter was felt. Gentle adhesiolysis of the anterior epidural space by intermittent balloon inflation was performed as described for Case 1, and the spread of contrast medium above the level of disc herniation was confirmed. At the end of the procedure, a Perifix epidural catheter (B. Braun Melsungen AG, Melsungen, Germany) was left at the target site through the balloon catheter lumen. After test injection of 1 ml lidocaine, 6 ml of a mixture of 1% lidocaine and 1,500 IU hyaluronidase was administered through the Perifix catheter. After 10 to 15 minutes of monitoring, another 4 ml of a mixture of 10% hypertonic saline and 20 mg triamcinolone was injected through the catheter. The catheter was removed on the day of the procedure. There were no complications during the procedure. At the follow-up visit after one month, the patient's pain was found to be reduced and was scored as a 1 on the NRS. The patient had no walking limitations, and his functional status was improved, with a change in the ODI score from 38 to 2. The effect has been maintained for more than 13 months, and the patient is currently being monitored on follow-up.

[[37.0, 'year']]

M

{'27631213': 1, '31058860': 1, '27826538': 1, '16906184': 1, '30313103': 1, '21273107': 1, '15262072': 1, '16094269': 1, '22270752': 1, '33633419': 1, '32244742': 1, '16906207': 1, '22622905': 1, '23615883': 1, '28246488': 1, '10338168': 1, '17339579': 1, '23703408': 1, '22259719': 2, '22828693': 1, '28163566': 1, '30985668': 1, '31257823': 1, '33940768': 2, '27574583': 1, '23615889': 1, '7604329': 1, '16906205': 1, '15658126': 1, '24748948': 2}

{'3990828-1': 2, '3990828-3': 2, '3990828-4': 2, '3259140-1': 1, '3259140-2': 1, '3259140-3': 1, '8107254-1': 1}

3990828-3

noncomm/PMC003xxxxxx/PMC3990828.xml

A Novel Balloon-Inflatable Catheter for Percutaneous Epidural Adhesiolysis and Decompression

A 70-year-old man presented with pain in the lower back and both legs. He had undergone a decompressive surgery at the L4-5 level seven years previously. However, his pain had again developed six months prior to presentation. He complained of numbness and a cramping sensation in both legs and could not walk more than 100 meters because of his pain. He scored his pain as 8 on the NRS, and his functional score on the ODI was 40. Left neural foraminal stenosis at the L4-5 and L5-S1 levels and right neural foraminal stenosis at the L3-4 level with degenerative spondylolisthesis, a bulging disc, and facet osteoarthritis were noted by lumbar MRI. The patient had been treated with an epidural steroid injection before visiting our clinic. However, the effect lasted for only two weeks, and his pain was reduced by only 10%.\nTo relieve the patient's pain and extend the duration of pain relief, PEA and decompression with the inflatable balloon neuroplasty catheter were performed as described for Cases 1 and 2. A caudal epidurogram showed a filling defect from the central epidural space above the L5-S1 level to both the L5 and S1 intervertebral foramina. After anterior epidural adhesiolysis and decompression of both neural foramina by mechanical adhesiolysis and balloon inflation as described in Case 1, contrast agent spread throughout both the L5 and S1 intervertebral foramina and the anterior epidural space above the L4-5 level. At the end of the procedure, 6 ml of a mixture of 1% lidocaine, 20 mg triamcinolone, and 1,500 IU hyaluronidase was administered through the catheter. After two months, the patient's pain scores on the NRS and ODI decreased to 4 and 36, respectively. His walking distance also increased to 500 meters. Interestingly, his pain nearly disappeared three months after the procedure, and he has been doing well without pain for more than 18 months following PEA and decompression with the inflatable balloon neuroplasty catheter.

[[70.0, 'year']]

M

{'27631213': 1, '31058860': 1, '27826538': 1, '16906184': 1, '30313103': 1, '21273107': 1, '15262072': 1, '16094269': 1, '22270752': 1, '33633419': 1, '32244742': 1, '16906207': 1, '22622905': 1, '23615883': 1, '28246488': 1, '10338168': 1, '17339579': 1, '23703408': 1, '22259719': 2, '22828693': 1, '28163566': 1, '30985668': 1, '31257823': 1, '33940768': 2, '27574583': 1, '23615889': 1, '7604329': 1, '16906205': 1, '15658126': 1, '24748948': 2}

{'3990828-1': 2, '3990828-2': 2, '3990828-4': 2, '3259140-1': 1, '3259140-2': 1, '3259140-3': 1, '8107254-1': 1}

3990828-4

noncomm/PMC003xxxxxx/PMC3990828.xml

A Novel Balloon-Inflatable Catheter for Percutaneous Epidural Adhesiolysis and Decompression

A 44-year-old female presented with pain in the lower back radiating to the right leg. Her symptoms first developed three years ago. When she walked for 10 minutes, her pain was aggravated and accompanied by numbness with a cramping sensation in the right leg. There was no weakness or sensory changes. No abnormal signs were seen on physical examination. For three years, she had been treated with oral medication and three sets of epidural steroid injections. The effect of the third epidural steroid injection did not last for more than one month. Moreover, PEA with the Racz catheter did not effectively reduce her pain level. The patient continued to complain of pain with a score of 8 on the NRS and she could not walk for more than ten minutes. His functional score on the ODI was 64. Her lumbar MRI revealed central disc extrusion at the L4-5 level with central canal stenosis, and bilateral L5 nerve root compression.\nWe planned PEA and decompression with the inflatable balloon neuroplasty catheter, and prepared as described above. A caudal epidurogram showed a filling defect from the central epidural space at the L4-5 level to both L5 intervertebral foramina (especially the preganglionic area). Gentle adhesiolysis of the preganglionic area at the right L5 level by intermittent balloon inflation was performed as described above, and the preganglionic spread of contrast medium was confirmed. At the end of the procedure, a Perifix epidural catheter was left at the target site through the balloon catheter lumen. After test injection of 1 ml of lidocaine, 6 ml of a mixture of 1% lidocaine and 1,500 IU hyaluronidase was administered through the Perifix catheter. After 10 to 15 minutes of monitoring, another 4 ml of a mixture of 10% hypertonic saline and 20 mg triamcinolone was injected through the catheter. The Perifix catheter was left in place for a 2-day drug injection. The catheter was then removed on the second day of the procedure, after injection of the same drugs, including the hypertonic solution. There were no complications during the procedure. At the follow-up visit after two months, the patient's pain was found to be reduced and was scored as a 2 on the NRS. The patient reported an improvement in her walking distance, and her functional status was also improved, with a change in the ODI score from 64 to 26. The effect has been maintained for more than seven months, and the patient is currently being monitored on follow-up.

[[44.0, 'year']]

F

{'27631213': 1, '31058860': 1, '27826538': 1, '16906184': 1, '30313103': 1, '21273107': 1, '15262072': 1, '16094269': 1, '22270752': 1, '33633419': 1, '32244742': 1, '16906207': 1, '22622905': 1, '23615883': 1, '28246488': 1, '10338168': 1, '17339579': 1, '23703408': 1, '22259719': 2, '22828693': 1, '28163566': 1, '30985668': 1, '31257823': 1, '33940768': 2, '27574583': 1, '23615889': 1, '7604329': 1, '16906205': 1, '15658126': 1, '24748948': 2}

{'3990828-1': 2, '3990828-2': 2, '3990828-3': 2, '3259140-1': 1, '3259140-2': 1, '3259140-3': 1, '8107254-1': 1}

3991402-1

noncomm/PMC003xxxxxx/PMC3991402.xml

Paratesticular leiomyoma in an azoospermic patient and successful testicular sperm extraction (TESE) for intracytoplasmic sperm injection (ICSI) with an ongoing pregnancy

A 31 years old man with a primary infertility of 7 years was referred to our center because of azoospermia. The medical history of the patient and his wife showed no specific problems. Clinical examination revealed normally sized testes with a testicular volume of 15 ml as measured by a Prader orchidometer. Both epididymis and vasa deferentiae, were present at both sides.\nSix months before, the couple underwent a first unsuccessful TESE-ICSI treatment in another clinic. No paratesticular mass was reported and scrotal ultrasound was reported normal.\nRoutine laboratory examinations showed a serum follicle-stimulating hormone (FSH) of 11.8 IU/L, luteinizing hormone (LH) of 8.4IU/L and free testosterone of 56.6 ng/L. Sperm analysis showed azoospermia on several occasions.\nThe couple was planned for a combined TESE-ICSI trial. The wife of the patient had a regular menstrual cycle and the ovarian hyperstimulation was performed using a classical protocol with 0.25 mg/day of gonadotrophin releasing-hormone antagonist (Orgalutran®, Merck Sharpe & Dohme) and 150IU/day of recombinant gonadotrophins (Gonal-F®, Merck Serono). Ovulation triggering was done with 10000 IU of human chorionic gonadotophin (Pregnyl®, Merck Sharpe & Dohme). Oocyte pick-up was performed under general anesthesia 36 hours later and 8 mature oocytes were retrieved.\nThe patient underwent a TESE on the same day of the oocyte retrieval.\nDuring this surgery, an ovoid paratesticular mass was observed on the left testis, adjacent to the epididymis, measuring 2.5 × 2.5 × 2 cms. The mass was excised. Grossly it was firm and well circumscribed with a gray-white homogeneous surface.\nSeveral testicular biopsies were taken to check the presence of spermatozoa and one of the biopsies was sending for pathological evaluation.\nThe microscopic examination of the paratesticular mass revealed a tumour composed of interlacing fascicles of spindled smooth muscles (). There was also focal inflammation with giant cells. The immunohistochemistry for smooth muscle actin (SMA) (Dako, clone 1A4, dilution 1/100) was positive. The final diagnosis of paratesticular leiomyoma was made. The analysis of the testicular biopsy showed a complete germ cell aplasia (Sertoli-cell-only syndrome). However, after multiple TESE, testicular spermatozoa were observed in the wet preparations which were used for ICSI. Based on morphology in the morning of day 3 after ICSI (van Royen E, 1999), 2 good quality embryos were transferred. The pregnancy test was positive and a single ongoing pregnancy was established.

[[31.0, 'year']]

M

{'18286504': 1, '3354127': 1, '3721756': 1, '9309777': 1, '9864578': 1, '12775098': 1, '2047777': 1, '10332467': 1, '8442311': 1, '10573001': 1, '10469708': 1, '1863475': 1, '8908593': 1, '30875294': 1, '2858113': 1, '16236398': 1, '10435559': 1, '940202': 1, '15175778': 1, '24753910': 2}

{}

3991807-1

noncomm/PMC003xxxxxx/PMC3991807.xml

A Case of IgG4-Related Disease with Bronchial Asthma and Chronic Rhinosinusitis in Korea

A 55-yr-old female with BA and CRS presented swelling of both eyes and neck aggravated 1 yr ago. The symptoms first developed 10 yr ago with cough, sputum, wheezing, nasal obstruction and rhinorrhea, which had remained with no change in size for 2 yr. She visited a local clinic due to the enlargement of a mass-like lesion 8 yr ago and then started to take 5 mg of prednisolone every other day. The swelling was temporarily reduced with a systemic steroid; however, the mass lesions were again aggravated whenever the steroid was stopped. She suffered from chronic cough with sputum and recurrent upper respiratory infections recent as of 1 yr; in addition, she was diagnosed with bronchial asthma 6 months ago. Her mass lesions were also aggravated in recent 1 yr; subsequently, she visited our hospital (October 2, 2012) for an evaluation of swelling of eyes and neck as well as recurrent respiratory infections. She experienced neither eye pain nor neck pain, did not complain of any visual problems or show systemic symptoms (such as febrile sensation and general weakness). Her asthmatic symptoms were well-controlled after being prescribed an inhaled corticosteroid. She had no previous history of any drug or food allergies. Her physical examination on the first visit revealed bilaterally swollen eyes and enlarged submandibular glands, with a size of 4×5 cm (). The diffuse swelling of both eyes was fairly well-demarcated, nodular and movable. There was no visual field defect or a limitation of ocular movement. The palpable masses of submandibular glands were movable and nodular without tenderness. Other organomegalies (except the lesions of eyes and neck) were not observed. The abdomen was not distended, there was no palpable lymph node, and her breath sound was clear without wheezing. Laboratory findings included a blood eosinophilia of 1,900/µL and elevated levels of erythrocyte sedimentation rate (ESR) 73 mm/hr, serum creatinine 1.6 mg/dL, and pancreatic enzymes (amylase 268 U/L, lipase 713 U/L). Total IgE level and eosinophil cationic protein (ECP) were also elevated (913 KU/L and >200 µg/L respectively). Serum lactate dehydrogenase (LDH, 113 U/L) level, liver function test and cardiac enzymes were within the normal range. Chest radiography and electrocardiogram showed no specific findings. To evaluate her asthmatic status, we performed a methacholine challenge test and the result was positive: provocative concentration causing a 20% fall in FEV1 (PC20), 0.86 mg/mL; FEV1/FVC, 64.57%; FEV1, 1.78 L; FEV1% predicted, 64.9%. A skin prick test (SPT) to all of the common inhalant allergens (Bencard, Bradford, UK) showed negative responses. We checked the serum levels of total IgG and IgG subclasses suspecting an IgG subclass deficiency due to an increased susceptibility to upper respiratory infection. The levels were markedly elevated: serum total IgG, 4,486 mg/dL (normal: 916-1,796 mg/dL); IgG1, 11,102.9 mg/L (normal: 3,824.0-9,286.0 mg/L); IgG2, 17,958.0 mg/L (normal: 2,418.0-7,003.0 mg/L); IgG4, 2,106.4 mg/L (normal: 39.2-864.0). Therefore, we suspected IgG4-RD on the basis of the mass lesions and elevated IgG4 level. Considering the possibility of systemic involvement of IgG4-RD, we performed multiple computed tomography (CT) scans of the neck, chest, and abdomen to establish the extent of the disease and to find any subclinical diseases. Neck CT imaging disclosed hypertrophies of extraocular muscles and the bilateral enlargements of lacrimal, submandibular and sublingual glands as well as mucoperiosteal thickening of maxillary and ethmoidal sinus indicating CRS (). Chest CT imaging study revealed that both lungs were diffusely involved with bilateral hilar lymph nodes, peribronchovascular bundle thickening, multifocal centrilobular opacities and interlobular septal thickening (). Irregular low density lesions of both kidneys and multifocal strictures as well as an irregular dilatation of the pancreatic duct were noted in the abdominal CT scan (). The right submandibular gland was biopsied to obtain a key pathological finding of IgG4-RD. The pathological features showed an abundant infiltration of IgG4-positive plasmacytes around the lymphoid follicles and glandular tissues. Cartwheel-like fibrosis (which is strongly indicative of IgG4-RD) was also noted (). Finally, we could confirm the diagnosis of IgG4-RD according to the criteria in 2011 (, ). We started a systemic steroid therapy with methylprednisolone 0.4 mg/kg/d. The nasal and asthmatic symptoms of the patient substantially improved and the elevated serum creatinine and pancreatic enzyme level was normalized at 2 weeks of follow-up. The masses significantly diminished with the treatment of a systemic steroid, which has been maintained with no recurrence. We performed follow-up measurements of lung function test 2 months later. Her FEV1% had improved to 103.8% predictive (2.82 L) compared to her initial FEV1 level (64.9% predictive, 1.78 L).

[[55.0, 'year']]

F

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{}

3991808-1

noncomm/PMC003xxxxxx/PMC3991808.xml

A Case of Pulmonary Arterial Hypertension Associated with Congenital Extrahepatic Portocaval Shunt

In October 2012, a 20-yr-old male was referred to our department with pulmonary hypertension of unknown etiology. He underwent surgical closure of ventricular septal defect (VSD) at 10 months of age. Eleven months before admission, the patient underwent laparoscopic appendectomy at another hospital. During the preoperative evaluation, screening abdominal ultrasound (US) showed multiple liver masses, and transthoracic Doppler echocardiography (TTE) showed pulmonary hypertension of unknown origin.\nOn admission, the patient had mild exertional dyspnea (New York Heart Association, NYHA class II). Physical examination revealed pectus excavatum but was otherwise unremarkable. The electrocardiogram demonstrated regular sinus rhythm with right bundle branch block (RBBB), and the chest X-ray showed mild cardiomegaly and increased pulmonary vascularity with bulged pulmonary conus (). At admission, the patient's laboratory values were within normal limits except for slightly reduced serum total protein (6.3 g/dL; reference range, 6.6-8.3) and mildly elevated direct bilirubin (0.53 mg/dL; reference range, 0.13-0.47) and blood ammonia (105 µg/dL; reference range, 20-80). Serologic markers for hepatits B and C virus and for AFP and CA-19 were negative.\nTTE showed a significantly dilated right ventricle (RV) chamber with a D-shaped left ventricle (LV). The LV chamber was mildly dilated, but the LV ejection fraction was normal. The estimated RV systolic pressure (RVSP), calculated as the maximal velocity of tricuspid regurgitation (TR Vmax), was 64 mmHg, which indicated moderate pulmonary hypertension (). We found no definite shunt flow through the inter-ventricular or inter-atrial septum and main pulmonary artery. In addition, there was no evidence of pulmonary thromboembolism or pericardial effusion. These findings were confirmed by transesophageal echocardiography (TEE).\nCardiac catheterization was performed to confirm the diagnosis and to classify the pulmonary hypertension based on the Dana Point classification recommended by the World Health Organization (WHO) (, ). Right catheterization, performed with a Cournand catheter, showed a pulmonary capillary wedge pressure (PCWP) of 7 mmHg, mean pulmonary arterial pressure (mPAP) of 44 mmHg (), pulmonary vascular resistance (PVR) of 608 dyn·s·cm-5 and a cardiac index (CI) of 2.89 L/min per m2. Consequently, pulmonary arterial hypertension (group 1 pulmonary arterial hypertension) was diagnosed by right heart catheterization (RHC). Interestingly, significant oxygen step-up was observed between the inferior vena cava (IVC) and the low level of right atrium (RA) during O2 saturation analysis of the right heart. This findings suggested significant arterial blood shunt in this area.\nAbdominal computed tomography (CT) and magnetic resonance imaging (MRI) were performed to further evaluate the multiple liver masses that were found incidentally at the patient's local hospital. CT showed ill-defined low-density nodular lesions in the bilateral hemiliver. These lesions exhibited hyperintensity on T1-weighted MR images, with the larger ones containing a central scar with a high signal intensity on T2-weighted MRI images and a low signal intensity on T1-weighted MR images (). Based on the CT and MR imaging results, initially we thought that the pulmonary arterial hypertension was caused by portal hypertension, which is known as portopulmonary hypertension associated with nodules of liver cirrhosis (LC). A percutaneous liver biopsy was performed under US guidance for histological diagnosis, which was multifocal nodular regenerative hyperplasia with no evidence of LC. Therefore, CT angiography and portal venography were performed to investigate whether intra- or extra-cardiac shunt was present and also to determine the anatomical relationship between the portal venous system and the right heart; both can cause pulmonary arterial hypertension.\nCT angiography demonstrated the presence of a portocaval shunt in which the left portal vein (PV) and left hepatic vein joined and drained directly into the suprahepatic IVC without passing through the liver (). Portal venography revealed abnormal communication between the left PV and IVC with obliteration of the right PV (Abernethy type 1b) (). The main PV and hepatic venous wedge pressure were both 6 mmHg. The superior mesenteric and splenic venous pressures were 6 mmHg and 9 mmHg, respectively. In addition, we reexamined the TTE that was not able to detect this communication at first, in which type 1 CEPS could be clearly visualized on the subcostal window ().\nWe confirmed the diagnosis as a pulmonary arterial hypertension caused by CEPS (Abernethy type 1b) and multifocal nodular regenerative hyperplasia of the liver. However, there was no deinite evidence of other cardiac, gastrointestinal or genitourinary anomalies that are also known to be associated with type 1 CEPS. The patient began inhalation of iloprost (40 µg/day) and was taught to use a nebulizer. The patient's condition improved and he was discharged on day 7. At a 5-month follow-up appointment, his 6-min walking test improved from 380 m to 525 m, and TTE showed a reduction in RVSP from 64 mmHg to 49 mmHg.

[[20.0, 'year']]

M

{'9094026': 1, '19555858': 1, '56646': 1, '17868331': 1, '32337399': 1, '31196005': 1, '18362102': 1, '1150113': 1, '19796040': 1, '1142284': 1, '32494552': 1, '10875741': 1, '8665788': 1, '19555859': 1, '1079535': 1, '7807356': 1, '30671377': 1, '24753712': 2}

{}

3991953-1

noncomm/PMC003xxxxxx/PMC3991953.xml

Hashimotos Thyroiditis with Coexistent Papillary Carcinoma and Non-hodgkin Lymphoma-thyroid

A 32-year-old female with solitary nodule and hypothyroidism since 6 months, presented with a sudden increase in size since 15 days. Local examination showed a solitary nodule in the left lobe of the thyroid. General, physical, and systemic examinations were within normal limits. There were no clinically palpable cervical lymphnodes. Thyroid function test showed high thyroid stimulating hormone and decreased T4 levels. Ultrasound neck showed enlarged thyroid with nodularity and hyperechoic areas. Fine needle aspiration cytology (FNAC) of the nodule showed features of HT with papillary carcinoma.\nHence, a total thyroidectomy was performed and revealed nodularity on the outer surface. Left lobe measured 4 cm × 2.5 cm × 1.5cm and right lobe measured 3 cm × 2 cm × 1 cm. Cut surface of both the lobes was homogenous, grey white with tiny colloid filled areas []. Histology showed areas of HT with prominent lymphoid follicles having germinal center and atrophied thyroid follicles lined by hurthle cells []. A tiny focus of follicular variant of papillary carcinoma was also seen [Figure and ]. Another focus showed effacement of the thyroid parenchyma by diffuse monotonous lymphoid infiltrate suggestive of NHL []. Immunohistochemistry showed these cells immunoreactive for CD 45, CD 20, and bcl 2, which suggested a B-cell origin []. Areas of papillary carcinoma showed positivity for both low and high molecular weight cytokeratin [Figure and ]. Hematological parameters and marrow evaluation were within the normal limits. Hence, the final diagnosis of HT coexisting with papillary carcinoma and primary NHL (B-cell lineage) was made. Levothyroxine was initiated at 300mcg/day and patient was treated with chemotherapy (R-CHOP regime). Patient tolerated the chemotherapy well and with 12 months of follow-up, no recurrence or metastasis was noted.

[[32.0, 'year']]

F

{'21112862': 1, '31938394': 1, '26871795': 1, '20625656': 1, '29435379': 2, '18318579': 1, '20591920': 1, '10598190': 1, '19041823': 1, '22568399': 1, '30089952': 2, '24761251': 2}

{'6060575-1': 1, '5757112-1': 1}

3991954-1

noncomm/PMC003xxxxxx/PMC3991954.xml

Reservoir Complete Denture in a Patient with Xerostomia Secondary to Radiotherapy for Oral Carcinoma: A Case Report and Review of Literature

A 67-year-old male patient reported to the Department of Prosthodontics with the chief complaint of difficulty in mastication due to dryness of mouth and absence of teeth. Medical history revealed that the patient had undergone RT 2 years back for the moderately differentiated squamous cell carcinoma involving posterior 1/3rd of left lateral border of the tongue.\nExtraoral examination revealed reduced lower facial height and unsupported lips. Intraoral examination revealed maxillary and mandibular edentulous residual ridges and decreased salivary flow [Figure and ]. A diagnosis of xerostomia secondary to RT was made after calculating unstimulated whole saliva flow rate by absorbent (swab) method (whole saliva flow rate was < 0.1 ml/min).\nTreatment plan included either (1) fabrication of implant supported or conventional upper and lower complete dentures with external application of salivary substitute in the oral cavity or (2) fabrication of lower complete denture with artificial saliva reservoir in it and upper conventional complete denture. It was discussed with the patient and informed consent was obtained for the agreed treatment, which included rehabilitation of the upper arch with conventional complete denture and reservoir denture in the lower arch.\nPrimary impressions were recorded in irreversible hydrocolloid impression material. After border molding, final impressions were made in medium body elastomeric impression material [Figure and ] Jaw relation was recorded with wax occlusal rims fabricated on self-cure acrylic denture base. The vertical height of the lower rim was measured. Accordingly, teeth selection was carried out and size of the reservoir was determined, so that maximum space for the reservoir is gained while maintaining 2 mm thickness of the reservoir wall. Then using face bow, only upper cast was mounted on the semi-adjustable articulator. Upper and lower wax rims with the centric records were preserved and set aside for later use Shellac base plate was adapted on the lower final cast. According to the predetermined dimensions, putty type of elastomeric material was placed in the center of the base plate and modeling wax (modeling wax, DPI, Mumbai, India) was added at the periphery to create the walls of the reservoir []. Space for reservoir was created by removing putty from the center []. Five stainless steel rods (3 mm in length and 2 mm in diameter) were positioned parallel to each other in the wax []. The two parts of the reservoir lower denture would be attached to each other using these rods. A bevel was carved 1-1.5 mm above the inferior border at the periphery of the base Then flasking and dewaxing was carried out as a routine procedure. Clear heat cure polymerized resin was used for packing the mold space (Trevalon HI, Dentsply India Ltd., Gurgaon, India) and after curing a permanent clear acrylic base was obtained with five stainless steel rods embedded in it and having a reservoir in the center. Thus, the tissue bearing plate of the two piece reservoir denture was fabricated [] Next, the lower cast was retrieved from the flask and with the preserved wax occlusal records it was mounted on the semi-adjustable articulator. After this, the lower temporary record base was replaced with the permanent clear acrylic base [] Teeth arrangement was carried out on the semi-adjustable articulator with putty maintaining the reservoir space []. Extra bulk of wax was added to the mandibular trial denture to gain optimum thickness. Then trial dentures were finished and tried in the patient's mouth to check for retention, stability, esthetics, phonetics and comfort [] Flasking followed by dewaxing of the lower trial denture was carried out to obtain base portion of the flask containing permanent denture base [] and a counter portion containing the teeth [] Aluminum foil was adapted on the denture base for easy separation of the two halves of the mandibular denture []. Packing was carried out with pink heat cure acrylic resin (Trevalon HI, Dentsply India Ltd., Gurgaon, India) and processed to obtain the teeth bearing plate of the reservoir denture [] After careful deflasking aluminum foil was removed. The teeth bearing plate of the mandibular denture rested on the bevel created on the tissue bearing plate. Finishing and polishing was carried out with the segments together to ensure a flush smooth finish, without any damage to the edges [] Two outlet holes were drilled for the salivary substitute on each side in the retromylohyoid region of the teeth bearing plate and were adjusted in size similar to the thickness of a 23 gauge orthodontic wire [] Artificial saliva substitute (Wet mouth, ICPA Health Products Ltd., India) was then filled in the reservoir space of the lower denture with a capacity of 3.8 ml The upper denture was fabricated in the conventional manner Denture insertion was carried out and post-insertion instructions were given to the patient. Furthermore, he was taught how to open and close the reservoir denture for filling the artificial salivary substitute and cleaning the reservoir space. In addition, fine orthodontic wire was provided to him for cleaning the drainage holes if they get blocked Recall appointments were scheduled after 24 h, 1 week, 4 weeks and every 6 months. At recall appointments, good retention was observed and relief from the symptoms of dry mouth and improvement in dietary intake was reported by patient. Patient found it easy to clean the dentures as taught and informed that once filled saliva substitute lasts for 4-5 h. Patient has now been successfully wearing the dentures for over 2 years.

[[67.0, 'year']]

M

{'23449825': 1, '6389837': 1, '8648574': 1, '24293925': 1, '14640373': 1, '17564151': 1, '22379309': 1, '21397583': 1, '24761252': 2}

{}

3991955-1

noncomm/PMC003xxxxxx/PMC3991955.xml

Mucoepidermoid Lung Carcinoma in Child

A 6-year-old male child was presented with fever, cough, hemoptysis and wheezing since1 month. Chest X-ray showed features suggestive of foreign body with post-obstructive pneumonia-left lung and was treated for the same with medication without much improvement. Family history and developmental history was unremarkable. Routine hematological, biochemical and microbiological investigations were unremarkable. Subsequently CT scan chest was carried out, which showed oval mass with speculated margin in right hilar region [, shown in arrows] with distal segmental atelectasis. Bronchoscopy showed small growth with nodularity in the apical segmental bronchus of the right lower lobe with mucosal erosion and hence carried out bronchoalveolar lavage showed few atypical squamous cells. Post-bronchoscopy sputum was unremarkable. CT abdomen and pelvis showed no evidence of metastatic deposits. Hence, patient underwent left lower lobectomy. The right lower lobectomy showed a grey white oval mass with solid and cystic areas in the right hilar region with extension in to the lung parenchyma []. Histology of the tumor showed mixed solid and cystic areas with sheets of epidermoid cells and mucus-filled cysts of irregular size [Figure and ]. Areas of solid growth were composed of squamoid and intermediate cells [ and ]. Epidermoid cells showed inter cellular bridges []. Cysts were lined by columnar cells with mucin-rich cytoplasm. These cells were positive for periodic acid-Schiff stain []. Hence, the final diagnosis of mucoepidermoid carcinoma-intermediate grade of right lower lobe was made. Lymph-vascular invasion and lymph node metastasis were negative. The post-operative course was good. Since the tumor was low-grade, no adjuvant treatment was administered. Patient had no signs of tumor recurrence for 1 year, to date, since the resection of the tumor.

[[6.0, 'year']]

M

{'27994904': 2, '15720070': 1, '21985459': 2, '2930303': 1, '17824797': 1, '1871698': 1, '34377224': 1, '11936541': 1, '24761253': 2}

{'3207949-1': 1, '5138474-1': 1}

3991957-1

noncomm/PMC003xxxxxx/PMC3991957.xml

Unilateral Closed Lip Schizencephaly with Septo-Optic Dysplasia

Our case was a 30-year-old male patient, known case of seizure disorder since childhood. He presented to us with two episodes of generalized tonic-clonic seizures. Patient had decreased visual acuity (6/12) in both eyes since childhood.\nOur subject's mother was 18-year-old at the time of birth and he was a full term normal delivery child with no history of birth asphyxia.\nNo history of developmental delay (Informant-Mother).\nNo history of any congenital anomalies in the family.

[[30.0, 'year']]

M

{'19623216': 1, '2928524': 1, '12238909': 1, '10895038': 1, '21026933': 1, '21647999': 1, '6476009': 1, '17587179': 1, '9153481': 1, '16423603': 1, '29663010': 1, '25848158': 1, '15888615': 1, '3259384': 1, '24761255': 2}

{}

3992334-1

noncomm/PMC003xxxxxx/PMC3992334.xml

Improved severe hepatopulmonary syndrome after liver transplantation in an adolescent with end-stage liver disease secondary to biliary atresia

A 16 years-old female was born with biliary atresia, and she underwent porto-enterostomy (Kasai's procedure) on the 55th day after birth. She had intermittent attacks of cholangitis during her childhood. She had been pretty good and developed normally until the age of 15 years. Although she had hepatosplenomegaly, there was no overt symptom. However, she had progressed liver failure aggressively for 6 months before LT. In addition, she was on a bed ridden status because of dyspnea for last 2 months before LT. Both fingers showed clubbing (), ankles were swollen and lips were cyanotic, those were suspected as secondary changes of chronic respiratory insufficiency. Her chest X-ray showed no abnormal findings, except elevated left diaphragm due to splenomegaly. However, her partial pressure of arterial oxygen and arterial oxygen saturation was markedly decreased (PaO2 54.5 mmHg, O2sat 84.2%). Her hepatic and renal profiles were as follows: total bilirubin 42.3 mg/dL, albumin 2.5 g/dL, AST 241 U/L, ALT 93 U/L, INR 2.39, ammonia 2.54 µg/mL and creatinine 0.5 mg/dL. Her Child-Turcotte-Pugh classification was C and MELD (Model of End-Stage Liver Disease) score was 30. The transesophageal echocardiography (TEE) with agitated saline bubble showed an extracardiac right to left shunt, which suggested intrapulmonary arterio-venous shunt ().\nShe underwent orthotopic LT donated from a 13-year old deceased donor, in February 2010. For the liver transplant procedure, there shows marked adhesion of entire perihepatic area, and 1.5 cm sized two gallstones in the Roux-limb of jejunal loop, just above the jejunal stenosis, which was removed by jejunotomy. Otherwise, there was no notable event during a routine orthotopic LT procedure. The first PaO2/O2sat level of postoperative 2nd day was 51.3 mmHg/88.0%; however, she was free from ventilator on the morning of that day. In spite of supplying oxygen with a mask, the lower partial pressure of arterial oxygen was persisted, ranging from 36.2 to 53.9 mmHg during the 48 hours after extubation. Although her PaO2 and O2sat level were shown to be very low, her breathing and physical activity with consciousness was rapidly recovered and very stable. She was transferred from the ICU to the isolation ward, on postoperative day 17. Bile leakage was developed from the enterotomy site to remove the gallstones, which was detected by DISIDA scan; it was healed spontaneously by percutaneous drainage and conservative management. Her partial pressure of arterial oxygen remained as low as 55-60 mmHg during a month after surgery. She was allowed to go home on postoperative day 75.\nRoutine regimen for immunosuppression was applied. Steroid and Simulect® (basiliximab) were administered during anhepatic period, and Prograf® (tacrolimus) and Cellcept® (mycophenolate mofetil) were added on postoperative day 2 and was followed by a routine protocol of our institution. The steroid was tapered until postoperative month 3 and mycophenolate mofetil was used for postoperative 6 months. Tacrolimus monotheray has been maintained since postoperative month 6.\nThe partial pressure of arterial oxygen improved progressively during the postoperative follow up period and on postoperative month 11, the level was normalized (PaO2 118 mmHg). Follow-up transthoracic echocardiography (TTE) with agitated saline bubble on postoperative 11th months did not show pulmonary arteriovenous shunt any more (). Clubbing of both fingers also recovered to normal shape in postoperative month 11 (). The patient recovered successfully, not only physically, but also pychosocial activity, including school performance during the 48-months follow-up period.

[[16.0, 'year']]

F

{'15621142': 1, '18509123': 1, '19686444': 1, '21365433': 1, '29192374': 1, '12792501': 1, '19775311': 1, '21365434': 1, '18310172': 1, '12500204': 1, '10981002': 1, '10915189': 1, '15828054': 1, '24757662': 2}

{}

3992336-1

noncomm/PMC003xxxxxx/PMC3992336.xml

Sonography of hepatic hemangioma accompanied by arterioportal shunt

A 58-year-old man visited our hospital with right upper quadrant pain. His clinical history did not include any specific disease, family history was unremarkable, and physical examination was unremarkable. The results of routine laboratory investigations were unremarkable as well. Serologic tests for hepatitis A, B, and C were negative.\nHepatic sonography showed increased liver echogenicity, suggestive of hepatic steatosis. Gallbladder was unremarkable, and there was no remarkable abnormal finding in the biliary tree and pancreas as well. In the subcapsular area of the right hepatic lobe, there was a 2-cm, well-defined nodule with echo-poor appearance, surrounded by large geographic perinodular hypoechoic area, suggestive of peritumoral sparing of hepatic steatosis (). There was no thrombus at the portal branch, in the spared area of hepatic steatosis around the tumor. Doppler study revealed hypervascularity of the tumor and the reverse hepatofugal flow of the peritumoral portal vein parallel to the feeding artery, indicating the presence of arterioportal shunt accompanying the tumor. Based on grayscale and Doppler sonographic findings, hepatic hemangioma with arterioportal shunt was highly suspected.\nUnenhanced and postcontrast dynamic CT scans were performed for further evaluation of hepatic tumor. Unenhanced CT scan showed decrease of hepatic parenchymal attenuation, suggestive of hepatic steatosis. The tumor was seen as low attenuation nodule in the subcapsular area of the right hepatic lobe, surrounded by subtle hyperdense area, suggesting peritumoral sparing of steatosis. Dynamic contrast-enhanced CT showed strong homogenous enhancement of the tumor, surrounded by large wedge-shaped parenchymal hyperenhancement during the arterial phase. The tumor showed persistent enhancement similar to hepatic vessels and the surrounding parenchymal hyperenhancement was also appreciated during the venous phase. Several small nodules (< 1 cm) with similar enhancement pattern as the one described above were also noted in both hepatic lobes. The diagnosis of hepatic hemangiomas with arterioportal shunt was made by typical CT features.

[[58.0, 'year']]

M

{'9762989': 1, '16985113': 1, '11376258': 1, '8626890': 1, '21385916': 1, '11868785': 1, '9933672': 1, '24757664': 2}

{}

3992345-1

noncomm/PMC003xxxxxx/PMC3992345.xml

Coronary Artery Fistula Draining into the Left Ventricle

A 48-year-old male presented with abdominal pain that had lasted for 2 months. He had no cardiovascular risk factor, and no cardiovascular symptom such as chest pain or dyspnea. He was diagnosed as gallbladder stone and admitted to our hospital for laparoscopic cholecystectomy. Preoperative electrocardiography was within normal limit, and chest X-ray showed no pathologic abnormality. He was consulted to cardiovascular department because surgeon heard a continuous cardiac murmur and ordered echocardiography for a preoperative evaluation. The echocardiography showed normal ejection fraction (64%). The mitral inflow E/A ratio was 1.63, and E/E' ratio was 12.0. The valvular morphology and function was normal. However, there was abnormal color flow within left ventricle predominantly during diastole (, ,, , ). It was originated from basal posterior wall and drained into the left ventricular cavity. The maximal velocity of blood flow draining into left ventricle was approximately 3.0 m/s. In short-axis great arterial view, left coronary artery appeared dilated. Multiple tortuous dilated vascular structures with internal blood flows disclosed by color Doppler image were also found around left ventricular myocardium. Especially, dilated large echo-free vascular structure was detected in the apical area. The connection between those dilated vascular structures and left coronary artery was suspected, but clear visualization of the connection was limited in 2-dimensional echocardiography. Coronary artery computed tomography (CT) scan was performed to confirm the pathologic anatomy of these abnormal findings. Coronary CT revealed markedly dilated (up to 16 mm) and serpentine whole left coronary arteries (). The left anterior descending artery was communicating with left circumflex artery at the apical posterior epicardium, and was directly connected to the basal posterior side of left ventricular cavity (). He was finally diagnosed as having CAF.\nSince the patient had no cardiovascular symptom, he underwent laparoscopic cholecystectomy without specific treatment of CAF. No clinical events occurred during his admission. The patient visited outpatient clinic a month after discharge without clinical events or symptoms.

[[48.0, 'year']]

M

{'29137066': 2, '17762067': 1, '1417232': 1, '9477461': 1, '19891792': 1, '9482144': 1, '3518378': 1, '27377631': 1, '7656302': 1, '20332380': 1, '22560322': 1, '18299514': 1, '24753806': 2}

{'5690759-1': 1}

3992346-1

noncomm/PMC003xxxxxx/PMC3992346.xml

Dilated Cardiomyopathy Secondary to Hypothyroidism: Case Report with a Review of Literatures

A 36-year-old man presented to the emergency room with dyspnea of New York Heart Association functional class III/IV and fatigue. The patient had a 1-year-history of chief complaints of weakness of all four extremities, weight gain and bilateral lower extremity edema. For two months prior to admission, the patient had a progressive worsening of bilateral lower extremity edema. On physical examination, the patient had body mass index (BMI) 28.6 kg/m2 and vital signs such as blood pressure 130/90 mmHg, pulse rate 90 beats/min, respiratory rate 20 breaths/min and O2 saturation 96% in room air. In addition, the patient had pale and dry skin. Heart rate was regular and systolic murmur was heard at the apex. Breath sounds were decreased with inspiratory crackles on bilateral lung bases. The patient also had bilateral presence of non-pitting edema of the foot and ankle. On chest X-ray, the patient had cardiomegaly with perihilar congestion and blunting of both costophrenic angles. These findings are suggestive of pleural effusion (). On electrocardiographic findings, the patient had normal sinus rhythm with low voltage of limb leads, interventricular conduction delay and non-specific ST-segment and T-wave changes (). On clinical laboratory examinations, the patient showed elevated serum levels of N-terminal pro-brain natriuretic peptide (5026 pg/mL) and normal range of cardiac enzymes. Renal functions were normal with blood urea nitrogen of 14.8 mg/dL and creatinine of 1.2 mg/dL. Lipid panel showed total cholesterol 231 mg/dL, triglyceride 188 mg/dL, high-density lipoprotein cholesterol 34 mg/dL and low-density lipoprotein cholesterol 88 mg/dL. Liver function test showed elevated serum levels of transaminases with total bilirubin 1.34 mg/dL, aspartate transaminase 402 IU/L, alanine transaminase 340 IU/L and alkaline phosphatase 44 IU/L. On complete blood counts, the patient had white blood cell counts 9260/mm3 with 56% neutrophils, hemoglobin 10.8 g/dL and platelets 190000/mm3. Serum electrolytes showed [Na+] = 120 meq/L, suggesting hyponatremia, and [K+] = 4.3 meq/L. Serum creatinine kinase was elevated (2738 U/L). On echocardiography, the patient had a dilated left ventricular cavity with a diastolic dimension of 6.1 cm, a decreased global systolic function with an ejection fraction of 16% and functional mitral regurgitation of moderate grade (). The patient had a ratio of transmitral early peak velocity (E) to septal mitral annulus velocity (E') of 13. The patient was started on loop diuretic therapy using furosemide and angiotensin converting enzyme (ACE) inhibitor (enalapril) for heart failure. On day 2, the patient underwent thyroid function test. This showed that the patient had elevated serum levels of thyroid stimulating hormone (100 µIU/mL) (reference range: 0.5-5 µIU/mL), decreased serum levels of T3 (60 ng/dL) (reference range: 80-180 ng/dL) and decreased serum levels of free T4 (0.054 ng/dL) (reference range: 0.7-1.9 ng/dL). Furthermore, the patient underwent additional tests to reveal the cause of hypothyroidism. This showed that the patient was positive for thyroglobulin antibody but negative for anti-microsomal one. On thyroid ultrasonography, the patient had an atrophic thyroid gland with hypoechoic parenchyma with two small nodules of 5 mm and 8 mm in size in the right lobe. On Tc 99-mm radionuclide thyroid scan, there was an increased uptake in the above two small nodules. On fine-needle aspiration biopsy of the nodules, the patient had adenomatous hyperplasia on lymphocytic thyroiditis background (). These findings were suggestive of Hashimoto's thyroiditis accompanied by atrophic autoimmune thyroiditis. Based on these findings, the patient was started on thyroid hormone replacement with thyroxine. Thyroxine dose was titrated up to 50 µg/day after two weeks and then up to 100 µg/day. This was followed by the adjustment of thyroxine dose based on thyroid functions. At a 1-year follow-up, the patient had a gradual decrease in the enlarged left ventricular chamber and a normalization of the decreased left ventricular systolic functions (). Furthermore, the patient also had a normalization of clinical laboratory findings such as transaminases and creatinine kinase. Follow-up echocardiography findings are shown in . Three months after the treatment, the patient had a decrease in the BMI to 23.4 kg/m2. The patient discontinued use of loop diuretics (furosemide) but continued use of ACE inhibitor (enalapril), β-blockers (bisoprolol) and thyroid hormone replacement therapy.

[[36.0, 'year']]

M

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{'6726413-1': 1}

3992347-1

noncomm/PMC003xxxxxx/PMC3992347.xml

Congenital Absence of the Pericardium

A 19-year-old woman was referred to our clinic for further evaluation of cardiomegaly on chest radiography. She had no chest pain, shortness of breath, or other specific signs and symptoms. Her past medical history and family history were unremarkable. She had not taken any medications and denied use of illicit drugs and tobacco or alcohol abuse. On cardiac examination, a regular heart rhythm was heard without heart murmur. A 12-lead electrocardiogram (ECG) showed normal sinus rhythm, with a heart rate of 62 bpm and right deviation of the heart axis (). The chest radiograph revealed that the heart had bulging contour of the left superior cardiac border and leftward shift (). The echocardiography showed a globe-shaped heart and bulbous ventricle due to suspension of the heart from its basal pedicle (). It also revealed mitral valve prolapse. The estimated left ventricular ejection fraction was 65%. Chest computed tomography (CT) revealed outpouching of the right ventricle (RV), which contacted the left chest wall, and interposition of the lung between the aortic arch and prominent pulmonary trunk (). The patient was diagnosed with congenital absence of the left pericardium.\nA 56-year-old man was referred to our clinic for ECG abnormality. He had no chest pain, dyspnea, or other specific signs and symptoms. His past medical history and family history were unremarkable. He neither took medications nor used tobacco or alcohol. On examination, his blood pressure was 126/76 mmHg. A systolic ejection-type murmur was present with regular heart rhythm. A 12-lead ECG showed sinus rhythm with a heart rate of 59 bpm, an incomplete right bundle branch block, and a slight increase in left ventricular voltage (). Chest radiography revealed flattening of the left heart border and a lucent area between the aorta and pulmonary artery due to lung interposition (). The patient underwent an echocardiogram and chest CT because of the abnormal chest radiography, murmur, and ECG. The echocardiography showed a left laterally displaced left ventricle (LV) apex with a swinging motion that was highly suggestive of congenital absence of the pericardium (). The RV cavity was enlarged as 38 mm and demonstrated paradoxical septal motion. LV systolic function was normal. The chest CT revealed nonvisualization of the pericardium and leftward displacement of the entire heart with mild RV dilatation (). The patient was diagnosed with congenital absence of the pericardium.\nA 71-year-old male patient presented with a history of dyspnea on exertion. He reported atypical chest pain and shortness of breath. He suffered from asthma and was taking medication. Medical and family histories were otherwise unremarkable. He was a current, 100 pack-year smoker. On examination, his blood pressure was 120/70 mmHg. Regular heart rhythm without murmur and clear breath sounds were heard on auscultation. A 12-lead ECG showed normal sinus rhythm, with a heart rate of 73 bpm and left deviation of the heart axis (). Q-waves were seen in leads II, aVF, V1, V2, and V3. Chest radiography showed bulging contour of the left superior cardiac border (). Due to his symptoms, abnormal chest radiography, and ECG, the patient underwent an echocardiogram and heart CT. The echocardiography revealed a laterally displaced LV apex that was highly suggestive of congenital absence of the pericardium (). It also showed an enlarged LV cavity with mild global hypokinesia without regional wall motion abnormality. Valvular morphology and function were normal, and the estimated LV ejection fraction was 47%. The cardiac CT revealed absence of the pericardium at the left side of the heart without evidence of associated anomaly such as atrial septal defect or ventricular septal defect (). The patient was diagnosed with congenital absence of the left pericardium.

[[19.0, 'year']]

F

{'8172237': 1, '9609093': 1, '21220242': 1, '17513224': 1, '20444762': 1, '29569049': 1, '34221487': 1, '30972237': 1, '10800821': 1, '8001315': 1, '1536171': 1, '15676161': 1, '19733526': 1, '12135126': 1, '19448561': 1, '34527238': 2, '839275': 1, '24753808': 2}

{'8429913-1': 1}

3992348-1

noncomm/PMC003xxxxxx/PMC3992348.xml

Multiple Papillary Fibroelastomas and Thrombus in the Left Heart

A 68-year-old male with hypertension and atrial fibrillation, was admitted with progressive worsening dyspnea and chest pain. Physical examination at the time of the first admission revealed a temperature of 36.5℃; respiration 20/min; pulse, 100/min and irregular; and blood pressure, 120/80 mmHg. There was a prolonged diastolic murmur at the apex and laboratory data were unremarkable. Electrocardiogram revealed atrial fibrillation with rapid ventricular response. A chest X-ray showed cardiomegaly. TTE revealed a large left atrium of 7.22 cm diameter, severe mitral stenosis, mild mitral regurgitation, moderate aortic regurgitation, and presence of a multiple oscillating variable sized masses in the left ventricle and aortic valve, non-mobile 3.5 × 4.4 cm sized mass in the left atrium. The mitral valve leaflets were heavily thickened and calcified. The masses in the left ventricle were 0.31 × 0.92 cm, and 0.54 × 0.98 cm in size, oscillating heterogeneous echogenic material attached to the interventricular septum basal to mid level and 1.46 × 1.64 cm, 0.47 × 1.07 cm in size, mobile oval shaped mass, which had some echolucent area attached to the posterolateral papillary muscle and aortic valve (). The mass of the left atrium was 3.5 × 4.4 cm in size, non-mobile echogenic mass in the left atrium posterior wall. Cardiac magnetic resonance imaging demonstrated non-enhanced masses in the left atrium between the orifice of the right superior and inferior pulmonary vein and ventricle, which were heterogeneous in its signal intensity in T2 image (). Coronary angiography was normal. Based upon the findings as above, a differential diagnosis was made, which included thrombus, myxoma, fibroelastoma and inflammatory mass. In view of the possibility of embolism, unknown nature of the pathology and multiple valve diseases with symptoms, the patient was taken for urgent surgical resection with valve replacements.\nHistopathology examination of the resected masses in the left ventricle and aortic valve revealed a papillary proliferation, including an avascular connective tissue core lined by a single layer of the endothelial cells, which was sufficient for a diagnosis of CPF (). The left atrial mass was composed of fibrin and red cells with a variable platelet and leukocyte component, revealed to thrombus.\nThe postoperative course was uncomplicated and the patient was discharged in a satisfactory condition on the 12th day.

[[68.0, 'year']]

M

{'17060810': 1, '9283541': 1, '12947356': 1, '13736942': 1, '1088858': 1, '10903697': 1, '19732420': 2, '1953134': 1, '20706573': 1, '18191538': 1, '19491551': 1, '24753809': 2}

{'2749808-1': 1}

3992349-1

noncomm/PMC003xxxxxx/PMC3992349.xml

Unique Congenital Malformation of the Mitral Valve Associated with Anomalous Coronary Arteries and Stroke

A 55-year-old male, smoker and previously healthy, presented to our emergency department for abrupt onset of difficulty reading and right sided weakness, signs and symptoms suggestive of a new onset stroke. Stat computed tomography (CT) and computed tomography angiogram (CTA) of the brain revealed no abnormality. Magnetic resonance imaging of the brain showed acute infarction of the left posterior insular cortex and left parietal subcortical area. The patient was started on aspirin, atorvastatin and clopidogrel. He underwent a routine transthoracic echocardiogram (TTE) as to rule out any possible cardiac source of embolism. TTE revealed an abnormally thickened anterior mitral leaflet associated with mild eccentric mitral regurgitation (MR). Transesophageal echocardiogram (TEE) was performed for further assessment. TEE revealed some form of redundant tissue along the anterior mitral leaflet and the base of the anterior leaflet in the left ventricular outflow tract (LVOT). It is thin and supple, the appearance was neither consistent with a fibroelastoma, nor a tumor, an abscess, a true aneurysm of the sinus of Valsalva nor perimembranous septum. The anterior mitral leaflet is itself thickened and prolapses, which might represent myxomatous disease. A mild eccentric posteriorly directed MR jet was noted, likely originating from the mild prolapse of the anterior leaflet. At the very distal end of the anterior leaflet, there is an echo bright, independently mobile soft tissue entity, 2-3 mm in size. The left circumflex coronary artery (LCX) appears to have both an anomalous origin (very low in the left sinus of Valsalva immediately above the annulus, in closer association to the mitral valve than usual). The ostium of the right coronary artery appears larger than the left coronary artery (, , and , , , and ). Based on these findings, an electrocardiogram-gated cardiac CT scan was suggested. Coronary CTA revealed; anomalous LCX originating from the proximal right coronary artery off the right sinus of Valsalva with a retro-aortic benign course. The mitral valve was described as; thickened anterior mitral valve leaflet with a band like attachment to the membranous inter-ventricular septum, the portion of the band closer to the anterior leaflet forms a thin curvilinear band ( and ). This abnormal appearance could represent a congenital anomaly, myxomatous changes are still probable although may not explain the atypical attachment site. The patient had no fever, blood cultures were negative and all other laboratory investigations were within normal limits. The patient remained in hospital for one week and discharged later with a minor neurological deficit. In the absence of obstruction of the LVOT, the patient is being followed up without surgical intervention.

[[55.0, 'year']]

M

{'23236337': 1, '23185658': 2, '21087557': 1, '11767185': 1, '23090815': 1, '25342190': 1, '19262977': 1, '7503011': 1, '23663062': 1, '21944149': 1, '24753810': 2}

{'3498312-1': 1}

3992744-1

noncomm/PMC003xxxxxx/PMC3992744.xml

Reversible electrophysiological abnormalities in hypokalemic paralysis: Case report of two cases

A 20-year-old girl with no significant past medical illness presented with flaccid are flexic quadriparesis of 2 day duration. She had bulbar and respiratory involvement in form of dysphagia and her single breath count was nine. She also had cranial nerve involvement in form of bilateral facial weakness, neck flexor weakness, and dysphagia. The power in all muscle groups was 1/5. There was no sensory loss, bladder disturbance, or higher function disturbance. She was evaluated for electrolyte abnormalities (suspecting a possible diagnosis of hypokalemic paralysis). The electrocardiography (ECG) showed U waves. Arterial blood gas analysis showed normal pH, normal partial pressures of oxygen and carbon dioxide, and normal bicarbonate levels. Simultaneously, she underwent NC study. The NC study showed significant reduction in CMAP amplitudes of all motor nerves. The distal latencies and conduction velocities were normal in the motor nerves. However, the F-waves were non recordable in all the tested motor nerves. SNAP were also normal. Based on the electrophysiological findings, an alternate diagnosis of acute motor axonal neuropathy (AMAN) form of Guillain-Barre syndrome (GBS) was also considered. In the meantime serum potassium report was available and was 1.9 mmol/L. With administration of potassium (160 meq intravenous over 24 h followed by 60 meq per day in three divided doses orally in form of potassium chloride) patient showed dramatic clinical improvement. Based on this, the original diagnosis of hypokalemic paralysis with quadriparesis with cranial nerve and respiratory involvement was confirmed. NC studies were repeated 24 h after the initial study, by which time patient's motor power was back to normal and serum potassium was 2.9 mmol/L. Repeat NC was found to be normal. The secondary causes of hypokalemia including thyrotoxicosis, renal tubular acidosis, gastrointestinal loss were ruled out (FT3-3.20 pg/mL, FT4-1.10 ng/dL, TSH − 3.80 uIU/mL, arterial pH − 7.45). The short and long duration exercise test to document channelopathy as cause of hypokalemia was planned, but patient did not give consent for the same. As no definite secondary cause of hypokalemia could be found, the patient was not put on any prophylactic therapy. The patient was advised against heavy manual labour and avoiding heavy carbohydrate meals.

[[20.0, 'year']]

F

{'19225109': 1, '9325474': 1, '18250508': 1, '15640425': 1, '12210395': 1, '10399749': 1, '30766289': 1, '28321307': 2, '24753672': 2}

{'3992744-2': 2, '5347489-1': 1}

3992744-2

noncomm/PMC003xxxxxx/PMC3992744.xml

Reversible electrophysiological abnormalities in hypokalemic paralysis: Case report of two cases

A 52-year-old male with no past medical illness presented with flaccid areflexic quadriparesis of 1 day duration. There was no sensory loss, cranial nerve involvement, bladder disturbance, or higher function disturbance. The power in upper limb muscle groups was 2/5 and in the lower limb muscle groups was 3/5. The ECG done in the emergency ward showed U waves. He was evaluated for electrolyte abnormalities (suspecting a possible diagnosis of hypokalemic paralysis) and while the reports were still pending, he underwent NC study. The NC study showed significant reduction in CMAP amplitudes of all motor nerves. However, distal latencies and conduction velocities of motor nerves were normal. F-wave latencies were non recordable in all tested motor nerves. SNAP amplitudes were also normal. Based on the electrophysiological findings, an alternate diagnosis of AMAN form of GBS was also considered. The serum potassium report was 2.0 mmol/L. With administration potassium (160 meq intravenous over 24 h followed by 60 meq per day in three divided doses orally in form of potassium chloride), the patient showed dramatic clinical improvement. Based on this, the original diagnosis of hypokalemic paralysis with quadriparesis was confirmed. NC study was repeated 24 h after the initial study, by which time the patient's motor power was back to normal and serum potassium was 3.9 mmol/L. Repeat NC study was found to be normal. The secondary causes of hypokalemia including thyrotoxicosis, renal tubular acidosis, gastrointestinal loss were ruled out (FT3-3.09 pg/mL, FT4-1.03 ng/dL, TSH − 2.90 uIU/mL, arterial pH − 7.4) The short and long duration exercise test to document channelopathy as cause of hypokalemia was planned, but patient did not give consent for the same. As no definite secondary cause of hypokalemia could be found the patient was not put on any prophylactic therapy. The patient was advised against heavy manual labor and avoiding heavy carbohydrate meals.\nThe NC study report before and after correction of hypokalemia and recovery of muscle power depicting the changes in the CMAP of the motor nerves.\nAs there was no asymmetry between nerve conduction findings of left and right side, only right-sided nerves are described for sake of convenience [].

[[52.0, 'year']]

M

{'19225109': 1, '9325474': 1, '18250508': 1, '15640425': 1, '12210395': 1, '10399749': 1, '30766289': 1, '28321307': 2, '24753672': 2}

{'3992744-1': 2, '5347489-1': 1}

3992745-1

noncomm/PMC003xxxxxx/PMC3992745.xml

Atypical Wernicke's syndrome sans encephalopathy with acute bilateral vision loss due to post-chiasmatic optic tract edema

A 69-year-old male presented with intermittent feeling of blurred vision with mild imbalance while walking for 2 days followed by acute loss of vision in both his eyes. He had undergone partial gastrectomy for poorly differentiated adenocarcinoma of the pylorus before 1 month. He had no other health related problems previously. His family history was unremarkable and he had no history of alcohol or tobacco consumption. The immediate post-operative period was unremarkable. Ophthalmologic evaluation revealed total loss of visual acuity with no light appreciation or finger counting with preserved bilateral pupillary reaction to light. There was mild opthalmoparesis with reduced saccadic and pursuit movements toward the sound and patient's own finger movements. There was bilateral horizontal gaze evoked nystagmus with fast component in the direction of gaze. Bilateral optic fundi were normal. He had symmetric trunk and gait ataxia, but no limb ataxia or dysarthria. His alertness, mood, memory, behavior and other cognitive functions were well-preserved. His other systemic and neurologic examination was unremarkable. An urgent plain and contrast magnetic resonance imaging (MRI) of the brain was done to rule out either of posterior circulation stroke (Bilateral Posterior Cerebral Artery infarct), intracranial metastasis and paraneoplastic neurological dysfunction in view of recently operated carcinoma of stomach.\nMRI brain revealed bilateral symmetrical hyper-intensities over the mammillary bodies and periventricular regions of the third ventricle, bilateral inferior colliculi on T2-weighted and fluid attenuated inversion recovery (FLAIR) images [Figure , , and ] with homogenous enhancement postcontrast [Figure and ] with no restriction on diffusion-weighted and apparent diffusion coefficient (ADC) images (ruling out ischemia/cytotoxic edema). In addition to these classic findings of WE, focal hyper-intensities were also observed in bilateral post-chiasmatic optic tract on FLAIR images []. Based on the imaging findings and clinical background of patient, diagnosis of non-alcoholic acute Wernicke's syndrome was considered and treatment with intravenous thiamine hydrochloride (500 mg/d) was promptly started. His visual symptoms significantly improved in 24 h and his vision became completely normal in 72 h. His ataxia improved gradually over the next 3 weeks. He was discharged with the advice to take intravenous thiamine injections once every month to prevent the thiamine deficiency. A follow-up MRI brain carried out after 1 month revealed complete resolution of MR signal intensities [Figure and ].

[[69.0, 'year']]

M

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{}

3992746-1

noncomm/PMC003xxxxxx/PMC3992746.xml

Essential thrombocythemia: Rare cause of chorea

A 55-year-old female patient presented to us with an acute onset of involuntary movements involving limbs, face and tongue. These movements were random and fleeting from one part of the body to another causing dysarthria and social embarrassment. There was no history of headache, visual disturbances or transient ischemic attack (TIA). There was no history of recent exposure to anti psychotic's medication. There was no family history of chorea or dementia and no history of rheumatic fever. On examination, patient had generalized chorieform movements involving limbs face and tongue. There was no extra pyramidal or pyramidal sign. Higher mental functions were normal with mini mental score of 28. There was no facial plethora or splenomegaly.\nOn investigation, she had total white blood cell count 14.2 × 103/uL, total red blood cell count 5.07 × 106/uL, platelet count 1092 × 103/uL, hemoglobin 15.1 g/dL, hematocrit 46.3%, mean corpuscular volume 91.3 fL, mean corpuscular hemoglobin 29.8 PG, mean corpuscular hemoglobin concentration 32.7 gm/dL and erythrocyte sedimentation rate 01 mm. The peripheral blood smear revealed no abnormal cell or acanthocytes. Neutrophil alkaline phosphatase was 240, ceruloplasmin was normal and bcr-abl gene expression was negative. Janus kinase 2(JAK2) V617F mutation was positive. Bone marrow showed hyper cellular marrow with a marked increase in megakaryocytes without any atypical blast cells. Magnetic resonance imaging (MRI) brain was normal and the ultrasound sonography abdomen did not reveal organomegaly. Renal, hepatic and other metabolic profiles were normal. Anti-nuclear antibody and anti-double-stranded deoxyribonucleic acid were negative. The chest X-ray and echocardiogram were normal. Hence, a diagnosis of ET was made and she was started on haloperidol initially to control chorea symptomatically. She showed only some improvement, but her platelet count was rising further and was started on hydroxyurea. On 3rd month of follow-up her chorea completely subsided, haloperidol was slowly withdrawn and her platelet count was 562 × 103/uL.

[[55.0, 'year']]

F

{'16673273': 1, '6370700': 1, '16325696': 1, '21485168': 1, '32832197': 1, '30931269': 2, '33426172': 1, '69781': 1, '17210076': 1, '11009585': 1, '24753674': 2}

{'6432831-1': 1}

3992747-1

noncomm/PMC003xxxxxx/PMC3992747.xml

Acanthamoeba meningoencephalitis

A 16-year-old boy from Orissa with complaints of non-pulsatile, holocranial headache and low-grade, intermittent evening rise of temperature for 3 months and was on anti-tubercular therapy with steroids and anti-edema measures for clinically suspected central nervous system tuberculosis. He reported transient improvement of constitutional symptoms over the next 15 days, following which he developed right hemiparesis, motor aphasia and altered sensorium and was referred to our hospital. There was no preceding history of seizures, myoclonus, history of dog bite or vaccination. No history of exposure to unsafe sexual practices or drug abuse. There was no recent history of travel or water related activities preceding this illness.\nOn admission, he was febrile, drowsy and unresponsive to commands. Neurological examination revealed neck rigidity, right-sided hemiplegia, with hypertonia, and bilateral extensor plantar responses. Routine investigations including serum biochemistry (liver and renal function tests) and hemogram were normal except for mild peripheral blood leukocytosis (total white blood cells count was 12,600/cubic milimeter with neutrophillic predominance). Serology for HIV, and venereal disease research laboratory test was non-reactive.\nA cranial magnetic resonance imaging (MRI) [] revealed multiple, coalescing, predominantly T1 and T2 hypointense lesions with ring enhancement located in left capsuloganglionic region, thalamus, brainstem and cortico-medullary junctions, also lesions involving left basal ganglia showed a characteristic peripheral thin rim of T1 hyperintensity with blooming on gradient-sequences and hyperdensity on plain-computed tomography (CT) scans indicative of bleed. Magnetic resonance spectroscopy (MRS) [] from the lesions revealed elevated lactate and choline peaks. Fluid attenuated inversion recovery images sequences revealed sulcal hyperintensities with contrast enhancement, suggestive of leptomeningitis. The left caudate head and lentiform nuclei showed features suggestive of acute infarct, corresponding to recurrent artery of Huebner territory.\nBased on MRI features, possibility of a hemorrhagic meningoencephalitis either of viral or fungal origin was suspected. He succumbed to his illness on the second day of admission. A complete autopsy was performed following informed consent from close relatives of the deceased. At autopsy, the brain was diffusely edematous and revealed large necrotizing lesions with yellowish center surrounded by zones of hemorrhage involving parietooccipital lobes bilaterally, left orbitofrontal and inferior occipital regions []. On coronal slicing, multiple hemorrhagic, necrotic lesions were seen along the cortical ribbon mostly located in the crown of gyrus/depth of sulcus in left middle and inferior frontal lobe. At the level of optic chiasm, the left insular cortex showed large nodular confluent coalescing necrotic lesion [] with central zones of yellowish xanthomatous areas with peripheral rim of hemorrhage [], extending along the sylvian fissure following the gyral pattern and superiorly into the left putamen compressing the ipsilateral ventricle. The surrounding white matter was edematous. Distinct pale necrotic lesions were seen in the left head of caudate, left uncus, left anterior hippocampus and anterior thalamic nucleus. The cingulate gyrus on the right also showed a hemorrhagic lesion involving the cortical ribbon.\nThe brainstem showed a nodular, hemorrhagic, necrotic circumscribed lesion in the upper pons on left side. No lesions were seen in mid-brain or cerebellum. Histologically these lesions revealed florid meningoencephalitis with mixed infiltrate of lymphocytes and histiocytes flooding the subarachnoid space. The larger leptomeningeal vessels were thrombosed with dense inflammation []. The inflammatory infiltrates were seen invading the underlying cortex. The smaller parenchymal venules entrapped in the inflammation were ruptured forming small pools of fresh hemorrhage. Parenchymal necrosis and hemorrhage was prominent with venulitis. Foci showed ill-formed granulomas with histiocytic aggregates and multinucleate giant cells. Special stains for fungal hyphae and acid fast bacilli were negative. Periodic acid Schiff stain highlighted several large trohphozoite form of amoeba surrounding penetrating venules and filling the Virchow Robin spaces in continuity with subarachnoid space []. In addition scattered cysts morphologically resembling Acanthamoeba were detected perivascularly by silver stains []. The trophozoites were large (25 microns to 40 microns), with thick cell wall and prominent nucleoli. The cysts were multinucleate with thick cell walls. Trophozoites and cysts were also found in necrotizing lesions in pons. The posterior half of eye ball with optic nerves removed at autopsy revealed dense inflammation expanding the subarachnoid space surrounding the optic nerve, particularly on the left side with scattered trophozoites detectable in the perioptic space and within the substance of the optic nerve.\nThe lungs were boggy, subcrepitant and revealed bilateral consolidation with evidence of bronchopneumonia on histology. No trophozoites were detectable. The liver and spleen were enlarged and revealed multiple small abscesses and necrotizing granulomas with scattered trophozoite forms of acanthamoeba. Cysts were not detectable in the organs. Dot polymerase chain reaction for acanthamoeba was positive in serum and in vitreous of the left eye and brain tissue [] but negative in Cerebro spinal fluid. Dot blot is the simplification of conventional method, a mixture containing the molecule to be detected is applied directly on a membrane as a dot and is then spotted through circulate templates on to the membrane. No electrophoresis is applied and hence saves time, it confirms the presence of the biomolecules which can be detected by DNA probes or antibody. The principle is that a single oligoprobe can hybridize to a second DNA molecule that contains the target sequence. So, it is speculated that, following primary parasitemia secondary to poor host defenses, the parasite might have seeded the choroid of the left eye, spread through the lamina cribrosa into the peri-optic subarachnoid space, and extended along the subarachnoid space into basal cisterns, along sylvian fissure and into the parenchyma. We were handicapped with the absence of history and a very brief stay of the patient at our hospital, it is likely that he harboured the organism as a normal commensal probably in his nasal mucosa. Parasitemia would have occurred following breakdown of the local barriers secondary to viral infection.

[[16.0, 'year']]

M

{'5825411': 1, '2193354': 1, '32318505': 2, '16988022': 1, '16775267': 1, '9725321': 1, '8232369': 1, '17552103': 1, '33970886': 1, '9720747': 1, '3586292': 1, '9159368': 1, '31309100': 1, '1457633': 1, '18407447': 1, '6991973': 1, '857580': 1, '26280011': 1, '16774587': 1, '24753675': 2}

{'7114032-1': 1}

3992748-1

noncomm/PMC003xxxxxx/PMC3992748.xml

Clinical, hematological, and imaging observations in a 25-year-old woman with abetalipoproteinemia

A 25-year-old lady presented with a history of progressive nyctalopia since the age of 10 years and impaired hearing since the age of 15 years. The latter was attributed to chronic suppurativeotitis media (CSOM) elsewhere. At the age of 20 years, she developed tremulousness of limbs that was prominent while reaching out for objects as well as with anxiety. This was associated with dysarthria and imbalance of stance and gait that worsened markedly on removing visual cues. There was no history of dystonia, hyperkinetic movement disorders, recurrent infection, malignancies, focal limb deficits, seizures, myoclonus, altered sensorium, psychiatric manifestations, or autonomic system involvement. There was no family history of similar illness.\nShe was born to non-consanguineous parents at term following an uneventful antenatal period. Postnatally, there was failure to thrive with a global delay in the acquisition of all milestones. She suffered from recurrent diarrheal episodes throughout the first decade of life. She was advised a gluten-free diet following a presumptive diagnosis of celiac disease by her pediatrician without any significant respite. Her gastrointestinal symptoms subsided at the age of 10 years. She was also transfused blood on three occasions for severe anemia. She attained menarche at the age of 13 and had normal menstrual cycles.\nOn examination, she was a short-statured (height: 143 cm), thin-built (weight: 31 kg) girl with a very low body mass index (BMI: 15.19 kg/m2), dysmorphic facies in the form of prognathism, hypertelorism, malar hypoplasia, and scoliosis. Fundus examination showed evidence of atypical RP []. She had cerebellar signs in the form of titubation, dysarthria, as well as impaired co-ordination on finger-nose and knee-heel testing. Motor system examination revealed wasting and hypotonia of distal extremities, normal power, and sluggish deep-tendon reflexes. There was a marked impairment of kinaesthetic sensations; bilateral plantar responses were flexor.\nShe had been evaluated elsewhere for malabsorption and anemia. Jejunal biopsy showed only mild focal atrophy; serum tissue transglutaminase (IgA) levels were not elevated (7.05; ref: <15 U/ml: negative). D-xylose excretion was less than normal (0.2 g/5 g; ref: 1 g/5 g), suggesting malabsorption from the small intestine. Peripheral smear done on at least five occasions until the age of 15 years showed varying degrees of anemia (hemoglobin ranging from 3.8 to 8.0 g%), dimorphic red blood corpuscles (RBCs), and poikilocytosis. Examination of bone marrow aspirate showed normoblastic erythropoiesis, with absent marrow iron stores. Stool examination for parasites and occult blood drew negative results. Serum iron (31.08; ref: 35-145 μg/dl) was reduced and total iron binding capacity (TIBC) (558.2; ref: 250-400 μg/dl) was elevated. She received vitamin and iron supplements.\nPresently, at the time of evaluation at our centre, hemogram revealed hemoglobin: 12.4 g%, total leucocyte count (TLC): 5500 cells/mm3, erythrocyte sedimentation rate (ESR): 2 mm (1st h), while the peripheral smear showed normocytic to macrocytic and normochromic RBCs and numerous acanthocytes []. Serum lactate (16.6 mg/dl; ref: 4.5-20 mg/dl), renal and hepatic function tests, serum creatine kinase (CK) (55 U/l; ref: 20-171 U/l), screening for inborn errors of metabolism (IEM) by tandem mass spectroscopy (TMS), thyroid profile (thyroid-stimulating hormone (TSH): 2.45 μU/ml, ref: 0.34-5.0 μU/ml; T3: 140.04 ng/dl, ref: 87-178 ng/dl; T4: 13.4 μg/dl, ref: 6.09-12.23 μg/dl), human immunodeficiency virus (HIV) antibody test, and abdominal ultrasound were within normal limits. Serum ammonia (50.9 μmol/l; ref: 11-35 μmol/l) was mildly elevated. Magnetic resonance imaging (MRI) of brain revealed a normal study; there was no cerebellar atrophy, while the cervical cord showed T2-hyperintense signal changes in the dorsal column []. Routine peripheral nerve conduction studies showed absent sensory nerve action potentials in median, ulnar, and sural nerves with preserved motor conduction parameters. Audiometry showed moderate to severe mixed bilateral hearing loss, suggesting it to be due to combination of conductive (CSOM-related) and sensori-neural (disease-related) deafness.\nThe serum lipid profile was abnormal, with extremely low levels of total cholesterol (34; ref: 110-220 mg/dl), triglycerides (TG) (4; ref: 50-150 mg/dl), high density lipoprotein (HDL) (23; ref: 35-65 mg/dl), very low density lipoprotein (VLDL) (1 mg/dl; ref: 10-40 mg/dl), and low density lipoprotein (LDL) (10; ref: 60-160 mg/dl). Serum apolipoprotein B level was also very low (<20; ref: 60-117 m%). Serum levels of vitamin E (<0.3; ref: 5-18 mg/l) and D (5.24; ref: <10 ng/ml: deficient) were significantly reduced, while B12 (1841; ref: 243-894 pg/ml) and folic acid (12.9; ref: 3-17 ng/ml) were within normal limits.\nBased on the described phenotype, the presence of acanthocytes and low serum cholesterol, TG, HDL, LDL, VLDL, and apolipoprotein B levels, a diagnosis abetalipoproteinemia was considered with secondary vitamin E deficiency. She was initiated on treatment with oral vitamins E (2400 IU/d), D (1000 mg/d), A (400 IU/kg/d), and iron supplementation (ferrous sulphate containing 60 mg of elemental iron/day), and parenteral vitamin K (5 mg/day). There was no follow-up.

[[25.0, 'year']]

F

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{}

3992749-1

noncomm/PMC003xxxxxx/PMC3992749.xml

Intractable vomiting and hiccups as the presenting symptom of neuromyelitis optica

A 24-year-old lady developed recurrent projectile vomiting, 8-10 times/day for initial few days and 2-3 episodes/day later, associated with hiccups which used to come intermittently. Symptoms continued for 1.5 months. There were no other systemic or neurological complaints. Initially patient was seen by a general practitioner and was treated symptomatically. She did not experience weight loss, dehydration, or electrolyte disturbances as she was being treated with intravenous (IV) fluids. Later, she was evaluated by an ear, nose, and throat (ENT) specialist and a neurologist. A computed tomography (CT) scan was done which was normal again she was continued on symptomatic treatment. Later she was evaluated by another neurologist and MRI of brain was done, which showed T2/fluid attenuated inversion recovery (FLAIR) hyperintensity in periaqueductal grey matter of midbrain, midbrain tectum, medulla, and right temporal periventricular region [Figure and ]. The diagnosis considered were Wernicke's encephalopathy/acute disseminated encephalomyelitis (ADEM). There were no symptoms/signs of encephalopathy. Electroencephalogram and lumbar puncture were not performed. Vomiting and hiccups stopped after a 5-day course of IV methylprednisolone (IVMP). She was continued on oral steroids 1 mg/kg (weight 62 kg) initially and later on tapered for 5-6 months and she was asymptomatic subsequently. Five months later (11 months after initial symptom) she developed numbness of the right upper limb followed by right lower limb without facial involvement over 2 weeks. There was no weakness of limbs and bowel bladder disturbances. She was again given 5-day course of IVMP, but there was no significant improvement. Oral steroids were not given. Patient was independent for her daily activities.\nThree months later she developed bilateral visual loss which improved completely over 1 month following another course of IVMP. Oral steroids 1 mg/kg were given initially and gradually tapered over 1 year along with single dose of IV methylprednisolone injection every month. Later (2 years 2 months after onset of first symptom and 1.5 years of steroid therapy) she developed painful restriction of movements of left hip and imaging with MRI was done and was diagnosed to have avascular necrosis of femur both sides for which she underwent core decompression. Two and half years after the first symptom again she developed weakness of all four limbs requiring two person's support to walk, numbness below the neck, and urinary retention. This time she presented to our institute. MRI of spine showed longitudinally extensive transverse myelitis (LETM) involving first to fifth cervical vertebra []. We considered the diagnosis of NMO. Her NMO antibody test was positive. Other autoantibodies were negative. Cerebrospinal fluid examination showed six lymphocytes and protein of 41 mg/dL. Human immunodeficiency virus (HIV) and venereal disease research laboratory (VDRL) tests were nonreactive. Vitamin B12 level was normal. She was treated with five cycles of large volume plasmapheresis and she made significant improvement (expanded disability status scale was 6.5 at the time of admission and it was 3.5 during last follow-up 2 months later). For immunomodulation, azathioprine has been started, after explaining the need, short and long term side effects.

[[24.0, 'year']]

F

{'21368286': 1, '20399665': 1, '18420727': 1, '22042189': 1, '25972717': 2, '33927537': 1, '16717206': 1, '31565627': 2, '17350413': 1, '34080180': 1, '34566866': 1, '32140029': 1, '21031587': 1, '30088219': 1, '30122843': 2, '16275842': 1, '24753677': 2}

{'6758964-1': 1, '4426530-1': 1, '6073970-1': 1}

3992751-1

noncomm/PMC003xxxxxx/PMC3992751.xml

Pregnancy related symptomatic vertebral hemangioma

A 23-year-old primigravida presented at 28 weeks of gestation with progressive asymmetric weakness of both lower limbs for last 15 days. She also complained of diminished sensation over the lower limbs, along with plaster cast like sensation over the lower limbs and band like feeling at lower chest. She had no back or radicular pain, visual complain, urinary or bowel symptoms. There was no history of trauma, fever, weight loss or anorexia. Past and personal history was non-contributory. General physical examination including the spine was normal. Neurological examination revealed mild spasticity in lower limbs; motor power in left lower limb was Medical Research Council grade 4/5 and in right lower limb was 4/5 except at the ankle dorsiflexors where it was 2/5. Deep tendon reflexes in both lower extremities were brisk, abdominal reflex was absent and had bilateral extensor planter reflex. Sensory examination showed impaired sensation for touch and pain with a sensory level at D10 (spinal segment) and zone of hyperesthesia at D8 spinal segmental level. Posterior column sensations were impaired in both lower limbs and Romberg's sign was positive. Other systemic examination was unremarkable. A working diagnosis of compressive myelopathy (compression at D4-5 vertebral level) was considered.\nComplete hemogram, erythrocyte sedimentation rate, coagulation tests, blood glucose, renal and liver function tests were normal. Ultrasound of abdomen revealed 28 weeks single live intrauterine fetus. Magnetic resonance imaging (MRI) of dorsal spine showed marrow signal alteration in D3-D5 vertebral bodies and associated para-vertebral and posterior epidural extension compressing the spinal cord. Any osseous destruction or collapse of the involved vertebrae was not evident. The MRI findings were consistent with vertebral hemangioma with paravertebral-epidural component [Figure , and ].\nPatient was advised for surgery; however, she declined for it. When her weakness further worsened over next 3 weeks leading to paraplegia and bladder disturbance, she agreed for the surgery. Although the lesion was confined to three vertebrae, the epidural component was relatively more extensive, hence extended laminectomy at D1-5 vertebrae and tumor decompression was done. Histopathology of tumor tissue was also suggestive of hemangioma []. Post-operative ultrasonography showed 32 weeks live intrauterine fetus. There was significant improvement in motor deficit after a week of surgery and she was able to stand with support. Four weeks post-operatively she was able to walk with minimal assistance and also regained normal urinary bladder function. Six weeks postoperatively she delivered a full term normal baby by elective lower segment caesarean section. After delivery there was further clinical improvement and at 3 months follow-up she had minimal residual deficit with brisk deep tendon reflexes in lower limbs and normal sensory examination. Repeat MRI of dorsal spine at 3 months postoperatively showed reduced epidural component of vertebral hemangioma [Figure and ].

[[23.0, 'year']]

F

{'3734828': 1, '13526922': 1, '28695052': 2, '16190606': 1, '18224354': 1, '32913613': 2, '33948320': 2, '31852104': 2, '28819591': 1, '25918662': 2, '8416240': 1, '32699766': 1, '30956475': 1, '30290682': 1, '24753678': 2}

{'8088490-1': 1, '5473073-1': 1, '7459382-1': 1, '6922397-1': 1, '4397049-1': 1}

3992752-1

noncomm/PMC003xxxxxx/PMC3992752.xml

Glutamate-based magnetic resonance spectroscopy in neuroleptic malignant syndrome

A 55-year-old man was admitted with a history of acute-onset high-grade fever, severe generalized tremors and an altered level of consciousness for the last 2 days. On admission, the patient had a pulse rate of 116 beats/min, blood pressure 140/80 mm Hg, temperature 103.4°F respiratory rate of 32/min, and oxygen saturation of 95% although inhaling room air. The patient was being treated for bipolar disorder for the last year. He was on risperidone (30 mg/day), clonazepam (0.5 mg/day) and olanzapine (7.5 mg/day). Neurological examination revealed Glasgow coma score 12/15, disorientation, lead-pipe rigidity, brisk jerks, and coarse tremors. Examination of the other systems was normal.\nThe patient's treatment was initiated with cooling blankets, intravenous infusion of acetaminophen, and lorazepam. Routine investigations of blood revealed elevated erythrocyte sedimentation rate (100 mm 1st h), raised serum creatinine (1.5 mg/dl), and a very high creatine phosphokinase level (3522 Units/dl). His electrocardiogram and chest X-ray were normal. Bacterial and fungal cultures of blood were negative.\nMagnetic resonance imaging of the brain was obtained with a 1.5T scanner (General Electric, USA). T2 sequences showed mild hyperintensities in basal ganglia bilaterally []. Simultaneously, magnetic resonance spectroscopy was carried out with single [inner green box in ] and multi-voxel regions [outer white box in ] of interest. The regions of interest (ROI) were specified manually. shows a similar image at a different level. shows the presence of increased levels of glutamate in the single-voxel ROI (625 mm2) (arrowhead) with relaxation time (TR) 4200 and excitation time TE 103.8. A heat map of the glutamate concentration was generated [Figure and ], which showed increased levels of glutamate in both the basal ganglia.\nThe contribution of each hemisphere to the clinical scenario was analysed by parallel-beam radon transformation analysis of the heat map generated by magnetic resonance. This was carried out using the image analysis toolbox of MATLAB (MATLAB 2008a, MA, USA). The result showed marked symmetry [], confirming equal participation of both hemispheres.

[[55.0, 'year']]

M

{'21513803': 1, '23108793': 1, '18234683': 1, '8105799': 1, '20041172': 1, '21921084': 1, '21041067': 1, '22986449': 1, '24753679': 2}

{}

3992753-1

noncomm/PMC003xxxxxx/PMC3992753.xml

Multiple cerebral infarctions with severe multi-organ dysfunction following multiple wasp stings

A 40-year-old male, normotensive, non-diabetic, reported was stung by 50-60 wasps all over the body including face, head, and neck region. He was complaining of redness, swelling, and pain all over the body. He was treated at peripheral hospital with chlorpheneramine and Hydrocortisone injection. He remained stable for next 16-18 h, after which he developed rapid progressive deterioration in consciousness and became unresponsive within a period of next 4-6 h with associated history of vomiting and incontinence of urine. There was no history of headache, fever, breathlessness, trauma, abnormal body movement, drug intake, bleeding from any site, and jaundice. He was then brought to our emergency, where his initial assessment showed Glasgow Coma Scale of 6/15 with Blood Pressure of 170/100 mmHg. He was febrile to touch, multiple wasp sting marks [] with swelling of right upper limb (a total of 73 sting marks), moving left side of body on deep painful stimuli, gaze preference towards left side and with bilateral extensor response.\nA provisional diagnosis of stroke after multiple wasp sting was made, baseline laboratory investigation [] (complete blood count, renal and liver function tests, arterial blood gas analysis, electrocardiograph, x-ray chest, blood glucose, electrolytes, urine examination, Creatine Phosphokinase/Lactate Dehydrogenase, and coagulogram) were sent along with Non contrast Computed Tomography of head and was started on i.v hydrocortisone, i.v avil, and i.v antibiotics along with supportive measures.\nNon contrast Computed Tomogarphy of head was suggestive of hypodense areas in left thalamic region and occipital area. Later, further investigation like Fibrin degradation product, D-Dimer, and C-reactive protein was done which were also positive and next day magnetic resonance imaging of brain with diffusion weighted images was performed which revealed multiple hyperintense lesions in cortical and subcortical areas with loss of grey white contrast in both cerebral hemispheres, pons bilateral thalami, and left parieto-occipital region with evidence of marked diffusion restriction [].\nHis ultrasound abdomen, X-ray chest, electrocardiograph, electrolytes, arterial blood gases, liver function tests, urine examination was normal and antinuclear antibody, anti-double stranded DNA was negative.\nAfter 4 days, his NCCT head was repeated which showed hypodensities in left thalamic, left parieto-occipital, bilateral cerebellar hemispheres, and in pontine region.\nDuring the hospital stay of 23 days, he remained hemodynamically stable but his clinical condition did not improve much and was finally discharged in a vegetative state with GCS of 5/15 on oral steroids and antibiotics.

[[40.0, 'year']]

M

{'9563993': 1, '24299671': 1, '10201441': 1, '27857993': 1, '18523527': 1, '22566738': 2, '22715562': 1, '32055140': 1, '28702114': 1, '31223213': 1, '24753680': 2}

{'3345601-1': 1}

3992754-1

noncomm/PMC003xxxxxx/PMC3992754.xml

Vogt-Koyanagi-Harada syndrome presenting with encephalopathy

A 57-year-old Iranian blind woman was admitted to the Al- Zahra Hospital Emergency Room in Isfahan, with complaints of fever and loss of consciousness. She was blind since 38 years ago because of the VKH syndrome. Her underlying syndrome was diagnosed in an ophthalmology center in London, UK, and she was on prednisolone for a while. Since then, she had no other symptoms. She also had no co-morbidities and had no head trauma during her life. Five days before referring to the hospital, she developed fever, headache, vomiting and intermittent disorientation to the time and place. At the day of admission, she gradually lost her consciousness. On arrival, her exam was: axillary temperature 39°Cand Glasgow Coma Scale 3/15. No sign of meningeal irritation was detected. Cerebrospinal fluid (CSF) analysis showed a mild increase in the protein level (60 mg/dL), while other parameters such as herpes simplex virus- polymerase chain reaction (HSV-PCR) were in normal limits. Brain magnetic resonance imaging (MRI) showed diffuse hypointensities in T1, hyperintensity in T2 and FLAIR techniques in the right temporal, both frontal and right parietal areas []. Other laboratory data were normal. The patient dramatically responded to systemic corticosteroid therapy and was discharged from the hospital with a good general condition.

[[57.0, 'year']]

F

{'17103022': 1, '19201191': 1, '26425031': 1, '20547624': 1, '17384920': 1, '21051514': 1, '15891420': 1, '11141638': 1, '16770158': 1, '18600484': 1, '24753681': 2}

{}

3992755-1

noncomm/PMC003xxxxxx/PMC3992755.xml

Cerebral tubercular thrombophlebitis presenting as venous infarct: Magnetic resonance imaging and pathologic correlation

A previously healthy 23-year-old man presented with fever, occasional headache and vomiting since 4 days, one episode of generalized tonic clonic seizures 2 days prior to admission to the hospital followed by altered sensorium and left sided weakness. At admission to the neurological services, he was afebrile, not opening eyes to painful stimuli. Neurological examination revealed Glasgow Coma Scale (GCS) of 7/15, E1V2M4 with left hemiparesis. Both pupils were asymmetric and not reactive to light. The extraocular movements were restricted and ocular fundus revealed blurring of disc margins. Deep tendon reflexes were brisk and plantar response was extensor on the left and flexor on the right side. Routine hematological and biochemical parameters were normal. The serological tests for HIV, HBsAg, homocysteine, rheumatoid factor and antinuclear antibody were negative. Antemortem cerebrospinal fluid (CSF) analysis could not be done as lumbar puncture was clinically contraindicated. Electrocardiogram showed T wave depression in V1-V4 leads. Chest X-ray revealed inhomogeneous opacities in the left mid and lower zones with bilateral hilar prominence.\nCranial computed tomography (CT) scan highlighted hemorrhagic lesion in the right thalamus and right medial temporal lobe with multiple cerebral and cerebellar ring enhancing lesions. MRI brain [Figure –] revealed heterogeneous mixed signal intensity changes in the right thalamus, caudate, medial temporal region suggestive of hemorrhagic infarct with extensive perilesional edema extending into right internal and external capsules and corona radiata. The lesions bloomed on flash 2D sequences suggesting accumulation of paramagnetic substance, due to evolving hemorrhage. Lesions which were iso to hyper intense on T1WI and predominantly hypo intense on T2WI (T2 shortening) were noted in the right cerebral peduncle of midbrain suggestive of tuberculoma. Diffusion weighted imaging (DWI) revealed hyper intensity in the right thalamus, medial temporal and midbrain (facilitated diffusion) and hypo intensity in pons (restricted diffusion). Hemorrhage was extending into the lateral ventricle in both the occipital horns. The third and lateral ventricles were dilated with minimal periventricular hyper intensity suggestive of uncompensated hydrocephalus. Multiple rounded lesions iso intense on T1 and hypo intense on T2WI suggesting tuberculous granulomas were noted in the left side of pons, bilateral parasaggital basifrontal zones and left postero medial parietal lobe. There was diffuse sulcal hyper intensity on fluid-attenuated inversion recovery imaging (FLAIR) images suggestive of meningitis. MR venogram revealed non-visualization of the bilateral internal cerebral veins, vein of Rosenthal, vein of Galen and proximal segment of straight sinus and left transverse sinus (images are not available for documentation).\nA diagnosis of pulmonary tuberculosis with multiple intracranial tuberculomata and thrombosis of cerebral deep venous system was made. Possibility of cerebral toxoplasmosis was also considered in view of multiple ring enhancing lesions. He received both antituberculous and antitoxoplasma chemotherapy with folinic acid for 5 days. He succumbed on the 6th day of admission to the hospital. Smear from the basal exudates of the brain revealed acid fast organisms by Ziehl-Neelsen stain. Serum and CSF samples collected at autopsy were negative for IgG/IgM antibody to Mycobacterium tuberculosis, Toxoplasma gondii and Cysticercosis.\nAutopsy confined to the examination of the brain only was conducted 18 h postmortem with informed consent of close relatives. The brain weighed 1200 g and was edematous. Dural venous sinuses and superficial anastomotic veins were patent. The leptomeninges were hazy and had occasional tubercles in the parietal area along the course of the veins. The base of the brain had thick hemorrhagic exudate filling the chiasmatic, interpeduncular and pontine cisterns extending to foramen of Lushka, entrapping the cranial nerves and cerebral vessels. The internal carotid and vertebro basilar system were patent with no evidence of atherosclerosis. The crus cerebri on the right was necrotic and hemorrhagic dissecting down from the thalamus to midbrain and the medial temporal lobe on the right was softened. Bilateral cerebellar tonsilar herniation was noted, in spite of mega cisterna magna. On slicing the brain small tuberculomata were found in the left parietal cortex, pons and cerebellum corresponding to lesions on imaging. The right thalamic nucleus, internal capsule, putamen, hippocampus and right half of splenium of the corpus callosum showed hemorrhagic softening, rupturing into the third and lateral ventricle and extending down. The pons and medulla oblongata were enclosed in hemorrhagic inflammatory exudates. At the lower pontine tegmentum and along the foramina of Lushka on both sides, close to choroid plexus tiny tuberculomas were seen in the cerebellum. On the surface the pontine and cerebellar veins were found thrombosed and enclosed in the exudate [Figure –].\nThe histological examination of the representative neuroanatomical areas revealed multiple tuberculomas with caseous necrosis, perilesional edema and reactive astrocytosis. Small venous channels draining into the pontomesencephalic veins and the cerebellar veins were found thrombosed and enclosed in tuberculous inflammatory exudates. Similar to arteries, some of the small veins revealed granulomatous phlebitis. The topographic distribution of hemorrhage lesions correspond to the venous drainage area of basal vein of Rosenthal, anterior and posterior mesencephalic veins. The transverse pontine veins, the retrotonsilar veins of the cerebellum and segment of internal cerebral veins and thalamo-striate veins bilaterally but asymmetrically revealed tuberculous thrombophlebitis along with arteritis of the small perforator vessels, thus highlighting the hemorrhagic lesions and masking the small arterial ischemic lesions. Though the tuberculomas indicate chronic pathology, the acute phlebitis suggests an acute exacerbation of an immune complex mediated granulomatous pathology (Theortical possibility of immune reconstitution secondary to ATT needs to be considered).

[[23.0, 'year']]

M

{'11353098': 1, '19970915': 1, '842274': 1, '506839': 1, '11594914': 1, '612660': 1, '11156766': 1, '24753682': 2}

{}

3992777-1

noncomm/PMC003xxxxxx/PMC3992777.xml

Mycotic aneurysms of the intracranial and peripheral circulation: A rare complication of bacterial endocarditis

A 16-year-old boy presented to us with 5 days history of sudden onset right hemiparesis with speech difficulty. There was also history of recurrent fever for last 6 months.\nHe was also a known case of rheumatic heart disease and was on penicillin prophylaxis for last 5 years.\nOn general physical examination, patient was pale and febrile. The neurologic examination showed spastic dysarthria along with right hemiparesis with medical research council (MRC) grade 4/5 power in right upper and lower limb.\nAmong the routine investigations, urine analysis revealed albuminuria, red blood cells, epithelial cells and hyaline cast suggestive of glomerulonephritis. Echocardiogram was carried out to look for vegetations, but none could be visualized other than severe mitral regurgitation and mild aortic regurgitation with enlarged left atrium and left ventricle. Blood cultures were repeatedly sent in view of history of longstanding recurrent fever and clinical suspicion of bacterial endocarditis, but were negative each time however still a diagnosis of possible infective endocarditis could be made from Duke's minority criteria[] as there was predisposing heart condition, presence of persistent fever, evidence of vascular phenomenon in the form of mycotic aneurysm and intracranial hemorrhage (as detailed in discussion) and immunological phenomenon in the form of glomerulonephritis.

[[16.0, 'year']]

M

{'11265084': 1, '10770721': 1, '11383721': 1, '18303107': 1, '24753666': 2}

{}

3992778-1

noncomm/PMC003xxxxxx/PMC3992778.xml

Acute flaccid paralysis due to West nile virus infection in adults: A paradigm shift entity

A 55-year-old man developed fever of 1 week duration, followed by altered sensorium of 1 day duration. On admission, he had neck rigidity with intermittent opisthotonus. Computed tomography brain and routine blood investigations were normal. He developed hypotension after admission and required intubation and vasopressors. Cerebrospinal fluid (CSF) showed 700 cells/cmm with 43% polymorphs, 57% lymphocytes, normal sugar and elevated protein of 75 mg/dl. He was started on ceftazidime, vancomycin and acyclovir. After 2 days, his condition deteriorated. On examination, he was in a “locked in state” (conscious, opened eyes and blinked and tracked his eyes and protruded his tongue to command). He had a flaccid quadriplegia with grade 0 power in all limbs and global are flexia. Sensory examination was normal. Magnetic resonance imaging (MRI) spine showed hyperintensities in the cervical cord extending from C2 to C7 levels. Axial MRI sections showed intense hyperintensities predominantly involving the grey matter (polio-myelitis) []. MRI brain was essentially normal. His chest X-ray showed bilateral fluffy infiltrates. He then developed intermittent dysautonomia with intermittent tachycardia, tachypnea, blood pressure swings and hypersalivation. Nerve conduction (NCV) studies showed normal motor and sensory responses with absent F waves in all nerves. The initial diagnosis was AFP with polyradiculopathy due to a meningo-encephalitis. The differential diagnosis included paralytic rabies, Cytomegalovirus (CMV), human immunodeficiency virus (HIV) infection and leptomeningeal metastases []. On day 5, he developed oliguric renal failure and persistent hypotension following which he became comatose. CSF polymerase chain reaction (PCR) panel was positive for WNV and negative for CMV, human herpes virus-6, rabies, John Cunningham virus, herpes simplex virus (HSV) 1 and 2, dengue, Japanese encephalitis (JE), nipah, chikungunya, chandipura, mumps, measles and enterovirus including poliovirus, fungi and bacteria including Myobacterium tuberculosis on day 7 (Xcyton acute encephalitis syndrome [AES], Bangalore). The serum and CSF samples were positive for both Japanese encephalitis virus (JEV) and WNV immunoglobulin M (IgM) antibodies by IgM capture enzyme-linked immunosorbent assay (ELISA) (JEV IgM ELISA, National Institute of Virology [NIV] Pune and WNV IgM ELISA, InBiosinc. USA). However, the serum sample on microneutralization assay showed a high titer of neutralizing antibodies to WNV (titer: 40) and undetectable neutralizing antibodies to JEV (titer <10). Hence, the WNV etiology was confirmed.[] CSF was negative for malignant cells. He was offered sustained low efficiency dialysis (SLED) due to persistent hypotension. He underwent three sessions of SLED. On day 14, the relatives decided to withdraw treatment and he expired on day 15.

[[55.0, 'year']]

M

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{'3992778-2': 2, '3992778-3': 2, '8702647-1': 1, '8702647-2': 1, '7381993-1': 1, '7381993-2': 1, '7381993-3': 1}

3992778-2

noncomm/PMC003xxxxxx/PMC3992778.xml

Acute flaccid paralysis due to West nile virus infection in adults: A paradigm shift entity

A 42-year-old man presented to us with buttock pain of 1 week duration. Two days prior to admission, he developed high grade fever and back pain followed the next day by weakness of the right leg and intense twitching of the right thigh. He had grade 0/5 power in the right leg, 4/5 power in the left leg with absent deep tendon reflexes bilaterally and a normal sensory exam. Fasciculations were noticed over both thighs. An MRI spine with contrast was normal. Routine blood investigations were normal. CSF showed 135 cells with 93% lymphocytes and 7% polymorphs and normal sugar and protein. PCR for bacteria, including Mycobacterium tuberculosis, Streptococcus pneumonia, Neisseria meningitidis and HSV, CMV and varicella zoster virus were negative. He was treated for presumptive viral myelitis with acyclovir, ceftazidime and vancomycin for 10 days. Three serum samples collected within 2 weeks after the onset of central nervous system (CNS) symptoms were positive for both JEV and WNV IgM antibodies by IgM capture ELISA (JEV IgM ELISA, NIV Pune and WNV IgM ELISA, InBiosinc., USA). However, the serum samples on microneutralization assay showed significantly high titre of neutralizing antibodies to WNV (titre: 320) and undetectable neutralizing antibodies to JEV (titer <10) confirming the WNV etiology. His fever subsided, but he had residual flaccid paralysis of the right leg, proximal > distal at follow up 1 month later.

[[42.0, 'year']]

M

{'6099760': 1, '34956995': 2, '30124385': 1, '32724683': 2, '22461779': 1, '15709126': 1, '25935909': 1, '15714427': 1, '23760372': 1, '23682140': 1, '16983682': 1, '14700342': 1, '12773646': 1, '30575890': 1, '12847156': 1, '10563521': 1, '12754368': 1, '31392241': 1, '12869104': 1, '18729783': 1, '29695953': 1, '11749765': 1, '24753667': 2}

{'3992778-1': 2, '3992778-3': 2, '8702647-1': 1, '8702647-2': 1, '7381993-1': 1, '7381993-2': 1, '7381993-3': 1}

3992778-3

noncomm/PMC003xxxxxx/PMC3992778.xml

Acute flaccid paralysis due to West nile virus infection in adults: A paradigm shift entity

A 45-year-old man presented to us with high grade fever of 5 days duration, generalized weakness, twitching of both thighs and difficulty in walking of 1 day duration. He had grade 3 power in the right hip flexion and knee extension, absent deep tendon reflexes in both lower limbs and generalized fasciculations all over the body, including the facial muscles. Sensory examination was normal. MRI spine showed an ill-defined non-enhancing hyperintensity in the cervico-thoracic cord. CSF showed 246 cells, 80% polymorphs and 20% lymphocytes, with normal sugar and protein. CSF PCR panel for multiple organisms including WNV was negative. Routine blood investigations including erythrocyte sedimentation rate were normal. He was treated with acyclovir and antibiotics and made a near complete recovery. At follow up 3 weeks later, he complained with severe fatigue and occasional buckling at the right knee. The serum and CSF samples were positive for both JEV and WNV IgM antibodies by IgM capture ELISA (JEV IgM ELISA, NIV Pune and WNV IgM ELISA, InBiosinc. USA). However, the serum samples (three samples collected within 2 weeks of onset of CNS symptoms) on micro-neutralization assay showed significantly high titer of neutralizing antibodies to WNV (titer: 320) and undetectable neutralizing antibodies to JEV (titer <10) confirming the WNV etiology. Demographics are shown in [].

[[45.0, 'year']]

M

{'6099760': 1, '34956995': 2, '30124385': 1, '32724683': 2, '22461779': 1, '15709126': 1, '25935909': 1, '15714427': 1, '23760372': 1, '23682140': 1, '16983682': 1, '14700342': 1, '12773646': 1, '30575890': 1, '12847156': 1, '10563521': 1, '12754368': 1, '31392241': 1, '12869104': 1, '18729783': 1, '29695953': 1, '11749765': 1, '24753667': 2}

{'3992778-1': 2, '3992778-2': 2, '8702647-1': 1, '8702647-2': 1, '7381993-1': 1, '7381993-2': 1, '7381993-3': 1}

3992780-1

noncomm/PMC003xxxxxx/PMC3992780.xml

Isolated primary craniosynostosis in an adult: Imaging findings of a case

A 31-year-old female was brought with a history of severe mental retardation since birth. She had a history of global developmental delay also. Both the parents were normal with no consanguinity. On physical examination, she had a peculiar face with hypertelorism and deformed calvarium. There was no mandibular hypoplasia or midfacial deformity. No microcephaly or abnormal nasal configuration was seen []. Her hands and feet were normal with no syndactyly. X-ray of the skull [Figure and ] showed prominent convolutional markings on the calvarium with complete closure of all calvarial sutures. No harlequin eyes were seen. Plain computed tomography (CT) confirmed the X-ray findings. All the sutures were closed and showed bone bridging and heaping. Inner table of skull showed extensive convolutional markings [Figure and ]. The brain parenchyma was normal with no atrophy. Corpus callosum, both leaves of the septum pellucidum, and posterior fossa structures were well seen. However, the subarachnoid space and cisterns showed effacement. The ventricular system was normal []. The paranasal sinuses were hypoplastic. All these imaging findings along with the supporting history were consistent with primary isolated craniosynostosis.\nThe uniqueness of our case lies in the presentation of imaging findings of the patient with primary craniosynostosis who survived into adulthood without undergoing any corrective surgical procedure, whereas the literature describes such findings in infants and children only.

[[31.0, 'year']]

F

{'15026597': 1, '8730180': 1, '21852568': 1, '8623653': 1, '5769296': 1, '24753669': 2}

{}

3992781-1

noncomm/PMC003xxxxxx/PMC3992781.xml

Rare ocular manifestation in a case of West Nile virus meningoencephalitis

A 40-year-old male presented with confusion, short-term memory loss, and unsteady gait for one month. He also complained of intermittent right facial numbness, diplopia, bilateral lower extremity numbness and weakness, and severe choking spells while coughing. The patient mentioned that when he had visited Ohio four weeks ago, a dead bird was found with West Nile virus infection. On examination, he was drowsy, but oriented to time, place, and person with mild maculopapular rash on his upper back, chest, and face. Cranial nerve examination revealed a subtle downbeating nystagmus. His motor strength, sensory exam, and deep tendon reflexes were normal. The cerebrospinal fluid (CSF) showed lymphocytic pleocytosis, while the remaining results were normal. The patient was started on empirical antibiotics, while the culture results were awaited. Magnetic resonance imaging (MRI) of the brain and complete spine were unremarkable. The patient had pronounced bilateral subconjunctival hemorrhage with progressive drowsiness the next day. West Nile IgM in the CSF was noted to be positive, while his mental status deteriorated and he required intubation within the next 24 hours. Electroencephalography (EEG) showed mild bicentral slowing, with no evidence of epileptiform discharges. An ophthalmology examination showed acute hemorrhagic conjunctivitis, conjunctival chemosis, and periorbital edema, with no chorioretinitis on fundoscopy (). Supportive management was continued with gradual improvement of his mental status.

[[40.0, 'year']]

M

{'12270973': 1, '16102302': 1, '16038762': 1, '16860390': 1, '12847156': 1, '15522373': 1, '16704798': 1, '15140603': 1, '15621074': 1, '11407341': 1, '24753670': 2}

{}

3992805-1

noncomm/PMC003xxxxxx/PMC3992805.xml

First reported cases of diffuse cutaneous leishmaniasis in human immunodeficiency virus positive patients in Jaipur District of Rajasthan, India

This was a case report of a 50-year-old male agriculturist, diagnosed as HIV positive 1½ years back on antiretroviral therapy (ART), who presented with a 6 month history of asymptomatic skin lesions over his limbs. Physical examination revealed multiple, diffuse, non-ulcerating, papulonodular and non-itchy skin lesions of size 2-18 mm []. History revealed that the lesions first appeared on the feet and then over the hands. There was no history of travel to endemic areas of leishmaniasis. There was no hepatosplenomegaly and lymphadenopathy. The laboratory investigations revealed anemia hemoglobin (Hb - 8.3 g/dL). The liver function tests, renal function tests, lipid profile and blood sugar were within the normal limits. The platelet count was 2 lacs/μL and the total leucocyte count was 5,100/μL.\nChest X-ray and ultrasound of abdomen were normal. His CD4 count was 126 cells/μL and HIV viral load was <47 copies/mL. The patient was initially suspected to be having histoplasmosis, which was ruled out by skin biopsy.\nPunch biopsy of skin lesions showed sheets of histiocytic cells in the sub epithelial tissue, stuffed with numerous amastigotes of Leishmania. Mild lymphocytic and plasma cell infiltrate was also noted [].\nThe patient was treated with ketoconazole 200 mg twice a day and 450 mg rifampicin daily for 1 month along with ART (nevirapine, stavudine and lamivudine). The patient improved on treatment but later was lost to follow-up.

[[50.0, 'year']]

M

{'30505791': 2, '15964970': 1, '22693548': 1, '31579666': 1, '20606960': 1, '17901650': 1, '32394886': 1, '21734126': 1, '7779927': 1, '23504228': 1, '24754029': 2}

{'3992805-2': 2, '6232997-1': 1}

3992805-2

noncomm/PMC003xxxxxx/PMC3992805.xml

First reported cases of diffuse cutaneous leishmaniasis in human immunodeficiency virus positive patients in Jaipur District of Rajasthan, India

This was a second case of a 43-year-old male laborer, diagnosed as HIV positive 2 years back who was on ART and anti-tubercular treatment for the past 9 months. He presented with a 7 month history of asymptomatic skin lesions all over his body. Physical examination revealed multiple bilateral asymmetrical diffuse, papulonodular, non-itchy skin lesions of size 2-25 mm on the face, trunk and extremities. Lesions first appeared on the arm and progressively spread to involve the face, legs and trunk []. There were no signs of ulceration and scarring. There was no lymphadenopathy and hepatosplenomegaly. There was no history of travel to endemic areas of leishmaniasis. The patient was initially suspected to be suffering from histoplasmosis, but skin biopsy taken from the nodules ruled it out. Laboratory investigations revealed anemia (Hb-9.1 g/dL). Liver function tests, renal function tests and lipid profile were normal. Ultrasonography of the abdomen was normal. His CD4 count was 50 cells/μL and HIV viral load was 1750 copies/mL. Punch biopsy of skin lesions revealed sheets of histiocytic cells in the sub epithelial tissue, stuffed with numerous amastigotes of Leishmania. Mild lymphocytic and plasma cell infiltrate was also noted [].\nThe patient was treated with ketoconazole 200 mg twice daily and 450 mg rifampicin daily for 1 month along with ART (nevirapine, stavudine and lamivudine). The patient initially responded to treatment but later on expired due to chest infection.

[[43.0, 'year']]

M

{'30505791': 2, '15964970': 1, '22693548': 1, '31579666': 1, '20606960': 1, '17901650': 1, '32394886': 1, '21734126': 1, '7779927': 1, '23504228': 1, '24754029': 2}

{'3992805-1': 2, '6232997-1': 1}

3992807-1

noncomm/PMC003xxxxxx/PMC3992807.xml

Unusual presentation of acute pancreatitis in falciparum malaria

The present case report is about a 40-year-old male patient who presented with high-grade fever associated with chills, jaundice vomiting and abdominal pain for 4 days. There was no history of cough, burning micturition, diarrhea or altered sensorium. On physical examination, he was alert, but febrile (103° Fahrenheit) with mild jaundice. He gradually became drowsy 3 days after admission. Systemic examinations were within the normal limit except epigastric tenderness and abdominal distension with normal bowel sounds. Laboratory investigations revealed hemoglobin - 10.2 g/dl, total leucocyte count - 15,100 (with Neutrophil - 87%) and platelets - 2.75 lacs/cu.mm. Peripheral blood smear revealed ring forms of P. falciparum. Immunochromatographic test for P. falciparum histidine-rich protein 2-based assay was strongly positive. Liver function testing showed serum Total Bilirubin - 4.4 mg/dl (Direct Bilirubin - 2 mg/dl) and serum aminotransferases and alkaline phosphatase were within normal limits. Serum amylase was 525 IU/L and serum lipase was 250 IU/L. Renal function and electrolytes were normal (Serum urea - 32 mg/dl, serum creatinine - 1.2 mg/dl, serum sodium - 140 meq/L and serum potassium - 4.1 meq/L). Urine and blood cultures came out to be sterile. Serum calcium was 9.2 mg/dl and fasting lipid profile was within the normal limits (cholesterol - 170 mg/dl, triglycerides - 103 mg/dl, high density lipoprotein - 36 mg/dl, low density lipoprotein - 114 mg/dl and very low density lipoprotein-20 mg/dl). Chest X-ray was normal and abdominal X-ray showed “Ileus” without air-fluid levels. Ultra sonography abdomen demonstrated an edematous, enlarged pancreas with minimal fluid in the peritoneal cavity. Computed tomography (CT) scan of the abdomen revealed edematous, enlarged pancreas with multiple fluid collections around pancreas and in the peritoneal cavity []. A diagnosis of severe falciparum malaria with acute pancreatitis (Grade E, CT severity index-4) was made and treatment was initiated with intravenous artesunate. There was marked improvement in his clinical symptoms in next 48 h. Acute pancreatitis was managed with analgesics, hydration and supportive therapy. Ryle's tube was initially instituted for bowel rest. After 3 days, his spikes of fever came down. From day 5, he started tolerating oral feeds. His pain abdomen and jaundice subsided after 8 days. He was discharged after a hospital stay of 12 days. On his follow-up visit, 2 months later, he was symptom free and doing well.

[[40.0, 'year']]

M

{'28571194': 1, '26816452': 2, '28217609': 1, '17438439': 1, '17374979': 1, '11280593': 1, '17437476': 1, '4412798': 1, '9799920': 1, '24754031': 2}

{'4711211-1': 1}

3994261-1

noncomm/PMC003xxxxxx/PMC3994261.xml

Endoscopic Treatment of Various Gastrointestinal Tract Defects with an Over-the-Scope Clip: Case Series from a Tertiary Referral Hospital

A 47-year-old male patient who had undergone minigastric bypass for diabetes mellitus experienced anastomotic site leakage. Despite a successful surgical repair, he developed additional leakage at multiple sites, including a jejunocutaneous fistula. Furthermore, he developed a delayed allergic response to vicryl. We decided to use the OTSC system for fistula closure. Gastroduodenoscopy with the OTSC system was performed with fluoroscopic guidance with the patient under conscious sedation. A total of three fistulas were identified and successfully closed during three separate sessions, each with a single OTSC. The patient was discharged with no further complications.\nA 32-year-old woman underwent sleeve gastrectomy for morbid obesity. Two weeks after the gastrectomy, computed tomographic (CT) scans revealed a large intraperitoneal abscess due to anastomotic leakage at the esophagogastric junction. After percutaneous drainage of the abscess, we decided to use the OTSC system for primary closure. The fistula opening was approximately 10 mm wide. One OTSC was placed, successfully sealing the deficit, as confirmed by the introduction of gastrografin under fluoroscopy.\nA 56-year-old man presented with fever and abdominal\npain. He had been treated 2 months previously for necrotizing pancreatitis and a pancreatic pseudocyst, which was drained percutaneously. On admission, a colonopseudocystic fistula was detected by using contrast fluoroscopy. After identification of the fistula opening by using both indigo carmine dye and contrast, the OTSC system was used for primary closure of the fistula tract. A single t-type OTSC, with only suction applied, was used to completely seal the fistula. The fistula was completely healed after 5 days ().\nA 50-year-old man underwent endoscopic full-thickness gastric resection (EFTGR) for early gastric cancer. He had a history of chronic hepatitis B and had undergone transarterial chemoembolization for hepatoma. His tumor stage was T1bN0M0 according to endoscopic ultrasonography and abdominal CT findings. Although radical gastrectomy with nodal dissection is the standard treatment, we performed EFTGR with OTSC closure considering his comorbidities and surgical risk. After the EFTGR, the size of the gastric opening was approximately 30 mm. With laparoscopic guidance, we used an OTSC twin grasper to approximate the opposing margins of the opening and three t-type OTSCs for closure. Successful closure was confirmed by performing a leak test with indigo carmine dye and room air. Three days later, we performed an upper GI series with gastrografin. The seal at the opening was confirmed with the introduction of gastrografin under fluoroscopy. The patient was discharged 13 days later with no complications ().\nA 57-year-old man underwent endoscopic en bloc resection for a gastric subepithelial tumor (SET) involving the muscle layer. The preresection diagnosis was a leiomyoma or a GI stromal tumor. The 1.2-cm tumor was removed by performing conventional endoscopic mucosal resection with a standard endoscopic snare. However, after resection, the muscularis proper was exposed at the base of the tumor. Because of the possible risk of delayed perforation, we decided to use the OTSC to prevent perforation. We used the OTSC twin grasper to grasp both ends of the resection margin, then successfully closed the wound with a t-type OTSC. Two days later, we performed gastroduodenoscopy. The lesion was completely sealed by using the OTSC, and the patient was discharged the following day ().

[[47.0, 'year']]

M

{'22978826': 1, '21108175': 1, '18930700': 1, '17453289': 1, '19899033': 1, '27571898': 1, '19899030': 1, '18984107': 1, '9402126': 1, '26191340': 1, '19685422': 1, '19018468': 1, '17591492': 1, '20172156': 1, '26416380': 1, '24765601': 2}

{}

3994262-1

noncomm/PMC003xxxxxx/PMC3994262.xml

Endoscopic Removal of a Migrated Coil after Embolization of a Splenic Pseudoaneurysm: A Case Report

A 63-year-old man was found to have advanced gastric cancer on a routine cancer screening examination. Preoperative abdominal computed tomography (CT) was performed, and there was no specific finding besides advanced gastric cancer. He underwent total gastrectomy. The tumor was located at the posterior wall of the high body. The gross type of the tumor was Bormann type II. The size of the tumor was 4.5×3.8×0.8 cm, and the depth of invasion was at the subserosal level (pT2b). Sixty-six lymph nodes were dissected, and no metastases were observed (pN0). Lymphatic, venous, and perineural invasions were present.\nOne month after the surgery, he came to the emergency department with complaints of a febrile sense and abdominal pain. An abdominal CT scan was carried out, and a pseudoaneurysm of the splenic artery and a small amount of hemoperitoneum were detected (). The total gastrectomy performed 1 month ago was thought to be the cause of the pseudoaneurysm. The size of the pseudoaneurysm was 2.7×1.9×3.6 cm. On the day after admission, a celiac angiography was performed. A large pseudoaneurysm of the splenic artery was observed on angiography (). Extravasation of the contrast agent was not observed, and there was no evidence of ongoing bleeding or rupture of the pseudoaneurysm. However, the risk of rupture seemed high, and we decided to perform embolization. The splenic artery was selected by using a microcatheter, and coils (Tornado embolization microcoil; Cook, Bloomington, IN, USA) were inserted to obliterate the pseudoaneurysm. The large size of the pseudoaneurysm and the fast blood flow required the use of 22 coils. After the coils were placed, splenic angiography was done and successful embolization of the pseudoaneurysm was confirmed (). He was discharged without any complication. As a routine surveillance, an abdominal CT scan was taken 5 months after the embolization, and it showed no evidence of cancer recurrence or any complication associated with embolization.\nNine months after the embolization of the pseudoaneurysm, the patient presented to the emergency department with epigastric pain. On upper gastrointestinal endoscopy, several strands of wire were noted at the inferolateral side of the esophagojejunal anastomosis (). A simple abdominal radiograph showed that the wires protruding through the jejunal wall were part of a coil used for pseudoaneurysm embolization (). We tried to cut the wires by using endoscissors (FS-5L-1; Olympus, Tokyo, Japan); however, it was difficult because the wires were thick and stiff. Thus, we tried to use hot biopsy forceps (Radial Jaw 3; Boston Scientific, Natick, MA, USA) for cutting the wires, which proved to be easy and effective. The hot biopsy forceps were used with an electrosurgical generator (VIO-300D; ERBE Elektromedizin, Tübingen, Germany) in the Endocut Q mode (effect 2, cut duration 2, and cut interval 2) (). It took about 1 to 2 seconds to cut each wire, and five wires were cut in total. Residual thin strands of wires were removed with endoscissors. There was no immediate complication during and after the procedure.\nThe patient was discharged from the hospital without epigastric pain and remained asymptomatic. He was followed up with upper gastrointestinal endoscopy 3 months after the endoscopic coil removal, and annually thereafter. Abdominal CT scans were performed every 6 months. There had been no symptom or complication related to the coil during the 2-year follow-up period.

[[63.0, 'year']]

M

{'29988858': 1, '18158056': 1, '23078441': 1, '17614039': 1, '7954570': 1, '34040915': 2, '21944789': 1, '22068647': 1, '25925841': 2, '14603202': 1, '11381514': 1, '32328377': 2, '29479413': 2, '17296711': 1, '17882482': 1, '33430578': 2, '8858739': 1, '18504106': 1, '12354829': 1, '16552377': 1, '22875411': 1, '9354712': 1, '17418076': 1, '16026434': 1, '33134404': 1, '32547670': 1, '29725660': 1, '24765602': 2}

{'7174856-1': 1, '5810436-1': 1, '8652176-1': 1, '4423092-1': 1, '8139854-1': 1}

3994263-1

noncomm/PMC003xxxxxx/PMC3994263.xml

An Unusual Case of Duodenal Perforation Caused by a Lollipop Stick: A Case Report

A 23-year-old woman presented to the emergency department of our hospital with epigastric and right upper quadrant pain that started 2 days ago. She had no significant medical history and not taking any medicine. Physical examination revealed epigastric and right upper quadrant tenderness, with rebound tenderness in the right upper quadrant. Her vital signs were as follows: blood pressure, 130/90 mm Hg; heart rate, 78 beats per minute; body temperature, 36.6℃; and respiratory rate, 18 breaths per minute. Plain radiographs of the abdomen did not reveal any abnormal findings. Laboratory tests revealed a white blood cell count of 12,800/mm3 (neutrophil, 81.7%); hemoglobin level of 11.4 g/dL; platelet count of 175,000/mm3; and C-reactive protein level of 10.7 mg/dL (reference limit, 0.1 to 1 mg/dL). Liver function tests, renal function tests, and electrolytes were all within the reference limits. An abdominal CT scan revealed a 7-cm-long, stick-like foreign body situated vertically from the duodenal bulb to the third portion of the duodenum. Mottled air density and blurred periduodenal fat planes with streaky soft tissue stranding were also observed around the third portion of the duodenum; however, no pneumoperitoneum was observed (). The patient was unaware of ingesting the foreign body. Emergency esophagogastroduodenoscopy was performed to identify the foreign body. A surgical team was contacted to ascertain whether emergency surgery could be carried out immediately if bowel perforation is detected during esophagogastroduodenoscopy or if the abdominal pain becomes worse. A lollipop stick was found in the duodenum, with a shallow ulcer in the proximal third portion of the duodenum, and it was endoscopically removed with rat-tooth forceps. Two small ulcers, one proximal with exudates and the other distal with air bubbles, were also seen in the third portion of the duodenum. Successful closure was performed by placing 3 hemoclips (HX-610-135; Olympus, Tokyo, Japan) to the proximal ulcer. Five hemoclips were placed circumferentially around the perimeter of the perforation edge of the distal ulcer. A detachable snare (SD 6L-1; Olympus) was placed around the perimeter base of the clips. The snare was then tightened, successfully bringing all the edges of the wound together (). The patient recalled having slept drunk with a lollipop in her mouth 2 weeks previously. The next day, abdominal CT was repeated to observe the hemoclips in the duodenum and the periduodenal inflammation; however, no pneumoperitoneum was yet observed. An intravenous proton-pump inhibitor and antibiotic treatments, including metronidazole and a third-generation cephalosporin, were used, and she was placed on a nothing-per-oral status with nasogastric tube drainage for 5 days. From the sixth day of hospitalization, feeding was gradually advanced from water to a liquid diet, and then to a soft diet. She refused to undergo follow-up endoscopy and was discharged on the ninth day of hospitalization. She remained asymptomatic at the subsequent follow-up 2 weeks after discharge.

[[23.0, 'year']]

F

{'21350325': 1, '16479337': 1, '34908865': 1, '17556153': 1, '8798356': 1, '10549750': 1, '21628009': 1, '23293675': 1, '27006854': 1, '15378256': 1, '28203127': 2, '7698623': 1, '21804366': 1, '20538351': 1, '1948617': 1, '23596543': 1, '1489367': 1, '25323288': 1, '30755893': 1, '20622631': 1, '8495838': 1, '10462667': 1, '26263453': 1, '27266827': 1, '29851786': 1, '31760218': 1, '20132426': 1, '24765603': 2}

{'5260512-1': 1}

3994264-1

noncomm/PMC003xxxxxx/PMC3994264.xml

A Case of Mucosa-Associated Lymphoid Tissue Lymphoma of the Sigmoid Colon Presenting as a Semipedunculated Polyp

A 54-year-old man visited Daegu Catholic University Hospital after a screening colonoscopy that revealed a sigmoid colon polyp that was diagnosed pathologically as a tubular adenoma. He denied other symptoms such as abdominal pain, weight loss, fever, general weakness, loss of appetite, or hematochezia. His blood pressure was 106/64 mm Hg, pulse rate 73 beats per minute, respiratory rate 20 breaths per minute, and body temperature 36.7℃. His consciousness was clear, and no lymphadenopathy was evident in the head and neck, axillary, or inguinal region. Abdominal examination revealed no tenderness or rebound tenderness. Bowel sounds were normal, and the liver and spleen were not palpable. The laboratory findings were as follows: white blood cells, 11,400/mm3 (neutrophils 81.8%, eosinophils 0.4%, lymphocytes 12.4%); hemoglobin, 13.4 g/dL; and platelet count, 202,000/mm3. The blood chemistry test showed the following results: aspartate aminotransferase, 16 IU/L; alanine aminotransferase, 21 IU/L; total bilirubin, 0.6 mg/dL; alkaline phosphatase, 129 IU/L; total protein, 6.5 g/dL; albumin, 4.4 g/dL; blood urea nitrogen, 12.2 mg/dL; creatinine, 0.9, mg/dL; Na, 139 mEq/L; K, 3.4 mEq/L; and Cl, 98 mEq/L. The serum carcinoembryonic antigen level was 2.69 ng/mL, which was within the reference range.\nColonoscopy revealed a semipedunculated polyp, approximately 2 cm in size, in the sigmoid colon. The surface of the polyp showed redness and nodularity (). In private clinics, the tumor was diagnosed as a tubular adenoma; however, a diagnosis of submucosal tumor was not completely ruled out. We performed EMR by en bloc resection of the polyp with a flex knife and a snare after injecting a glycerin solution into the submucosa ().\nResected specimens histologically showed lymphoepithelial lesions with diffuse proliferation of atypical lymphocytes, which immunohistochemically stained positively for CD20, CD5, and Bcl-6, but negatively for CD3, Bcl-2, and cyclin D1. In addition, the Ki-67 labeling index was 10% to 20%. These findings were compatible with low-grade B-cell MALT lymphoma ().\nThere was no evidence of lymph node metastasis or involvement of any other organ, except for a gallstone, in the thoracic and abdominal computed tomography performed for staging. According to the Ann Arbor staging system, the tumor was stage IE.\nThe resected lesion was replaced with normal mucosa on sigmoidoscopy 2 months after the EMR (). He has been free of disease during 10 months of follow-up.

[[54.0, 'year']]

M

{'8946607': 1, '12456507': 1, '6193858': 1, '28289662': 2, '16507274': 1, '20062639': 2, '6645123': 1, '28469125': 1, '15832010': 2, '17233195': 1, '16549831': 1, '25561821': 1, '20389173': 1, '31832456': 1, '29970607': 1, '19696541': 1, '31572011': 1, '8045524': 1, '28831450': 2, '27807552': 1, '15933708': 1, '33392331': 2, '33153250': 2, '10601069': 1, '28415161': 1, '24765604': 2}

{'2808615-1': 1, '5560452-1': 1, '2803979-1': 1, '5346780-1': 1, '8505188-1': 1, '7760443-1': 1}

3994265-1

noncomm/PMC003xxxxxx/PMC3994265.xml

A Case of Malignant Granular Cell Tumor in the Sigmoid Colon

A 43-year-old female patient visited SAM Medical Center for further evaluation of a submucosal tumor that was seen on prior colonoscopy in another clinic. She was asymptomatic, and a physical examination showed unremarkable findings. The laboratory results showed a white blood cell count of 4,100/mm2, hemoglobin of 7.7 g/dL, platelet count of 340,000/mm2, albumin of 4.4 g/dL, aspartate aminotransferase of 13 IU/L, and alanine aminotransferase of 7I IU/L. Colonoscopy showed a yellowish, round submucosal tumor with intact mucosa, approximately 1 cm in diameter in the sigmoid colon (). Endoscopic ultrasonography (EUS) revealed an approximately 1×1 cm hypoechoic heterogeneous mass with a smooth margin originating from the third echo layer (). Because the diagnosis was benign GCT or carcinoid tumor, and the tumor was relatively small, we decided to follow the patient after 1 year, after she was given sufficient explanation about the malignant potential of the lesion. At the follow-up colonoscopy 1 year later, the size of the tumor increased to approximately 3 cm. We performed segmental colon resection with lymph node dissection, and the pathologic gross finding showed the tumor to be well circumscribed and located at the submucosal and muscular layers with central infiltration of the serosa. Histologic examination revealed proliferation of large polygonal cells with abundant eosinophilic granular cytoplasm, which was positive for S-100 and invasion of local lymph nodes and vessels (). Two of the histologically malignant criteria of GCT-presence of vesicular nuclei with large nucleoli and pleomorphism-were met, and the tumor was diagnosed as a histologically benign or atypical but clinically malignant GCT occurring in the sigmoid colon.

[[43.0, 'year']]

F

{'30008819': 1, '20514678': 1, '26637199': 1, '20096083': 1, '17300677': 1, '29391355': 1, '24900100': 1, '20076822': 1, '28018455': 2, '22807961': 1, '21924561': 1, '29980826': 1, '15285042': 1, '17891685': 1, '19399282': 2, '12743780': 1, '16733867': 1, '24765605': 2}

{'2672140-1': 1, '5177722-1': 1}

3994266-1

noncomm/PMC003xxxxxx/PMC3994266.xml

A Case of Choledocholithiasis and Intestinal Malrotation in an Adolescent with Repaired Gastroschisis

A 17-year-old girl visited Chungbuk National University Hospital, presenting with fever and abdominal pain that had developed 7 days previously. She had undergone an operation for gastroschisis repair at birth. At the time of admission, her vital signs were as follows: blood pressure, 120/80 mm Hg; pulse rate, 70 beats per minute; respiration rate, 18 breaths per minute; and body temperature, 37.5℃. She appeared emaciated and acutely ill. Her body mass index was 18.1 (height, 151 cm; and weight, 41.3 kg). A physical examination revealed icteric sclera, a very thin abdominal cavity, and a longitudinal surgical scar at the midline. Tenderness was noted in the upper abdominal area, and normal bowel sounds were heard. There was no particular finding in the limb or neurological examinations. Laboratory analysis revealed a white blood cell count of 27,000 cells/mm3; hemoglobin level, 12.3 g/dL; platelet count, 277,000 cells/mm3; aspartate aminotransferase level, 108 IU/L; alanine aminotransferase level, 144 IU/L; alkaline phosphatase level, 476 IU/L; total protein level, 6.5 g/dL; albumin level, 3.7 g/dL; total bilirubin level, 14.1 mg/dL; direct bilirubin level, 9.2 mg/dL; amylase level, 592 U/L; lipase level, 825 U/L; blood urea nitrogen level, 5.0 mg/dL; and creatinine level, 0.5 mg/dL. These data were compatible with diagnoses of acute cholangitis and acute biliary pancreatitis. An abdominal computed tomography scan revealed a round calcifying lesion near the pancreas (), and the absence of the retroperitoneal duodenum and the anterior position of the spleen with respect to the left kidney. The anterior and left-sided position of the superior mesenteric vein compared with that of the superior mesenteric artery was observed in the abdominal computed tomography scan (). The coronal view revealed the distorted architecture of the liver and a high-attenuation lesion at the extrahepatic bile duct (). Results of a barium examination revealed a right-sided duodenojejunal flexure and malpositioning of the bowel, with the small bowel on the right side and the colon on the left side (). Intestinal malrotation could be diagnosed based on these findings. ERCP was performed by using a lateral-view endoscope in the usual way. After approaching the ampulla, the endoscope was pushed against the duodenal wall to maintain the papilla in the correct position, and a selective bile duct cannulation confirmed the presence of a 12-mm round stone in the common bile duct. With a guidewire-assisted technique, the single dark brown stone was removed by using a Dormia basket after the endoscopic sphincterotomy (). The procedure lasted for 15 minutes. A cholangiogram obtained through an endoscopic nasobiliary drainage tube revealed a distorted biliary system, which was characterized with diffuse dilatation of the intrahepatic and extrahepatic biliary trees, downward-positioned gallbladder and a right intrahepatic biliary tree, and a horizontally located common bile duct. The abnormal orientation of the duodenum suggested intestinal malrotation (). Clinical symptoms and liver function tests normalized after the ERCP procedure. The patient has been monitored for 3 years and is in a normal state.

[[17.0, 'year']]

F

{'15790327': 1, '10663862': 1, '16418964': 1, '18655099': 1, '2654854': 1, '19308378': 1, '19308379': 1, '2530328': 1, '19302840': 1, '7748034': 1, '18475100': 1, '9301359': 1, '24765606': 2}

{}

3994513-1

noncomm/PMC003xxxxxx/PMC3994513.xml

Amplification of Aminoglycoside Resistance Gene aphA1 in Acinetobacter baumannii Results in Tobramycin Therapy Failure

All isolates () were cultured from a 20-year-old male polytrauma victim sustained in combat operations in Afghanistan (day 1). Cultures obtained from day 3 grew A. baumannii (isolates MRSN 3361 and MRSN 3363) susceptible to tobramycin (MIC = 0.5 µg/ml). Tobramycin-susceptible MRSN 3364 was cultured on day 8 from a tissue sample collected from the left hip injury. Upon stabilization of the patient, he was transferred to the United States for definitive care, arriving on day 9, where antibiotics were changed to intravenous tobramycin, meropenem, and vancomycin based on culture results. A. baumannii MRSN 56 was cultured from the left hip wound on day 11 and was susceptible to tobramycin (MIC = 0.5 µg/ml). Throughout this escalation of care, tobramycin was continuously administered. On day 12, MRSN 57 was cultured from a tissue sample collected from the right hip but had an MIC of tobramycin of 8 µg/ml. The following day, MRSN 58 was cultured from a tissue sample collected from the left hip. MRSN 58 had a tobramycin MIC of = 16 µg/ml, which denotes resistance by CLSI guidelines (). Consequently, tobramycin therapy was discontinued, and the patient was prescribed colistin while continuing meropenem.

[[20.0, 'year']]

M

{'20833818': 1, '19246619': 1, '27441293': 1, '33757578': 1, '34460288': 1, '18931120': 1, '27974412': 1, '25293759': 1, '32884309': 1, '27594850': 1, '21537009': 1, '6356187': 1, '23812239': 1, '22543367': 1, '20833577': 1, '33024041': 1, '20375036': 1, '15585503': 1, '19364869': 1, '32752093': 1, '18024520': 1, '10835024': 1, '29914950': 1, '31307955': 1, '26195261': 1, '16894515': 1, '17438042': 1, '25313016': 1, '20542900': 1, '18007677': 1, '18444865': 1, '28223389': 1, '18588489': 1, '19609259': 1, '23587960': 1, '8601470': 1, '26645270': 1, '8381641': 1, '28855980': 2, '19686082': 1, '23139793': 1, '25870058': 1, '29259044': 1, '32681604': 1, '26558753': 1, '16415984': 1, '12709325': 1, '344891': 1, '19332680': 1, '7263566': 1, '18568430': 1, '20383326': 1, '25779578': 1, '25052812': 1, '15328088': 1, '6304464': 1, '27671066': 1, '30111627': 1, '29691340': 1, '32718956': 1, '4598297': 1, '20966089': 1, '24757213': 2}

{'5574246-1': 1}

3994599-1

noncomm/PMC003xxxxxx/PMC3994599.xml

Use of meso-Rex shunt with transposition of the coronary vein for the management of extrahepatic portal vein obstruction

A meso-Rex shunt with transposition of the coronary vein was performed in a 20-year-old man. The patient had a previous clinical history of increased abdominal volume and five episodes of gastrointestinal bleeding, and was diagnosed with idiopathic portal vein obstruction at 5 years of age. Hypercoagulability studies were performed at the time of thediagnosis. Antithrombin III level was 58% of normal, but other parameters were all unremarkable. One month before the shunt operation, an endoscopy identified aggravated esophageal and paraesophageal varices and hypertensive gastropathy. The size and patency of the umbilical portion of the intrahepatic left portal vein were assessed by preoperative Doppler ultrasonography and computed tomography; there was massive splenomegaly and no detectable intrahepatic left portal vein (). A preoperative percutaneous transhepatic liver needle biopsy showed a noncirrhotic liver without fibrosis, and hepatic venous pressure gradient was 28 mmHg (pressure in the inferior vena cava 7 mmHg, wedged hepatic venous pressure 35 mmHg).\nAfter laparotomy, the round ligament was dissected toward the distal part of the left portal vein at the level of the Rex recessus. The left portal vein was then approached, and its ventral and lateral aspects were dissected over a length of 3-4 cm. The intrahepatic left portal vein was evaluated by surgical exploration, and its diameter was approximately 3 mm. Splenectomy was performed because of massive splenomegaly. There was a nest of peripancreatic collaterals with flow toward the gastroesophageal junction through a series of large varices, which included the coronary vein with an adequate diameter and flow in the hepatopetal direction. This vein was fully mobilized, divided, and then transposed across the mesocolon and behind the pylorus to the intrahepatic left portal vein to which it was anastomosed end-to-side using nonabsorbable monofilament interrupted sutures (). Unclamping of the meso-Rex shunt immediately allowed adequate portal flow into the liver, as confirmed by intraoperative portography, and there were no remaining large portosystemic shunts (). Postoperative recovery was rapid and uneventful, with liver function tests within normal ranges and normal portal flow observed by Doppler ultrasonography and computed tomography (). Follow-up was uneventful, with improvement of the signs of portal hypertension, without any new episodes of gastrointestinal bleeding. Six months after surgery, computed tomography showed preserved portal vein flow via the shunt.

[[20.0, 'year']]

M

{'10494645': 1, '22008343': 1, '26475346': 1, '17618880': 1, '22943796': 1, '22498382': 1, '16552203': 1, '1733076': 1, '10646766': 1, '22409296': 1, '24761417': 2}

{}

3994601-1

noncomm/PMC003xxxxxx/PMC3994601.xml

Systemic metastasis of hepatocellular carcinoma responsive to multidisciplinary treatment including debulking surgery

A 52-year-old male patient with a history of type B viral hepatitis visited the hospital with abdominal distension; at that time, a huge mass (a mass measuring approximately 7 cm on segment 8, and a mass measuring 2.5 cm on segment 6) in the right hemiliver and hematomas around the liver were observed on abdominal computed tomography (CT) scan; the diagnosis was HCC rupture (). After transarterial chemoembolization (TACE), segment 8 segmentectomy and segment 6 wedge resection were performed (); hyperthermic intraperitoneal adriamycin irrigation was then performed for prevention of peritoneal seeding. According to the biopsy report, there was no viable tumor because of TACE. The patient was discharged with no specific complication and no evidence of recurrence was observed for seven years postoperative (During the seven years, ultrasonography or CT and tumor marker check was performed every 3 months, but there was no abnormal finding). However, 84 months after the initial operation, an abnormal splenic mass was observed on follow-up ultrasonography, and his tumor marker was elevated (α-fetoprotein, 1.94; protein induced by vitamin K absence or antagonist II, 309). Therefore, we performed positron emission tomography-CT, and multiple metastases were observed. The sites of metastases were brain, adrenal gland, spleen, kidney, skin (buttock), back muscle, and buttock muscle (, ); however, there was no intrahepatic recurrence. Skin biopsy confirmed metastasis of HCC (). The patient then received radiation therapy for brain metastasis, and took oral medication with sorafenib (Nexavar, Bayer Health Care, Leverkusen, Germany). After one month, a new lesion was observed on his right thumb (). However, follow-up abdominal CT showed stable condition of the previously mentioned multiple metastases (mass of spleen, left adrenal gland, left kidney, back muscle, and buttock muscle), and the brain mass had shrunk. We performed en bloc resection of intra-abdominal metastatic masses (splenectomy, left adrenalectomy, left nephrectomy) and excision of the right thumb mass (; Edmonson-Steiner grade of these masses are grade 2, and histologic type is trabecular, and cell type is hepatic cell). Currently, 18 months after initial diagnosis of multiple metastases, he is still alive, and he takes an oral medication with sorafenib for target therapy of remnant tumor in back muscle, buttock, and brain, which are unresectable ().

[[52.0, 'year']]

M

{'9058154': 1, '210712': 1, '18710423': 1, '4336632': 1, '19542932': 1, '28189067': 1, '18817997': 1, '11474320': 1, '17230611': 1, '24761416': 2}

{}

3994608-1

noncomm/PMC003xxxxxx/PMC3994608.xml

Primary malignant rhabdoid tumor of greater omentum in 10-year-old girl

A 10-year-old girl visited the Emergency Department for abdominal pain. The pain had developed 7 days prior after getting hit with a ball. There were no associated symptoms such as nausea, vomiting, or diarrhea. On physical examination, the patient complained of tenderness in the lower abdomen. Laboratory findings showed that hemoglobin was 10.8 g/dL and C-reactive protein was 8.06 mg/dL. Other results were not remarkable. Ultrasonography showed a multiseptated large hematoma. A computed tomography scan was undertaken and showed a lobulating hemorrhagic tumor (9 cm × 6 cm × 6.5 cm) with hemoperitoneum in the lower abdomen and pelvis (). Initially, the mass was suspected as a hematoma resulting from bleeding of the lymphangioma or hemangioma in the mesentery. After 3 days of antibiotics treatment, her pain was relieved. For follow-up, we examined the mass by ultrasonography. It revealed a necrotic solid tumor enhancing with peripheral vessels and a small amount of hemoperitoneum. We assumed that the mass was a malignant tumor of the mesentery or retroperitoneum, and performed a laparoscopic exploration. There was a huge omental solid mass that was freely movable and free of adhesions to any other intra-abdominal organs. The mass was removed completely including remnant omentum via laparotomy. Several seeding nodules were found on the small bowel mesentery and Pouch of Douglas and were removed for pathologic confirmation.\nGrossly resected multinodular solid masses showed irregular and infiltrative borders and the cut surface was tan gray and fleshy. There was multifocal hemorrhages and necrosis (). Microscopically nested round to polygonal tumor cells revealed infiltrative borders () and each tumor cell showed eccentric nuclei, prominent nucleoli, as well as a characteristic eosinophilic inclusion or globules in the abundant cytoplasm (). These findings were consistent to that of "rhabdoid" cells. Immunohistochemically neoplastic cells expressed cytokeratin (), vimentin (), and epithelial membrane antigen. However, tumor cells showed negative reaction for desmin, smooth muscle actin and myosin. Importantly neoplastic cells revealed the absence of nuclear expression of INI 1 (), which was recently discovered as a one of the most important histologic markers of malignant rhabdoid tumors [].\nPostoperatively, she recovered uneventfully and resumed her oral diet on the 3rd postoperative day. An fluorine-18 fluorodeoxyglucose positron emission tomography/computed tomography was undertaken and revealed no evidence of primary malignancy including kidney and central nervous system. At postoperative day 7, the patient began chemotherapy consisting of VDC/IE (VCR, Doxorubicin, Cyclophosphamide/Ifosfamide, Etoposide) regimen. Despite 4 cycles of chemotherapy of VDC/IE regimen, the mass in the Pouch of Douglas, where previously there had been documented seedings, was now apparent and showed peritoneal carcinomatosis through magnetic resonance imaging. She had been treated with intensive chemotherapy yet died after 9 months due to disease progression.

[[10.0, 'year']]

F

{'12478486': 1, '9057515': 1, '18288421': 1, '2216596': 1, '27057865': 2, '16528370': 1, '8897515': 1, '15254056': 1, '9866769': 1, '24761408': 2}

{'4998781-1': 1}

3994611-1

noncomm/PMC003xxxxxx/PMC3994611.xml

Very early-onset peritoneal recurrence following curative total gastrectomy for Borrmann 4 gastric cancer

A 39-year-old man with progressive weight loss of 10 kg during the past 6 months was referred to Departement of Surgery in June 2012. No definite abnormal findings in the stomach or duodenum were observed on gastrofiberscopy (GFS) 1 year ago at Yeouido St. Mary's Hospital (). However, diffuse engorged gastric folds with ulcerations at the mid body and greater curvature side of the stomach, suggesting a Borrmann-4 AGC were found during the current GFS (). A biopsy confirmed signet ring cell carcinoma. An abdominal computed tomography (CT) scan also showed diffuse gastric wall thickening, compatible with the GFS findings without definite regional lymphadenopathy (cT4aN0M0) (). Positron emission tomography (PET) CT found no active lesions in the abdomen including the stomach and liver. However, a mild hypermetabolic focus at the medial aspect of the left iliac bone was noted, which was equivocal to confirm the bone metastasis (). Tumor markers were all within normal limits including carcinoembryonic antigen of 0.6 ng/mL (normal range, 0-5 ng/mL), alpha fetoprotein of 1.6 ng/mL (normal range, <8.1 ng/mL) and carbohydrate antigen 19-9 of 6.68 U/mL (normal range, 0-37 U/mL).\nAn open total gastrectomy and splenectomy with D2 lymph node dissection was carried out for the R0 resection. No definite metastatic focus was detected during the operation, including definite metastatic lymphadenopathy in the entire abdominal cavity. No peritoneal washing cytology was performed. The postoperative course was uneventful until postoperative day 4 when he resumed soft meals.\nA pathological examination revealed Borrmann-4, 13.0 cm × 11.0 cm sized serosa-exposed signet ring cell carcinoma with 50 metastatic lymph nodes out of 84 retrieved lymph nodes resulting in pT4aN3bM0, stage IIIc according to Union of International Cancer Control seventh edition. There was no microscopic cancer cell involvement on either resection margin, resulting in a R0 resection.\nFive days following the gastrectomy, localized abdominal pain on the left upper quadrant with nausea and vomiting developed. A 500-mL volume of turbid whitish fluid without bile contents were aspirated via a reinserted Levin tube. An abdominal CT scan and Gastrografin swallowing radiography showed a markedly dilated jejunal Roux-limb with an abrupt cutoff near the jejuno-jejunostomy site (). All attempts to improve the intestinal obstruction, including nasojejunal decompression and correction of the fluid and electrolyte imbalance were unsuccessful. A re-exploration was considered to relieve the intestinal obstruction.\nA reoperation to relief the Roux-limb obstruction via a laparoscopic approach was performed at postoperative day 8. Adhesions were observed around the jejunojeunostomy site and the mesocolon compressed the Roux-limb just proximal to the jejunojejunostomy. Laparoscopic adhesiolysis relieved the Roux-limb obstruction without any problem. However, we incidentally found some whitish peritoneal nodules on the left diaphragmatic surface that were not present at the initial operation (). One of peritoneal nodules was excised for histologic examination, revealing a metastatic adenocarcinoma with signet ring cell features (). The patient tolerated the reoperation well and was transferred to the Department of Internal Medicine for systemic combination chemotherapy of capecitabine and cisplatin (XP).\nDuring the follow-up examination performed in December 2012, 6 months after the operation and after the eight cycle of XP chemotherapy, a CT scan showed newly developed ill-defined soft tissue density in the common hepatic space and retropancreatic space, suggesting nonspecific postoperative changes or a tumor recurrence. Then, the chemotherapy regimen was changed to oxaliplatin-based FOLFOX. In addition, no interval change in the 1.7 cm sized sclerotic bony lesion in the left iliac bone was observed on a serial bone and CT scan.\nThe patient tolerated a regular diet and chemotherapy relatively well until January 2013. Then, abrupt vomiting developed. A CT scan and an upper gastrointestinal series showed markedly distended jejunal limb due to cancer recurrence. Bypass jejunojejunostomy was performed to relieve the jejunal obstruction at the jejunojejunosotmy site. Marked carcinomatosis and ascites were found during the operation. After the jejunojeunal bypass, the symptoms were relieved temporarily, but the patient suffered from poor oral intake and a large volume of ascites. The patient died on March 9, 2013. He had survived 9 months following the initial operation.

[[39.0, 'year']]

M

{'21455599': 1, '12576435': 1, '10671934': 1, '19847567': 1, '21573742': 1, '21573743': 1, '15593458': 1, '10518099': 1, '27595490': 1, '24761407': 2}

{}

3994622-1

noncomm/PMC003xxxxxx/PMC3994622.xml

Mammary duct ectasia with bloody nipple discharge in a child

A 14-month-old boy exhibited a mass in the right breast with bloody nipple discharge for 2 weeks before presenting a our hospital. There were no abnormalities in the patient's medical, familial, or developmental histories or in the maternal medical history. On physical examination, a 1-cm palpable mass without tenderness was noted in the subareolar region of the upper right breast. When the mass was squeezed, dark brown nipple discharge appeared (). There were no signs of inflammation in the physical examination or laboratory findings.\nAn ultrasonogram revealed a 1.0 cm × 0.8 cm multiseptated cystic mass in the right subareolar region. The macrocystic portion of the mass exhibited internal echogenicity. Minimal septal vascular flow was noted, and the mass was thought to be a complicated hemorrhagic lymphangioma or mammary duct ectasia ().\nSurgical excision was performed via a circumareolar incision, and a dark, bloody, fluid-filled cystic mass was removed. The mass, which was connected to main duct, was completely excised ().\nThe pathologic diagnosis was mammary duct ectasia. A microscopic analysis of the specimen demonstrated multiple dilated ducts with periductal fibrosis. The lumens of the dilated ducts contained histiocytes and degenerated epithelial cells, and duct stasis was observed ().

[[14.0, 'month']]

M

{'15101674': 1, '12603810': 1, '11112815': 1, '21550735': 1, '11381445': 1, '3219531': 1, '3746598': 1, '16585292': 1, '18286517': 1, '2329427': 1, '24761426': 2}

{}

3994625-1

noncomm/PMC003xxxxxx/PMC3994625.xml

Relining technique for continuous sac enlargement and modular disconnection secondary to endotension after endovascular aortic aneurysm repair

An eighty-one-year-old male visited the clinic complaining of abdominal pain along with pulsating mass. He had been diagnosed with infrarenal aortic aneurysm and this was treated with EVAR 6 years previously. After EVAR, a gradual increasing of the aneurysm sac was found without evidence of any type of endoleak. Eventually, the aneurysm reached a diameter of 9.7 cm on the computed tomography (CT) angiography and abdominal pain redeveloped. CT angiography showed a huge aortic aneurysm without evidence of endoleak, and it was considered that this was due to endotension.\nCT-guided sac aspiration was performed through the translumbar puncture of the aneurysm sac, and 400 mL of a dark brown-colored liquid was aspirated (). CT scan was performed the day after the puncture and the sac shrunk back to its original size (). Abdominal pain subsided and the palpating mass disappeared. One month after the aspiration, a CT scan was retaken, and the scan showed that the aneurysm sac increased back to the size before the aspiration (). Additionally, the scan showed no signs of endoleak. A second aspiration was performed again, and a further 300 mL of the dark brown colored fluid was aspirated. During the second aspiration, small amounts of contrast media was administered through the lumbar puncture site in order to search for the presence of collateral flow induced endoleak and to detect any possible rupture of the aneurysm sac. But no contrast media leakage from the sac was found, and no endoleak was found. So it was concluded that the increase of the aneurismal sac was due to endotension.\nFinally, with the consent of the patient, the endovascular relining technique was performed on the patient to treat the endotension. Since the diameter of the main body of the original endograft was 28 mm, it was planned that the relining process would be carried out by inserting two customized, tubular stent-grafts each of 14 mm in diameter. The length of the relining stent-graft was calculated to cover not only the whole length of the original stent-graft but to cover the entire growing sac. The patient was put under general anesthesia, and both common femoral arteries were punctured and selection of both limbs of the original stent-graft was attempted. Unexpectedly, the guide wire escaped from the junction area of the left module to the aneurysm sac. Upon inspection, a modular disconnection was found at the left graft junction area resulting in large amounts of leakage from the disconnected area. The original main body was selected with difficulty, and two 14-mm- × 12-cm-sized stent-grafts were successfully implanted within the original endograft (). Ancillary attachment between the original and the new stent-grafts was made with a compliant balloon. A final aortogram was performed and no endoleak was detected and the leakage from the modular disconnection disappeared after the endovascular relining. The day after the procedure, CT angiography showed no endoleak but retroperitoneal hematoma around the aneurysm sac was found. It was determined that the contained aneurismal sac rupture and the retroperitoneal hematoma were caused by the leakage from the modular disconnection.\nSerial review of the plain x-rays taken since the initial EVAR 6 years prior showed very subtle but gradual modular migration unnoticeable by eye, and complete disconnection developed within 5 days between the day of the second aspiration and the relining procedure. It was determined that the modular disconnection was a result of the aspiration (). The patient showed no symptoms or signs of aneurysm sac rupture after the procedure and was discharged with no further complications. CT scan taken four months after the relining procedure showed no endoleak and the size of the aneurysm sac decreased from 9.7 to 9.3 cm.

[[81.0, 'year']]

M

{'27022336': 1, '16678679': 1, '17306953': 1, '21215940': 1, '23526100': 1, '16378143': 1, '27708782': 2, '10876210': 1, '19786241': 1, '22727839': 1, '32273926': 2, '19576721': 1, '10893129': 1, '28787913': 1, '24761425': 2}

{'7140164-1': 1, '5033069-1': 1}

3994683-1

noncomm/PMC003xxxxxx/PMC3994683.xml

Unusual hemodynamic stroke related to an accessory middle cerebral artery: The usefulness of fusion images from three-dimensional angiography

A 77-year-old female experienced repeated TIAs of motor aphasia and dysarthria. On admission, she was alert and well oriented. She had no cranial nerve deficits or focal neurological signs. Magnetic resonance (MR) imaging revealed no evidence of acute cerebral infarction []. MR angiography showed an occlusion of the left internal carotid artery (ICA) and stenosis of the right MCA [Figure and ]. Some anomalous arteries were also identified faintly on MR angiography and ordinary angiography, but the detailed anatomy was not clear. Fusion images of three-dimensional digital subtraction angiography (3D-DSA) demonstrated an occlusion of the cervical portion of the left ICA and stenosis of both the proximal segments (M1) of the MCA []. In addition, a left AMCA, originating from near the anterior communicating artery (ACoA), was identified [Figures and ].\nThree-dimensional DSA revealed the characteristic cerebral blood flow (CBF) supply pattern. The AMCA supplied CBF to the frontal lobe alone. The AMCA was perfused by the right ICA via the ACoA. In addition, the left MCA, which was perfused by the left posterior cerebral artery via the left posterior communicating artery, supplied CBF to the temporal and parietal lobes [Figures -]. Because the proximal segment (A1) of the left ACA was occluded, the flows of the AMCA and MCA were clearly separate []. Single-photon emission computed tomography (SPECT) showed a marked decline in the CBF to the left fronto-temporo-parietal lesion at rest, while cerebral vascular reactivity was impaired by acetazolamide loading []. After diagnosis, we started antiplatelet medication (ASA 100 mg/day) and it continued until bypass surgery.\nIt was concluded that bypass surgery was needed for the territory of both the AMCA and MCA. A double anastomosis was performed that consisted of: (1) the frontal branch of the left superficial temporal artery (STA) to the cortical artery of the left AMCA; and (2) the parietal branch of the STA to the cortical branch of the left MCA. Prior to anastomosis, intraoperative indocyanine green video angiography was performed and demonstrated bidirectional flow in the left frontal cortical artery []. After anastomosis, the flow in the frontal cortical artery improved. A remarkable improvement in CBF in all lesions was confirmed postoperatively. The patient was discharged with no neurological deficits and remained free from ischemic attacks without antiplatelet medication for at least 1 year.

[[77.0, 'year']]

F

{'7452329': 1, '4723180': 1, '12568319': 1, '9432156': 1, '33573270': 2, '9090429': 1, '3047592': 1, '4682708': 1, '19233548': 1, '1588429': 1, '7974142': 1, '2407970': 1, '31341713': 1, '4841880': 1, '14142582': 1, '15340873': 1, '18728585': 1, '951638': 1, '17104495': 1, '12826338': 1, '24778914': 2}

{'7912107-1': 1, '7912107-2': 1}

3994684-1

noncomm/PMC003xxxxxx/PMC3994684.xml

Hemangioblastoma of the optic nerve producing bilateral optic tract edema in a patient with von Hippel–Lindau disease

This patient is a 34-year-old right-handed female with a known history of VHL disease. She presented to the neurosurgical service at Houston Methodist Hospital with a chief complaint of right retro-orbital pain and proptosis. She had previously undergone removal of a right retinal hemangioblastoma and was blind in the right eye, but the progressive pain and proptosis led to the discovery of a progressively enlarging lesion of the right optic nerve. Past history was notable for VHL and gastroesophageal reflux disease. In addition to the retinal lesion, she has previously undergone suboccipital craniectomy for excision of a cerebellar hemangioblastoma as well as a left sided acoustic neuroma. She harbors intramedullary tumors at the craniocervical junction as well as in the cauda equina. Her family history is significant for a son who has VHL. She has no knowledge of other family members with VHL as she does not know her biological father. Neurological examination is significant for blindness of the right eye and numbness in the perineum.\nMagnetic resonance imaging (MRI) scans of the brain with and without gadolinium revealed an avidly enhancing mass of the right optic nerve distal to the optic chiasm involving the cisternal, canalicular, and orbital components of the nerve measuring 1.2 cm in maximal diameter []. The mass was noted to have doubled in size in comparison to imaging performed 5 years prior. In addition, increased FLAIR signal was noted in the optic tracts bilaterally, which was not observed in the prior study [], suggesting the diagnosis of an infiltrating optic nerve glioma.\nShe underwent elective craniotomy and excision of the mass, which was performed through a standard fronto-temporal craniotomy. The sphenoid wing was drilled flush with the orbital roof and the dura was opened in a curvilinear fashion based on the sphenoid wing. The proximal Sylvian fissure was dissected sharply and gentle frontal lobe retraction was applied. The tumor was noted to have a red-tan appearance and was noted to tent the dura propria of the optic canal upward. The dura propria was incised sharply, and the orbital roof was opened utilizing a high speed diamond burr and 1 and 2 mm Cloward punches. The distal optic nerve was identified and divided followed by section of the nerve 1-2 mm distal to the chiasm. The ophthalmic artery was then identified, coagulated and cut [].\nNeuropathological diagnosis confirmed hemangioblastoma with the tumor having marked vascularity with a vacuolated stroma [].\nThe patient had an initial uncomplicated postoperative course and was discharged to home. She returned to the hospital 3 days after discharge with headaches. Repeat MRI of the brain revealed gross total excision of the mass as well as resolution of the FLAIR signal in the bilateral optic tracts. She is presently doing well, with resolution of her retro-orbital pain and no visual defect in the left eye.

[[34.0, 'year']]

F

{'6784554': 1, '33442737': 1, '4473999': 1, '24138046': 1, '10326959': 1, '17219830': 1, '7753357': 1, '11310918': 1, '3050687': 1, '7196008': 1, '2909683': 1, '17527048': 1, '29911000': 2, '19068378': 1, '11152361': 1, '21293730': 1, '15747747': 1, '7199079': 1, '15534587': 1, '27928308': 1, '9440188': 1, '15508741': 1, '22953140': 2, '2482948': 1, '34868983': 2, '18395800': 1, '7959672': 1, '7946625': 1, '17218907': 1, '1632366': 1, '16793428': 1, '33143685': 2, '12834696': 1, '24778921': 2}

{'8632699-1': 1, '7640410-1': 1, '3420590-1': 1, '5989481-1': 1}

3994685-1

noncomm/PMC003xxxxxx/PMC3994685.xml

A case of Langerhans cell histiocytosis of the skull in which preoperative methionine positron emission tomography was useful in comprehending the spreading of the lesion

A 20-year-old female.\nNo major illnesses.\nThe patient consulted our institute after becoming self-aware of swelling and dull pain in the left side of her head from 3 months prior.\nShe was clearly conscious and no symptoms of neurologic deficit were observed. A soft flexible tumor was palpated in an approximately 3 × 3 cm region on the left side of her head and tenderness at that site was observed.\nThere were no inflammatory findings and the tumor marker was within the normal range.\nAn oval radiolucent line was observed in the left cranium upon simple head X-ray []. A slightly heterogeneously enhanced tumor in left parietal bone was observed inside the bone defect in a gadolinium-enhanced T1-weighted image upon head magnetic resonance imaging (MRI); wherein, the dura mater and subcutaneous tissue contacting the tumor widely exhibited an enhancing effect and was found to have thickened [Figure and ]. Nuclide accumulation was observed in the tumor inside the bone defect upon FDG-PET; however, the brain cortex accumulation was also high in the area adjacent to the brain surface, so the border was unclear, making evaluation difficult []. No significant abnormal accumulations in other areas of the body were observed. Meanwhile, such accumulation was observed to be poor in the center of the tumor upon Met-PET, while accumulation with a well-defined border was observed in the border as well as the dura mater and subcutaneous tissue adjacent thereto [].\nAccordingly, it was believed to be an extramedullary tumor such as LCH of the skull, meningioma, malignant lymphoma, etc. The tumor was symptomatic and enlarged within a relatively short period of time; therefore, surgery was carried out including pathological diagnosis.\nA U-shaped skin incision was made on the left side of the head. When the skin flap was reversed, the subcutaneous tissue was strongly adhered to the defective part of the bone. A craniotomy was carried out leaving a distance of approximately 3 cm from the defective part of the bone such that the range observed with accumulation upon Met-PET was sufficiently included [Figure -]. When the bone flap was reversed, the tumor was observed to be yellow in color. The tumor was adhered to the dura mater and the dura mater of the attachment site was yellow in color and particularly thick. The dura mater was excised, while leaving a border of approximately 1 cm from the thickened part of the dura mater [Figure -]. Tumor cells were not observed in the stump of the excised dura mater upon immediate pathological examination. The subcutaneous tissue adhered to the defective part of the bone was also resected and the excised stump was negative. The defective part of the bone was excised upon providing a border of approximately 1 cm [], and this was supplemented using artificial bone Biopex®. The defective part of the dura mater was sutured using artificial dura mater (GoreTex®).\nThe accumulation of tumor cells having a nuclear groove and constricted nucleus in the border part observed with accumulation upon Met-PET was observed inside the extracted skull [Figure -]. The tumor cells were immunohistochemically positive for CD1a, DEC205, and Langerin. The center part with poor accumulation lacked tumor cells, with fibrous tissue accounting for most parts []. Accordingly, it was diagnosed as LCH. The dura mater was observed to have undergone invasion of histiocyte-like tumor cells and eosinophil similar to the tumor itself in the region corresponding to the accumulation region upon Met-PET [Figure -]. Tumor cells and inflammatory cells were not observed in the dura mater stump.\nThe course was good and the patient was discharged without any deficiency symptoms. Relapse has not been observed as of 7 months following surgery.

[[20.0, 'year']]

F

{'27073529': 1, '3197424': 1, '7957291': 1, '18341013': 1, '26054903': 2, '15140741': 1, '18951435': 1, '26815698': 1, '10786099': 1, '10505036': 1, '18227990': 1, '8480200': 1, '10552020': 1, '24778915': 2}

{'4502045-1': 1}

3994687-1

noncomm/PMC003xxxxxx/PMC3994687.xml

Synchronous multicentric glioblastoma with PNET and O subtypes: Possible pathogenesis

A 47-year-old Caucasian male with no past medical history, presented with a four week history of episodic frontal headache and easy fatiguability. He also noted to have progressive difficulty with recall which was associated with occasional dizziness and an unsteady gait. On examination, there were no cranial nerve abnormalities and other focal neurologic findings. The rest of his clinical examination was unremarkable.\nMagnetic resonance imaging (MRI) brain scan was performed which revealed two intra-axial lesions with similar imaging characteristics []. The first lesion approximated 70 × 48 mm and was located at the left temporal lobe while the second lesion was at the left frontal parasagittal region and approximated 34 × 31 mm. Both lesions had solid and necrotic-cystic areas with areas of T1 hypointensity, T2 hyperintensity, with heteorgenous enhancement post-gadolinium contrast. Susceptibility within the masses suggested intra-lesional haemorrhage and/or calcification. Both lesions were associated with significant perilesional oedema causing mass effect and midline shift to the right. The radiological diagnosis was multi-centric glioblastomamultiforme, with differential diagnosis of metastasis.\nAdditional imaging workup included computed topography scans of his thorax, abdomen and pelvis and MRI of his whole spine, which did not demonstrate any further lesions.\nThe patient underwent an awake craniotomy for gross total resection of the left frontal and parieto-temporal tumours. Intraoperative frozen section was reported as suggestive of a high grade glioma. The patient recovered well postoperatively with no new focal neurological deficits. Post-operative MRI brain scan was performed 48 hours after surgery and showed no gross evidence of residual tumor. He was subsequently referred to the medical and radiation oncology teams for adjuvant therapy, and has since commenced on both chemotherapy (temozolamide) and radiotherapy to both cranium and spine.\nThe resection specimen from the left temporal lobe tumour showed two histologically distinct components. In some areas, the tumour resembled a glioblastoma (WHO grade IV) []. These areas consisted of a cellular proliferation of astrocytes with markedly enlarged, irregular, pleomorphic nuclei and moderate to abundant quantities of fibrillary cytoplasm. Neoplastic gemistocytic astrocytes and multinucleated astrocytes were seen. There was brisk mitotic activity, microvascular proliferation and pseudopalisading necrosis. In other areas, the tumour resembled a central nervous system primitive neuroectodermal tumour (CNS PNET, WHO grade IV) []. These latter areas consisted of densely packed cells with hyperchromatic oval to elongated nuclei, high nuclear cytoplasmic ratios, brisk mitotic activity and karyorrhexis. There were also areas where cells from both tumour types were closely intermingled. The lesion included large confluent areas of coagulative tumour necrosis. Immunoperoxidase staining for glial fibrillary acid protein (GFAP) was positive in the glioblastoma component [] and negative in the CNS PNET areas, while synaptophysin was positive in the CNS PNET areas [] and negative in the glioblastoma cells. The features were compatible with a malignant glioma with a PNET-like component.[]\nThe resection specimen from the left frontal lobe tumour showed features of a glioblastoma with an oligodendroglial component (WHO grade IV). The glioblastoma consisted of a cellular proliferation of astrocytes with irregular, hyperchromatic, pleomorphic nuclei and fibrillary cytoplasm. There was brisk mitotic activity, microvascular proliferation and pseudopalisading necrosis []. Focally, there was a proliferation of cells resembling oligodendrocytes with round regular nuclei, clear cytoplasm and distinct cytoplasmic borders. The oligodendroglial population was associated with a branching capillary network [].

[[47.0, 'year']]

M

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{'2958331-1': 1, '6935977-1': 1}

3994688-1

noncomm/PMC003xxxxxx/PMC3994688.xml

Pilomyxoid astrocytoma of the cerebellar vermis in an elderly patient

A 72-year-old male with a distant history of alcohol abuse presented with approximately 6 months of memory loss, difficulty expressing himself, and a progressively worsening gait. A magnetic resonance imaging (MRI) of the brain revealed a 2.5 × 3.7 × 2.5 cm heterogeneously enhancing cystic mass centered within the cerebellar vermis with mass effect on the fourth ventricle and mild ventriculomegaly [Figure and ] as well as an 8 × 6 × 4 mm satellite lesion within the right superior cerebellar peduncle [Figure and ]. On examination at an outpatient clinic, the patient had a slight expressive aphasia but was otherwise neurologically intact. At that time, the differential diagnosis of the lesion included primary glioma versus metastatic or granulomatous disease and the decision was made for surgical resection of the lesion.\nRoutine preoperative testing found the patient to be in rapid atrial fibrillation and he was sent to the emergency room. While undergoing evaluation of the arrhythmia, his rhythm converted to a junctional bradycardia, necessitating placement of transvenous pacemaker. In the absence of other identifiable etiologies for his sudden bradycardia, his cardiac symptoms were attributed to intracranial hypertension secondary to the obstructive hydrocephalus caused by the vermian lesion. A computed tomography (CT) scan of the head revealed ventriculomegaly but no frank hydrocephalus and the patient was taken to the operating room for placement of a ventriculoperitoneal (VP) shunt. Intraoperatively, he was found to have elevated intracranial pressure. His postoperative course was notable for immediate resolution of the cardiac arrhythmia.\nTwo days following placement of the VP shunt, the patient underwent a suboccipital craniectomy for resection of the cerebellar lesion. Intraoperatively, the lesion was found to be soft and mildly vascular with clean margins relative to the surrounding brain. Pathology specimens were sent for frozen histological analysis and were thought to be most consistent with a diagnosis of glioma. A postoperative MRI revealed a subtotal resection of the lesion. Permanent section of the lesion demonstrated a glial neoplasm composed of astrocytes with elongated, bipolar cytoplasmic processes, forming fascicles and focally, loose perivascular patterns, dispersed within an abundant myxoid background [Figure and ]. The tumor cells had round to irregular, hyperchromatic nuclei, with prominent perinuclear halos infiltrating the molecular layer of the adjacent cerebellar folia. They were strongly immunoreactive for GFAP and WT-1 with a MIB-1 labeling index of greater than 5% [Figure and ]. The lesion was diagnosed as a WHO grade 2 PMA. Postoperatively, the patient did well and was discharged to the inpatient rehabilitation service on postoperative day 4 and discharged home 12 days later with residual dizziness and gait imbalance. Following discharge, the patient refused further medical or surgical treatment. His neurologic status and overall health gradually deteriorated and he expired 11 months after initial symptom presentation and 4 months after surgery.

[[72.0, 'year']]

M

{'32656116': 2, '16048293': 1, '30363302': 1, '10515229': 1, '18536992': 1, '11758781': 1, '19938670': 1, '22031164': 1, '16645715': 1, '4016701': 1, '12924720': 1, '17894633': 1, '14683543': 1, '15775869': 1, '18958385': 1, '16521485': 1, '3392563': 1, '201364': 1, '24778917': 2}

{'7335121-1': 1, '7335121-2': 1, '7335121-3': 1}

3994689-1

noncomm/PMC003xxxxxx/PMC3994689.xml

Conservative surgery for osteoid osteoma of the lumbar vertebrae

A 20-year-old male presented with localized low back pain of 2 years duration, attributed to lifting a heavy object. Pain was persistent, worse at night, unrelated to activity, but characteristically relieved promptly with NSAIDS. He was misdiagnosed for over a year, and prescribed physiotherapy, analgesic/antiinflammatory therapy, and trycyclic antidepressants without improvement. On presentation he exhibited mild scoliosis, negative straight-leg-raise test and no focal neurological deficit. Plain X-rays of lumbosacral spine were normal, but the radioisotope bone scan (Tc-99m) showed increased uptake in left posterior half of the L2 vertebra. The CT scan confirmed that the L2 lesion was sclerotic with a lucent focus in the left postero-inferior quadrant []. Surgery, performed in the right lateral decubitus position utilizing an anterior retroperitoneal approach to the L2/L3 intervertebral space (X-ray confirmed) allowed for en-bloc resection of the involved quadrant of the L2 vertebral body while preserving the end-plates and posterior vertebral border []. Reconstruction of the bony defect was accomplished by impacting custom-sized tricortical bone graft harvested from the iliac crest []; no additional fusion was required. Postoperatively the patient was allowed to ambulate freely.\nAt 2-weeks postoperative follow-up the patient reported complete relief of his long-standing pain. At 12 postoperative weeks, the X-rays documented full incorporation of the bone graft []. In his last follow-up at 9 years, he was completely pain-free and had full function of the spine.

[[20.0, 'year']]

M

{'27893671': 2, '15973540': 1, '16550447': 1, '21304430': 1, '7985393': 1, '24778912': 2}

{'3994689-2': 2, '5134864-1': 1}

3994689-2

noncomm/PMC003xxxxxx/PMC3994689.xml

Conservative surgery for osteoid osteoma of the lumbar vertebrae

A 16-year-old male presented with persistent localized lower lumbar pain of 2 years duration. Pain was progressive, occurred at rest and at night, was relentless, was increased by walking, and immediately although transiently relieved with NSAIDS. He had been labeled neurotic and given antidepressants. On examination, he exhibited a mild postural scoliosis in the lumbar spine concave to the right, but had no focal neurological deficit and negative straight-leg-raise test. Radioisotope bone scan showed increased uptake over the right side of L2 vertebra on posterior view [] corresponding to X-ray showing a vague halo over the right neural arch of L2 []. High resolution CT scan confirmed a dense nidus and circular halo involving the right lamina []. Surgery, performed prone, consisted of removal of the right lamina utilizing a 3 mm high-speed burr. Careful preservation of the pars interarticularis, inferior articular process, and the facet joint [] avoided instability and the need for a fusion. The patient experienced a dramatic reduction in pain within one postoperative week. The patient was asymptomatic 5 years later. The histopathology confirmed an osteoid osteoma.

[[16.0, 'year']]

M

{'27893671': 2, '15973540': 1, '16550447': 1, '21304430': 1, '7985393': 1, '24778912': 2}

{'3994689-1': 2, '5134864-1': 1}

3994690-1

noncomm/PMC003xxxxxx/PMC3994690.xml

Sudden unexpected nocturnal death in Chiari type 1 malformation and potential role of opioid analgesics

A 29-year-old African-American male was admitted to our hospital because of headache associated with nausea, vomiting, and blurred vision. Intermittent headaches over the preceding 4 years were ascribed to CM1. In the month prior to admission, the patient's headaches had increased in frequency and in severity. He described the headaches as pounding and rated the intensity of the pain as 10 on a scale of 0 to 10, where 10 is the most severe. The pain began in the occipital region and extended to the forehead unrelated to coughing or straining. A few days before admission, nausea, vomiting, and blurred vision accompanied some of the episodes of headache. As the patient's headaches continued to worsen, he was admitted to an outside hospital. Magnetic resonance imaging (MRI) of the brain showed an 18 mm cerebellar tonsillar herniation and a disproportionately large communicating fourth ventricle with dilated but stable ventricular system, and no change from previous studies []. Cervical spine MRI was normal. In light of the patient's worsening symptoms, he was transferred to the University Hospital of Brooklyn for surgical intervention. The patient did not report limb weakness, paresthesia, or breathing difficulty, nor a history of cardiac arrhythmia, hypoglycemia, alcohol abuse, or epilepsy. The patient had no family history of neurologic or cardiac disease. Preadmission medications included variable amounts of acetaminophen, hydrocodone, and ibuprofen for headache control.\nOn evaluation, the patient's vital signs were normal, the lungs were clear and no bradycardia or cardiac pauses were observed. He was alert and oriented. There was no nuchal rigidity to passive flexion of the neck. The pupils were equal and reactive to light. The optic disc margins were sharp and the visual fields were normal. The remainders of the physical and neurological examinations were normal except for mild bilateral horizontal gaze-evoked nystagmus and a slightly unsteady gait. Laboratory studies, including complete blood count, serum electrolytes, blood glucose, urine specimen, and the results of the blood pressure and heart rate monitoring were normal. The patient was considered in stable condition because of a stable ventricular size with stable vital signs, relative preservation of motor and sensory pathways, and no respiratory stress during alertness. In light of his presumed stable condition, medical management of the patient's acute cephalodynia rather than urgent surgery became the priority. He was disconnected from the vital signs monitor and admitted to the neurosurgical ward for surgery to be scheduled after presurgical risk assessment testing, including routine laboratory studies, chest X-ray, and electrocardiogram. Medical management of the patient's pain during the first 24 hours of admission, starting in the emergency room and continuing in the neurosurgical ward, included 60 mg of codeine by mouth, 650 mg of acetaminophen by mouth, 10 mg of intravenous (IV) morphine sulfate (2, 4, and 4 mg at 4-hour intervals), 4 mg of IV hydromorphone, and 10 mg of IV metoclopramide. At 4:10 am on the second day of hospitalization, about 26 hours after admission, the patient complained of severe headache. Upon rising from bed, he became incontinent of urine. After the patient was placed in bed, hydromorphone 4 mg and metoclopramide 10 mg were given IV. At 8:00 am, the patient was found cold and pulseless in bed with no recordable blood pressure or cardiac activity on electrocardiogram and was pronounced dead. A complete postmortem examination revealed a CM1 with mild hydrocephalus without uncal herniation or syringomyelia. Toxicological screening was negative. The cause of death was not identified, but myocardial infarction, cardiac conduction defect, and suffocation due to vomiting or choking were convincingly excluded.

[[29.0, 'year']]

M

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{'3707328-1': 1}

3994691-1

noncomm/PMC003xxxxxx/PMC3994691.xml

Minimally invasive posterior cervical decompression using tubular retractor: The technical note and early clinical outcome

A 65-year-old female visited our clinic complaining neck pain and severe right side radicular arm pain with hand grip weakness for 12 months. She was conservatively treated at local clinic for 8 months without improvement. The cervical MRI showed right side neural foraminal stenosis from C3 to C6 levels and central spinal canal stenosis from C4 to C6 levels with myelopathy due to ossification of ligament flavumm (OLF). Cervical dynamic (flexion-extension) MRI showed aggravation of canal stenosis by posterior pathology on extension []. Her VAS scores for neck pain and radicular pain were 5 and 8, respectively. She underwent posterior Rt. side ULBD decompression with tubular retractor from C4 to C6 levels []. There was no complication during surgery except asymptomatic spinous process fracture discovered only after postoperative CT was taken. The operation time was 1.5 h and EBL was 40 cc after surgery, the VAS score for neck pain reduced from 5 to 3 and VAS score for radicular pain reduced from 8 to 3. She was discharged a day after surgery.

[[65.0, 'year']]

F

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{'6187890-1': 1}

3994692-1

noncomm/PMC003xxxxxx/PMC3994692.xml

Subtotal resection of an intradural mature teratoma in an adult presenting with difficulty initiating micturition

A 41-year-old male presented with a longstanding history of difficulty initiating micturition and lower back pain with recent onset of saddle paraesthesia and bilateral leg pain, which had been associated with decreased sensation on ejaculation and occasional fecal incontinence. There was no history of spinal dysraphism, congenital spinal abnormalities, previous spinal surgery, or lumbar puncture.\nClinical examination revealed no evidence of cutaneous abnormalities. Neurological examination was unremarkable.\nComputed tomography (CT) lumbar spine revealed no bony abnormalities. Magnetic resonance imaging (MRI) confirmed the presence of an intradural, extramedullary lesion at T12/L1, which was causing marked compression of the distal conus. The tumor measured 35 × 14 mm and displayed hyperintense signaling on pregadolinium T1 and low signal on T2 with a small crescentic element of fat on the dorsal superior border Figures and .\nThe surgical management consisted of a laminectomy from T11 to L1 and subtotal excision. At surgery, once the dura was opened the capsule was initially decompressed and a considerable amount of proteinaceous fluid was drained. Thereafter, the majority of the capsule was excised, however, the base of the tumor was found to be densely adherent to the distal conus. It was decided that this could not be safely dissected from the conus and therefore a thin rim of capsule was retained.\nPostoperatively, the patient developed transient urinary retention, however, he went on to make a good recovery with resolution of his back and leg pain. His bladder function improved although he does report occasional fecal incontinence.\nHistopathologic examination of the lesion demonstrated elements of endoderm, mesoderm, and ectoderm with fragments of degenerate keratin, cystic spaces lined with stratified squamous epithelium, adipose tissue, disorganized neural tissue as well as mucus secreting epithelium Figure and . There were no immature elements or malignant cells seen.\nPostoperative imaging at one year confirmed successful decompression of the conus and no evidence of tumor recurrence Figures and .

[[41.0, 'year']]

M

{'9817426': 1, '19119471': 1, '21107150': 1, '15239016': 1, '16523223': 1, '31227969': 1, '16770222': 1, '11198778': 1, '26396595': 2, '28110362': 1, '18084751': 1, '21897688': 2, '16753629': 1, '24778911': 2}

{'3159361-1': 1, '4553720-1': 1}

3994693-1

noncomm/PMC003xxxxxx/PMC3994693.xml

Orbital tuberculosis with coexisting fungal (Aspergillus flavus) infection

A 65-year-old male patient, with poorly controlled diabetes mellitus, presented to us with painless, progressive diminished vision in both eyes over 4 months (asymmetrical involvement; right eye defect more than left eye). On examination, right eye had only perception of light and left eye had vision of counting fingers up to 2 feet. Fundus showed features of optic atrophy. His neurological examination was unremarkable. There were no signs of meningeal irritation. He was negative for HIV, HBsAg and HCV done by ELISA as a routine presurgical investigation. His chest X-ray was unremarkable. Mantoux was negative. Sputum AFB (done in the postoperative period after the tissue cultures showed growth of tuberculosis) was negative. Sputum for acid fast bacilli was negative. He had an FBS = 176 mg/dl, PPBS = 231mg/dl, and Hb1Ac = 8.2%. Magnetic resonance imaging (MRI) of brain with orbit showed a lesion, which was heterogeneously hypointense on T1W and hyperintense on T2W, located in the orbit, encircling the optic nerve and was extending through the optic foramen into the cranial cavity. On gadolinium contrast T1W imaging, the lesion was brilliantly enhancing and was extending onto the planum sphenoidale []. Mild enhancement was also noted in the right orbit. The paranasal sinuses were normal. A working diagnosis of orbital meningioma was made. A left supraorbital craniotomy and deroofing of the orbit was followed by subtotal excision of the lesion. The tumor was grayish, mildly vascular, firm, nonsuckable and was encircling the left optic nerve and was extending into the optic canal. The frozen section examination was suggestive of granulomatous pathology and hence the specimen was subjected to microbiological examination as per our departmental protocol for suspected infections (aerobic, tubercular and fungal staining, and cultures). Histopathological examination showed multi-septate hyphae suggestive of fungus. On day 5, growth of Aspergillus flavus was noted on fungal culture. The patient was started on antifungal drugs immediately (Inj. Voriconazole 400 mg on day 1 followed by 200 mg daily for 14 days, followed by oral Voriconazole 200 mg, twice daily for 4 weeks, to be reviewed with repeat imaging). On day 28, all three cultures tubes for tuberculosis [BACTEC 460 Tb system (Becton Dickinson, USA) using the 12 B vials] were positive. He was started on antitubercular drugs as per his body weight (Isoniazid 300 mg once a day, Rifampicin 600 mg once a day, Pyrazinamide 750 mg twice daily, Ethambutol 800 mg once a day, and Benadone 20 mg once a day). He was discharged on 14th postoperative day with no change in his visual status. He, however, had a cerebrovascular accident and succumbed to it on 38th postoperative day.

[[65.0, 'year']]

M

{'3073939': 1, '15019377': 1, '7411335': 1, '22865977': 1, '18716964': 1, '16491039': 1, '24778920': 2}

{}

3994694-1

noncomm/PMC003xxxxxx/PMC3994694.xml

Long-term follow-up in two cases of intracranial Rosai–Dorfman Disease complicated by incomplete resection and recurrence

A 22-year-old male presented with progressive headache, focal convulsions, and monoparesis of his right arm and loss of vision of the right eye due to papillary congestion. In addition, he had noted a left supraclavicular swelling. Imaging showed a large extracranial space-occupying dura-based mass []. Lymph node and intracranial biopsy findings were compatible with RDD showing the emperipolesis phenomenon [] and a positive S-100 reaction. On operation, the tumor could be removed completely. Nineteen months later, a right submaxillary lymph node was extirpated confirming the diagnosis. After further 10 months, a left temporo-basal and a parietal tumor and after another year, a left retrobulbar lesion appeared and was operated as well. Because of this relapsing course, the patient received chemotherapy consisting out of 8 cycles of cyclophosphamide (1 g), vincristine (2 mg), doxorubicin (50 mg), and prednisone (50 mg) for 5 days every 3 weeks according to a modified CHOP regimen.[] Since then, no recurrences have been noted over a follow-up period of 7 years.

[[22.0, 'year']]

M

{'22652821': 1, '32661485': 1, '29720485': 1, '19659569': 1, '34221623': 1, '32983353': 1, '21557191': 1, '7680764': 1, '17380248': 1, '15764118': 1, '22029938': 1, '2180012': 1, '22725985': 1, '20350368': 1, '24778918': 2}

{'3994694-2': 2}

3994694-2

noncomm/PMC003xxxxxx/PMC3994694.xml

Long-term follow-up in two cases of intracranial Rosai–Dorfman Disease complicated by incomplete resection and recurrence

A 39-year-old male presenting with progressive headache since one year and a focal convulsion of the right side of his face on the day of admission. Computed tomography (CT) showed four space-occupying hyperdense lesions with prominent surrounding edema and enhancement in a left fronto-temporal, parietal/paramedian, occipital, and right central/periventricular localization []. The removal of the fronto-temporal mass was complicated by an extracranial cerebrospinal fluid (CSF)-containing cyst finally treated by duroplasty. Histology showed typical features of RDD. Two years later, because of persistence of the remaining lesions, the left parietal one was operated, and the others were treated successfully by chemotherapy following the CHOP regimen as in case 1. Since then, the patient has now been free from recurrences for 7 years.

[[39.0, 'year']]

M

{'22652821': 1, '32661485': 1, '29720485': 1, '19659569': 1, '34221623': 1, '32983353': 1, '21557191': 1, '7680764': 1, '17380248': 1, '15764118': 1, '22029938': 1, '2180012': 1, '22725985': 1, '20350368': 1, '24778918': 2}

{'3994694-1': 2}