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164,200 | 3830256-1 | 24,250,108 | noncomm/PMC003xxxxxx/PMC3830256.xml | Primary extra-nodal non-Hodgkin's lymphoma of gingiva: A diagnostic dilemma | Patient was a 50-year-old female of Indian origin who presented for evaluation of a slowly enlarging anterior mandibular mass, which she stated had been present for at least 12 months. She reported pain and swelling in association with paresthesia in the chin region for 12-14 months. Initially, her symptoms were thought by her dentist, to be a pyogenic granuloma and managed by excision and antibiotics. However, the lesion recurred after six months of excision and rapidly enlarged to the present size. Clinically, the lesion appeared as sessile, soft and friable mass, which bled on palpation []. The mass had displaced the teeth in the affected region and involved the mandibular labial sulcus. At the time of presentation, patient did not report any systemic symptoms and had no fever, weight loss or dysphasia. The patient's previous medical history was non-contributory. She was not on medications at the time of presentation and was a non-drinker and a non-smoker.\nExcisional biopsy was performed to determine the nature of the lesion. The H and E stained soft-tissue section [] revealed proliferation of lymphoblastic appearing cells that showed varying degrees of differentiation. Cells had round or oval nucleus with multi-lobed or cleaved nuclei. The section consisted of the population of monotonous proliferation of the lymphoblastic series with minimal cytoplasm. Lymphoblasts were scattered in diffuse pattern in the subepithelial connective tissue. At one area, the section was encapsulated and showed arteritis obliterans, extravasated red blood cells, collagen bundles, fibroblasts, adipocytes, chronic inflammatory cells mainly lymphocytes, calcifications, muscles fibers, eosinophilic material and bone. The epithelium was parakeratinized stratified squamous type, which was thin and atrophic at places.\nA diagnosis of primary extranodal non-Hodgkin's diffuse large B-cell type lymphoma of the gingiva with small cleaved nuclei type cells was made as CD20 marker was positive on immunohistochemistry [] and patient was then referred to the oncologist for definitive management. The oncologist confirmed that the lymphoma was localized to the anterior mandible only, without any diffuse disease or nodal involvement. She was categorized as stage IAE primary mandibular NHL. It was the recommendation of the oncologist that she should undergo four cycles of Cyclophosphamide hydroxydaunorubicin oncovin prednisolone-rituximab followed by radiotherapy. She attained a complete response and following therapy there appeared to be new healthy bone formation. | [[50.0, 'year']] | F | {'12167442': 1, '15291366': 1, '27656575': 1, '8475914': 1, '10707726': 1, '27694791': 1, '16012407': 1, '29264306': 2, '25954642': 1, '30967716': 2, '26088459': 1, '25810835': 2, '29731565': 2, '11036251': 1, '24250108': 2} | {'6421927-1': 1, '5717915-1': 1, '4368011-1': 1, '5917515-1': 1} |
164,201 | 3830269-1 | 24,251,123 | noncomm/PMC003xxxxxx/PMC3830269.xml | Dissociated hypopituitarism after spontaneous pituitary apoplexy in acromegaly | A 55-year-old smoker male presented to our out-patient clinic in 2004 with complaints of gradual onset increase in the size of hands and feet, bilateral knee pain, increased sweating and blurring of vision. Patient denied any history of headache. Physical examination revealed coarse facial features, large spade like hands, large feet, macroglossia, oily skin, and excessive sweating. The patient was hemo-dynamically stable with a blood pressure of 150/96 mm Hg.\nInvestigations revealed a normal complete blood count, liver and kidney function tests and electrolytes and evidence of left ventricular hypertrophy on electrocardiogram. Previously undiagnosed diabetes mellitus was uncovered by casual blood glucose of 243 mg/dl and HbA1c of 8.5%. GH suppression test using 75 g oral glucose showed a 60 min GH of 105 ng/ml. The basal levels of other pituitary and target hormones are depicted in . Magnetic resonance imaging (MRI) of the sellar region showed a 12.0 mm × 10.0 mm pituitary adenoma not compressing the optic chiasm []. The patient refused insulin and was started on metformin and glimepiride, and planned for transsphenoidal tumor decompression. However, the patient was lost to follow-up.\nEight years later, he presented in the emergency department of our institute with sudden onset headache, vomiting and decreased level of consciousness of 1 day duration. Examination revealed a Glasgow coma scale of 10 with right sided oculomotor nerve palsy and facial features suggestive of acromegaly. His blood pressure was 90/60 mm Hg. Subsequent investigations revealed random blood glucose of 67 mg% and normal electrolytes. Computed tomography scan of the head with focus on the sella was suggestive of apoplexy which was later confirmed by the MRI of the sellar region []. The patient was initially stabilized using intravenous glucocorticoids after which a transsphenoidal tumor debulking was done. Post-surgery the patient's condition improved. His post-operative endocrine workup after the apoplexy revealed a GH (post-glucose challenge) level of 1.48 ng/ml and secondary adrenal insufficiency and central hypothyroidism []. At present, the patient is doing well on metformin 500 mg, levothyroxine 75 μg/day and hydrocortisone 7.5 mg. | [[55.0, 'year']] | M | {'22200007': 1, '28567295': 1, '20400318': 1, '32923214': 2, '20140630': 1, '22340248': 1, '31310082': 1, '17785921': 1, '24251123': 2} | {'7478766-1': 1} |
164,202 | 3830270-1 | 24,251,124 | noncomm/PMC003xxxxxx/PMC3830270.xml | Deep vein thrombosis in a patient of Sheehan's syndrome: Autoimmunity or hypercoagulabilty | We present a 30-year-old female who presented with 1 month history of gradual onset swelling and pain involving the left leg. Physical examination revealed features of hypothyroidism, blood pressure of 100/70, pulse of 68/min and normally palpable peripheral pulses. The cardiovascular and respiratory system examination was normal. The left calf diameter was 5 cm greater than the right. Laboratory investigations revealed normocytic normochromic anemia, normal liver and kidney function test. Patient's blood glucose was 72 mg/dl; normal serum electrolytes; normal chest X-ray. Electrocardiogram revealed low voltage complexes with normal sinus rhythm. Doppler lower limbs revealed thrombosis in left popliteal vein. Patient's coagulation profile revealed normal prothrombin time of 12 s, activated partial thromboplastin time (APTT) of 30 s, positive D-dimer, negative protein C and protein S and normal titres of antinuclear antibodies. Echocardiography showed an ejection fraction of 52 percent. Patient was initially treated with heparin followed by warfarin. Endocrinology consultation was sought in view of clinical suspicion of hypothyroidism. Endocrinology review revealed a significant past history of primary postpartum hemorrhage, lactation failure and secondary amenorrhea since the delivery of the last child 6 years back. She had clinical features of growth hormone, thyroid hormone and adrenocorticotropic hormone deficiency. Hormonal analysis showed features of central hypothyroidism, secondary adrenal insufficiency and growth hormone deficiency which was confirmed by insulin tolerance test []. Patient was put on thyroxine; prednisolone and anticoagulants were continued for 3 months. Patient is regularly following in the endocrinology OPD with no further recurrence of DVT. | [[30.0, 'year']] | F | {'10817784': 1, '8123648': 1, '8949568': 1, '10468941': 1, '12213861': 1, '16410662': 1, '15256787': 1, '24251124': 2} | {} |
164,203 | 3830271-1 | 24,251,125 | noncomm/PMC003xxxxxx/PMC3830271.xml | Isolated adrenocorticotropic hormone deficiency due to probable lymphocytic hypophysitis in a woman | A 22-year-old unmarried female presented with a 4-year history of general fatigue, weight loss and hypotension. She was born of non-consanguineous parents after a normal full term vaginal delivery. She reported no family or personal history of autoimmune diseases. She had no history of trauma and she did not have a history of receiving glucocorticoids.\nThere were no abnormal findings on clinical examination, she was normally pigmented, blood pressure was 95/60 mmHg with no postural fall, and she had normal body hair. Her height was 170 cm and her weight was 53 kg. Thyroid palpation was normal. She had normal pubertal development. Her menarche started at the age of 12 years and she had regular periods. She had no galactorrhea. She had no headaches, visual disturbances, polyuria, or polydipsia.\nBlood examinations showed natremia of 138 mEq/L, kaliemia of 4.1 mmol/L, calcemiaof 2.38 mmol/L, plasma glucose of 4.3 mmol/L and normal blood cell count.\nClinical findings led us to consider the possibility of adrenocortical insufficiency, and the patient underwent detailed endocrine investigations, the results of which are shown in .\nCortisol deficiency was shown clearly by both insulin-induced hypoglycemia and depot Synacthen test [intravenous injection (IV), 1μg]. Secondary hypoadrenalism was confirmed by the finding of low basal ACTH level (13.8 pg/mL, reference range: 10.3-48.3), at which the plasma cortisol was 34 ng/mL. Prolactin level was elevated at 39 ng/mL (Normal range: 5-29 ng/mL in females). She had normal growth hormone levels concomitant to hypoglycemia. In contrast, basal concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol, thyroid stimulating hormone (TSH), and free thyroxine (FT4) were normal. These results excluded panhypopituitarism and led us to diagnose the patient with IAD. Magnetic resonance imaging (MRI) of the hypothalamus and pituitary showed a normal-sized pituitary (pituitary height 6 mm), with no mass lesion. Thepituitary stalk has a normal thickness of 2 mm and was not deviated. Thehyperintense signal of the posterior pituitary was in the normal location.\nThe diagnosis of IAD probably secondary to LYH was made. Investigation for autoimmune diseases, including assessment of anti-thyroid peroxidase antibody (anti-TPO), anti-thyroglobulin antibody (anti-TG), anti-ovarian antibodies, anti-adrenal antibodies, anti-glutamic acid decarboxylase (anti-GAD) antibodies, and antinuclear antibodies (ANA) was negative.\nA daily dose of hydrocortisone (25 mg) was administered. After 8 months of follow-up, the patient was well-controlled, and she experienced no signs or symptoms of endocrine dysfunction. | [[22.0, 'year']] | F | {'8013150': 1, '11314750': 1, '3014939': 1, '19121993': 1, '7791966': 1, '20039888': 1, '17077949': 1, '15613420': 1, '7611978': 1, '16421141': 1, '15826923': 1, '9030972': 1, '1660365': 1, '12852876': 1, '15634713': 1, '17341554': 1, '3701721': 1, '8006333': 1, '21521324': 1, '11383913': 1, '13211787': 1, '14585081': 1, '21623153': 1, '24251125': 2} | {} |
164,204 | 3830272-1 | 24,251,126 | noncomm/PMC003xxxxxx/PMC3830272.xml | Precocious puberty: A blessing in disguise! | A 9.5-year-old boy presented with enlargement of penis and appearance of pubic hair for 1 year and breaking of voice for 6 months. There was no history suggestive of raised intracranial tension and no history of head trauma, radiation exposure, cranial surgery or seizure. He was the first born child of a non-consanguineous union and had a younger brother who was healthy. He had a normal perinatal and developmental history had no history of any central nervous system infection or androgen exposure and his family history was non-contributory.\nOn examination, his height was 124.4 cm (standard deviation score [SDS] – 1.7), weight was 24.8 kg (SDS – 1.3) and his target height was 156.4 cm (SDS – 2.9). Testes were 5 ml in volume each and were firm, symmetric and without any irregularity. SPL was 8 cm and pubic hair was tanner stage 4 []. Examination of other systems including a detailed examination of the nervous system (with fundoscopic examination) revealed no abnormality.\nBiochemical tests showed an elevated testosterone (637 ng/dl) with prepubertal basal luteinizing hormone (LH) (0.128 mIU/ml) and post decapeptyl LH levels (30 min = 0.325 mIU/ml and 60 min = 0.334 mIU/ml) and a bone age of 12 years. Serum β-hCG was elevated (22.47 mIU/ml; normal = non-detectable to 5.3 mIU/ml) while 17-hydroxyprogesterone was normal (1.96 ng/ml). Ultrasonography of the abdomen and testes and chest X-ray were normal. Gadolinium contrast enhanced magnetic resonance imaging (MRI) revealed an ill-defined, heterogenous patchy enhancing lesion in bilateral basal ganglia with minimal compression and contralateral diaplacement of the third ventricle [Figures and ]. Cerebrospinal fluid (CSF) β-hCG was elevated (47.9 miU/ml; normal = non-detectable to 5.3 mIU/ml) but α-fetoprotein was normal (0.02 IU/ml; normal = 0-5.5). The next investigative step entailed a biopsy of the lesion, which could not be done in our institution for logistic reasons.\nHe was diagnosed to have isosexual precocity due to germ cell tumor involving bilateral basal ganglia, which in all likelihood was a germinoma and was referred to a specialty oncology institute. He received conformal radiotherapy following which serum testosterone dropped down to 137 ng/dl and MRI showed a slight decrease in the size of the lesion [].\nThe germ cell tumor was most likely a germinoma considering the age group, location, absence of elevated CSF α-fetoprotein and response to radiotherapy. | [[9.5, 'year']] | M | {'2178773': 1, '34357128': 1, '11862514': 1, '9763338': 1, '2991485': 1, '29682070': 2, '11965648': 1, '16768139': 1, '24251126': 2} | {'5898141-1': 1} |
164,205 | 3830274-1 | 24,251,128 | noncomm/PMC003xxxxxx/PMC3830274.xml | Suppurative meningitis: A life-threatening complication in male macroprolactinomas | A man aged 22, consulted for vomiting and fever. SM diagnosis was confirmed by lumbar puncture and blood cultures. SM was successfully treated by antibiotics. Cerebral MRI showed a PT invading cavernous sinuses, the sphenoid sinus and the brain []. Hormonal assessment [] demonstrated high PRL with gonadotroph deficit. After antibiotics, SM was sterilized. Then, the PT was treated with dopamine agonists that were successful on PRL (25 ng/ml) and on tumor size []. After a follow-up of 7 years, SM never relapsed, although the sellar floor was not surgically repaired. | [[22.0, 'year']] | M | {'1471531': 1, '1814656': 1, '9215279': 1, '18162729': 2, '2187637': 1, '23315667': 1, '11723327': 1, '15018331': 1, '21630035': 1, '25995804': 1, '25932390': 1, '22655691': 1, '19591087': 1, '12356971': 1, '11400039': 1, '4804459': 1, '21113283': 1, '662160': 1, '19555639': 1, '24251128': 2} | {'3830274-2': 2, '3830274-3': 2, '3830274-4': 2, '2694622-1': 1} |
164,206 | 3830274-2 | 24,251,128 | noncomm/PMC003xxxxxx/PMC3830274.xml | Suppurative meningitis: A life-threatening complication in male macroprolactinomas | A 49-year-old man was hospitalized in 2000 for the fourth SM. The previous ones were proved in 1984, 1988 and 1990. Clinical examination confirmed the meningeal syndrome and noticed rhinorrhea. Biochemical analyzes confirmed CSF leak and meningeal infection. The last one was treated successfully by antibiotics. Cerebral MRI showed an invasive and multidirectional PT measuring 47 mm × 40 mm × 30 mm destroying the sella floor and filling the sphenoid sinus []. The PT was secreting PRL []. That one was normalized by bromocriptine and the tumor size was significantly reduced. 13 years after, there was not any SM relapsing. | [[49.0, 'year']] | M | {'1471531': 1, '1814656': 1, '9215279': 1, '18162729': 2, '2187637': 1, '23315667': 1, '11723327': 1, '15018331': 1, '21630035': 1, '25995804': 1, '25932390': 1, '22655691': 1, '19591087': 1, '12356971': 1, '11400039': 1, '4804459': 1, '21113283': 1, '662160': 1, '19555639': 1, '24251128': 2} | {'3830274-1': 2, '3830274-3': 2, '3830274-4': 2, '2694622-1': 1} |
164,207 | 3830274-3 | 24,251,128 | noncomm/PMC003xxxxxx/PMC3830274.xml | Suppurative meningitis: A life-threatening complication in male macroprolactinomas | A man aged 25, with a history of chronic otitis and arrested puberty, was diagnosed as a multidirectional prolactinoma destroying the sella floor and measuring 30 mm × 30 mm × 30 mm []. The PT was responsible for optic atrophy, anterior pituitary insufficiency and diabetes insipidus. Pituitary lesion was diagnosed after SM due to pneumococcal infection. SM was sensitive to antibiotics. Under dopamine agonists PRL was normalized and the tumor volume decreased. After 2 years, there was not any SM relapsing. | [[25.0, 'year']] | M | {'1471531': 1, '1814656': 1, '9215279': 1, '18162729': 2, '2187637': 1, '23315667': 1, '11723327': 1, '15018331': 1, '21630035': 1, '25995804': 1, '25932390': 1, '22655691': 1, '19591087': 1, '12356971': 1, '11400039': 1, '4804459': 1, '21113283': 1, '662160': 1, '19555639': 1, '24251128': 2} | {'3830274-1': 2, '3830274-2': 2, '3830274-4': 2, '2694622-1': 1} |
164,208 | 3830274-4 | 24,251,128 | noncomm/PMC003xxxxxx/PMC3830274.xml | Suppurative meningitis: A life-threatening complication in male macroprolactinomas | A 29-year-old man was sent to our unit for a prolactinoma revealed by epilepsy crises. The PT was very large (68 mm × 50 mm × 50 mm) and multidirectional with an extension to the chiasm, cavernous sinuses, posterior and nasal areas []. He was operated on 3 times in vain. Then he was given dopamine agonists, which normalized PRL and reduced the tumor. After 3 months he had rhinorrhea, then one episode of SM sterilized by antibiotics. SM never relapsed after a follow-up of over 2 years.\nThe shows tumor sizes, hormonal parameters and bromocriptine dose which was used to treat the 4 prolactinomas. | [[29.0, 'year']] | M | {'1471531': 1, '1814656': 1, '9215279': 1, '18162729': 2, '2187637': 1, '23315667': 1, '11723327': 1, '15018331': 1, '21630035': 1, '25995804': 1, '25932390': 1, '22655691': 1, '19591087': 1, '12356971': 1, '11400039': 1, '4804459': 1, '21113283': 1, '662160': 1, '19555639': 1, '24251128': 2} | {'3830274-1': 2, '3830274-2': 2, '3830274-3': 2, '2694622-1': 1} |
164,209 | 3830275-1 | 24,251,129 | noncomm/PMC003xxxxxx/PMC3830275.xml | Microprolactinoma with visual field defect: An unsuspected etiology | A 32-year-old female patient presented to our department with history of headache, oligomenorrhea, and galactorrhoea for 2 years duration. The headache was located in the frontotemporal region with maximal intensity during the morning hours. She denied a history of vomiting, diplopia, or blurring of vision. She gave birth to 2 children with last childbirth about 7 years back. There was no history to suggest thyroid dysfunction, systemic or psychiatric ailment, and drug intake. Examination revealed normal vital parameters with a body mass index of 21.2 kg/m2 and there was no evidence of goiter. Her visual field examination by confrontation tests was apparently normal and she had no neurological deficit. Fundus examination showed mild pallor and was considered normal. Hormonal profile revealed hyperprolactinemia (serum prolactin – 1228 ng/mL) with normal thyroid and gonadal axes evaluation. Dynamic and contrast enhanced MRI study of the sella and pituitary gland showed well-defined intra-sellar mass of 0.8 × 0.4 × 0.6 cm3 over the left side of the pituitary gland without any supra-sellar extension and not in contact with the optic chiasm. There is mild thickening of the pituitary stalk with homogenous hyper-intensity in post-contrast images [Figure –].\nShe was diagnosed as a case of microprolactinoma and managed with 0.5 mg of cabergoline twice weekly. She showed clinical improvement in the form of regular menses and cessation of galactorrhoea. Her headache did not improve as we had expected and we continued her with cabergoline for another 6 months. Her repeat prolactin was normal and she continued to complain of headache and occasional blurring of vision. In view of persisting symptoms, a repeat neuro-imaging was done which revealed pituitary microadenoma (0.6 × 0.5 cm2) as described previously. Visual field examination revealed marked constriction of peripheral vision [] and bilateral early papilledema. Evaluation of the cortical venous sinuses by magnetic resonance venography revealed all patent sinuses. She was considered to have intra-cranial hypertension of obscure etiology and a guarded lumbar puncture was done after giving mannitol and acetazolamide. Her opening CSF pressure was 25-mm Hg and biochemical evaluation of the CSF was normal. She was diagnosed as a case of IIH and treated with acetazolamide along with cabergoline. Her symptoms and headache improved markedly and repeat perimetry showed completely normal visual fields [Figure and ]. During the last follow-up, she is asymptomatic with no headache, visual defect, diplopia, and normal fundus examination. | [[32.0, 'year']] | F | {'18996807': 1, '17857053': 1, '12744365': 1, '20831031': 1, '7148390': 1, '17008839': 1, '24251129': 2} | {} |
164,210 | 3830277-1 | 24,251,131 | noncomm/PMC003xxxxxx/PMC3830277.xml | Diabetes insipidus as a presenting manifestation of Rathke's cleft cyst | A 68-year-old Indian male patient presented with the complaints of generalized malaise, poor appetite, weight loss, headache and polyuria for last 2 months. He had a chronic ill-looking appearance, a dehydrated tongue and dry skin. Urine output was 5000-5500 mL/day with a history of nocturia and craving for cold fluids. No history of head injury, tubercular meningitis, central nervous system infections or chronic drug intake.\nHis physical findings on admission were height 156 cm; body weight, 44.5 kg and body mass index, 18.3. Blood pressure was 100/64 mmHg without postural change and pulse rate, 68/min with a regular rhythm. No edema was noted in his legs or feet. He had scant axillary and pubichair. Neurologic examination including visual field was found to be normal.\nLaboratory findings were as follows: White blood cell count 6400/mm3 (neutrophils 51%, lymphocyte 42%, monocyte 5%, eosinophils 2%, basophils 0%); hemoglobin, 13.4 g/dL; hematocrit, 35.5%; red blood cell count, 3.4 × 106/mm3; and platelets, 3.3 × 105/mm3 Serum sodium was 137 mmol/L; potassium, 3.9 mmol/L; and chloride, 103 mmol/L. Blood urea nitrogen was 12 mg/dL; serum creatinine, 0.8 mg/dL; and uric acid, 6.1 mg/dL. Fasting plasma glucose was74 mg/dL; hemoglobin A1c, 4.9% and serum calcium of 9.4 mg/dL.\nAnterior pituitary function tests revealed panhypopituitarism (serum cortisol 1.8 μg/dL, Adrenocorticotrophic hormone 15.6 pg/mL, total T3 56 ng/mL, total T4 4.2 μg/dL, thyroid stimulating hormone 1.86 mIU/mL, luteinizing hormone 0.8 mIU/mL, follicle stimulating hormone 1.67 mIU/mL, serum testosterone of 122 ng/dL and serum prolactin of 12 ng/mL. Water deprivation test revealed central diabetes insipidus [].\nMagnetic resonance imaging (MRI) revealed [Figures and ] a well-defined sellar-suprasellar lesion, which was heterogenous and mildly hyperintense on T1-weighted images and brightly hyperintense on T2-weighted (T2W) images. Internal well-defined hypointense nodule was also seen on T2W images. No obvious post contrast enhancement was seen. Pituitary tissue was compressed and stalk was central. The mass was abutting chiasma, but no obvious mass effect/compression seen. Findings were highly suggestive of RCC.\nTranssphenoidal surgery with complete excision of the mass was carried out and histopathological examination revealed cyst wall with columnar lining suggestive of RCC. Patient was started on replacement doses of levothyroxine, hydrocortisone tablets and testosterone injections. His symptoms improved and he was doing well in follow-up. Surprisingly his polyuria improved in postsurgical period without vasopressin replacement. | [[68.0, 'year']] | M | {'1545884': 1, '7054442': 1, '26837398': 1, '25431697': 2, '9442498': 1, '11590900': 2, '2002366': 1, '28272259': 2, '26464354': 1, '30097693': 1, '7889113': 1, '24251131': 2} | {'5348207-1': 1, '4531716-1': 1, '4241302-1': 1} |
164,211 | 3830279-1 | 24,251,133 | noncomm/PMC003xxxxxx/PMC3830279.xml | Growth hormone deficiency, secondary hypothyroidism, and empty sella following treatment of childhood macroprolactinoma | A 9-year-old girl presented with headache, nausea, vomiting, and decreased vision of 8 months duration. Automated perimetry revealed bitemporal hemianopia. Evaluation of anterior pituitary function revealed elevated serum prolactin (958 ng/ml), normal cortisol, thyroid function, and insulin-like growth factor 1 (IGF-1) []. Magnetic resonance imaging (MRI) brain (February 2009) showed 30 × 27 × 28 mm sellar mass with predominant suprasellar extension compressing the optic chiasma []. Cabergoline was initiated, initially at 0.5 mg/week increased to 1.5 mg/week over 6 months and continued. There was rapid improvement of symptoms with resolution of headache followed by resolution of nausea and vomiting by 2 months, vision became normal by 8 months of therapy. Revaluation after 10 months of initial diagnosis revealed normal serum prolactin with normal anterior pituitary function []. MRI brain that time (November 2009) showed a 91% reduction in tumor size, now measuring 11.5 × 13.6 × 12.7 mm.\nComplaints of lack of height gain, along with increased weight for 6 months, lead to revaluation in January 2012 (after 3 years of cabergoline therapy). Her height was 131 cm (<3rd percentile, height standard deviation score (SDS): –2.06; target height SDS: –1.4), height velocity 4 cm/year and body mass index (BMI) was 21.9 kg/m2 (85th percentile). Sexual maturity rating was prepubertal. Perimetry was normal this time. Hormonal evaluation revealed, low serum prolactin, secondary hypothyroidism, and growth hormone deficiency []. MRI brain showed complete resolution of pituitary adenoma with empty sella and absent posterior pituitary signal [].\nA diagnosis of complete regression of macroprolactinoma with growth hormone deficiency and secondary hypothyroidism with empty sella was made in an overweight adolescent girl who had received cabergoline for 3 years for macroprolactinoma. Cabergoline was stopped. Levothyroxine was initiated at 50 μg/day. She could not afford growth hormone replacement [Figures and ]. | [[9.0, 'year']] | F | {'15749410': 1, '21793295': 1, '6746860': 1, '15963057': 1, '11012580': 1, '7915824': 1, '9360509': 1, '28529200': 1, '10599692': 1, '24251133': 2} | {} |
164,212 | 3830280-1 | 24,251,134 | noncomm/PMC003xxxxxx/PMC3830280.xml | An interesting case of pituitary adenoma presenting as an invasive nasopharyngeal tumor | A 47-years-old man presented in the otorhinolaryngology department with a 4 month history of chronic left sided nasal obstruction, periodic epistaxis along with pain and difficulty in opening left eye. He also complained of frontal headache. Patient suffered from diabetes mellitus since last 10 yrs and had proliferative diabetic retinopathy in right eye.\nOn examination, patient had frontal sinus tenderness. There was complete third nerve palsy on left side []. Other cranial nerves were not affected. There was no periorbital edema. Ocular examination on right side was normal. There was no blackish discoloration of nasal or palatal mucosa. There was no conductive deafness. Patient was provisionally suspected of having an invasive nasopharyngeal malignancy or rhino-ocular mucormycosis of paranasal sinuses. However, nasal endoscopy revealed sphenoid sinus filled with expansive firm tumor. Biopsy from the mass showed nests and cords of synaptophysin positive cells with uniformly looking nuclei accompanied with necrotic fibro connective tissue consistent with possibility of pituitary adenoma with extensive necrosis. In view of the histopathological diagnosis, magnetic resonance imaging (MRI) of sella was planned and endocrine consultation was done.\nMRI revealed a heterogenous mass lesion in sphenoid sinus extending posteriorly in pituitary fossa with stalk displaced posteriorly and pituitary gland not separately discernible from the lesion. The fat plane between the pituitary gland and lesion was effaced [Figures –]. Upon endocrine evaluation, the patient had evidence of anterior pituitary hypofunction in the form of weakness, easy fatigability, reduced libido, nausea, vomiting, and increased episodes of hypoglycemia. He denied of having polyuria. Thyroid stimulating hormone (TSH) was 0.213 μIU/ml (0.2-5.1μIU/ml) with a free thyroxine (T4) of 0.6 ng/dl (0.95-2.25 ng/dl). Cortisol measured at 8:00 am was 4.93 μg/dl (5-23 μg/dl). His prolactin (PRL) level measured in serial dilutions was 2.0 ng/ml (2.7-17.0 ng/ml). Luteinizing hormone (LH) and Follicle-stimulating hormone (FSH) levels were normal. Transnasal transsphenoidal surgery was planned after optimization of thyroid and adrenal status. Postoperatively hormone supplementation was continued. Histopathological examination confirmed the diagnosis of pituitary adenoma. On immunohistochemistry, the cells were positive for synaptophysin and negative for prolactin, Adrenocorticotropic hormone (ACTH), and growth hormone (GH) markers. So the diagnosis was consistent with chromophobe adenoma of pituitary. | [[47.0, 'year']] | M | {'8666373': 1, '19288176': 1, '2769030': 1, '1548346': 1, '24251134': 2} | {} |
164,213 | 3830281-1 | 24,251,135 | noncomm/PMC003xxxxxx/PMC3830281.xml | Resistant prolactinoma: Is it monoclonal or polyclonal? | In January 2012, a 32-year-old lady was referred to our department for evaluation of a resistant prolactinoma. She presented to a peripheral hospital initially in February 2010 with a history of galactorrhoea and menstrual irregularity of 6 months duration. She complained of occasional episodic headache, not associated with vomiting, seizures, altered sensorium, and visual field defects. There was no history to suggest thyroid dysfunction, systemic or psychiatric ailment, and drug intake. She denied features to suggest a disturbance of any other hormonal axes or similar history in family members. Her initial evaluation revealed normal vital parameters with no evidence of goiter. Systemic examination was normal except for galactorrhoea. Her neurological examination was normal including visual fields and fundus examination. Hormonal profile revealed hyperprolactinemia (serum prolactin 289 ng/ml) with normal thyroid, adrenal, gonadal, and growth axes evaluation. Magnetic resonance imaging (MRI) sella revealed multiple, small, focal, well-defined, abnormal areas of signal intensity in the anterior pituitary on both sides []. Lesions appear homogeneously hypointense on T2 weighted images with minimal enhancement after contrast. Dynamic mean curve analysis shows slow uptake of contrast with low peak by the lesions suggesting a diagnosis of multiple pituitary microadenomas. There was no pressure effect on surrounding structures. The patient was treated with cabergoline 0.5 mg biweekly and continued for another 6 months. She had regular menstrual cycles and galactorrhoea subsided after 2 months of therapy.\nIn July 2010, the patient had conceived leading to withdrawal of cabergoline therapy. The patient did not have any features of raised intracranial tension throughout pregnancy and neuroimaging was not repeated for monitoring. She had an uneventful pregnancy and delivered a healthy baby at term. Nine months after delivery she presented with headache and occasional vomiting. Serum prolactin was elevated (158 ng/ml) and the patient underwent repeat neuroimaging. On dynamic and contrast enhanced MRI, pituitary gland appears heterogeneously bulky macroadenoma of 12 × 14 × 15 mm predominantly involving the right half of the anterior pituitary []. The lesion had a mixed pattern of contrast uptake and had no pressure effects on the surrounding tissue. The repeat hormonal panel revealed the normal function of anterior and posterior pituitary. Visual field examination by perimetry was normal and other hematological/biochemical parameters were normal including lipid profile. She was diagnosed to be a case of macroprolactinoma and was treated with cabergoline 0.5 mg weekly. The prolactin level normalized after 3 months with no recurrence of galactorrhea. However, repeat neuroimaging after 6 months did not show any resolution in the size of the pituitary macroadenoma. She continued to receive cabergoline and had no clinical features of hyperprolactinemia or pressure symptoms. | [[32.0, 'year']] | F | {'25884948': 1, '1988594': 1, '14674720': 1, '16705142': 1, '16299401': 1, '8100831': 1, '28766078': 1, '11081204': 1, '27347184': 1, '20058099': 1, '24251135': 2} | {} |
164,214 | 3830284-1 | 24,251,138 | noncomm/PMC003xxxxxx/PMC3830284.xml | Tale of two rare diseases | A 20-year-old male born of consanguineous union, resident of urban Kolkata presented with lack of development of secondary sexual characteristics. The patient was full term normal delivery with uneventful antenatal period. The neonatal period was uneventful, but history of hospitalization in infancy due to respiratory illness from which patient apparently recovered, although no past medical records could be retrieved. Growth development milestones were normally attained. There was history of hyposmia. There was no history of poor scholastic performance or other any systemic disease. On examination, height was 170 cm (97th percentile), arm span was 169 cm upper segment/lower segment ratio was 0.76, and body mass index (BMI) was 21. Facial features were normal except for high-arched palate []. Sense of smell tested on graded dilution of spirit revealed hyposmia. There was also synkinesis and bilateral horizontal nystagmus. Sexual maturity scores showed micropenis (stretched penile length (SPL) 4.6 cm); small testes (bilateral < 2 ml); [] gynecomastia; and absence of facial, axillary, and pubic hairs. Systemic examination was normal. Bone age as calculated from Greulich and Pyle chart was delayed at 14 years []. Total testosterone was <10 ng/dl (265-800). On investigation, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) values from three pooled sample were 0.25 mIU/ml (1.7-8.6) and 1.25 mIU/ml (1.5-12.4), respectively. Morning cortisol was 7.99 μg/dl. Thyroid stimulating hormone (TSH) and free thyroxine (T4) were 3.60 μIU/ml (0.27-4.2) and 1.12 ng/dl, respectively. Stimulated LH values after 100 μg of aqueous tryptorelin inj. subcutaneously was 11.42 mIU/ml. Magnetic resonance imaging (MRI) of hypothalamo-pituitary region revealed normal olfactory bulb [], but shallow olfactory sulcus []. Audiometry showed no sensorineural deafness. Two dimensional (2-D) echocardiography did not reveal any cardiac anomaly. Ultrasound of abdomen does not reveal any visceral organ anomaly. Karyotype revealed two cell lines: One showing deletion of chromosome 13 at band 13p10.8 and another showing trisomy 13 with homologous Robertsonian translocation []. As LH rise was pubertal, patient was put on follow-up for puberty onset. | [[20.0, 'year']] | M | {'21097773': 1, '9237504': 1, '19021638': 1, '17761590': 1, '11297579': 1, '21977150': 1, '16757108': 1, '23220825': 1, '24251138': 2} | {} |
164,215 | 3830285-1 | 24,251,139 | noncomm/PMC003xxxxxx/PMC3830285.xml | Epiphora and proptosis as a presenting complaint in acromegaly: Report of two cases with review of literature | A 37-year-old female was referred by Ophthalmologist to our endocrine unit with a presumptive diagnosis of acromegaly. She had primary complaints of increased watering from both eyes for the past 4 years, which increased on lying down and on exposure to sunlight. There had also been gradual protrusion of both the eyes (left > right) for the past 2-3 years. She had shown to multiple ophthalmologists earlier without much respite with the therapy. She had also received ayurvedic medications with no relief. The Ophthalmologist took note of her change in physical features and referred to the endocrine unit with a presumptive diagnosis of acromegaly.\nShe had noticed changes in physical appearance with gradual changes in face, feet and hands for the past 4 years. There had also been mild generalized headache for the past 3 years. She had been amenorrheic for 7 months. She had developed hypertension 2 years back. Examination revealed an average built female with body mass index - 25.6 kg/m2. There was frontal bossing, bulbous lips, prognathism, macroglossia, thickened skin of palms and feet and skin tags on the neck. Systemic examination was normal.\nEye examination revealed axial proptosis in the left eye with normaloculor motility and visual equity in both eyes. Lacrimal gland was enlarged in both eyes (left > right) []. Schirmer's test was normal.\nLab evaluation revealed normal hemogram, liver function and kidney function tests. Fasting and postprandial blood glucose levels were in the diabetic range (201 mg/dl and 220 mg/dl respectively) and lipid profile was deranged (T. cholesterol - 208 mg/dl, high density lipoprotein - 46 mg/dl, low density lipoprotein - 122 mg/dl, very low density lipoprotein - 40 mg/dl and triglycerides - 207 mg/dl). Hormone profile showed normal thyroid function test (TFT) and cortisol. Prolactin levels were 52.4 ng/ml and S. testosterone was low with normal luteinizing hormone (LH) and follicle stimulating hormone (FSH) levels (S. testosterone - 1.75 nmol/l, LH - 2.8 mIU/ml and FSH - 3.7 mIU/ml). Basal and post-glucose GH levels were elevated (0 h - 69.5 ng/ml, 1 h post-glucose GH - 358 ng/ml).\nMagnetic resonance imaging (MRI) brain showed a moderately enhancing sellar mass (1.6 cm × 2.2 cm × 2.3 cm) with extension into suprasellar cistern and left cavernous sinus causing left internal carotid artery encasement suggestive of pituitary macroadenoma.\nMRI orbit revealed proptosis left eye with bilateral lacrimal gland enlargement [Figure and ]. | [[37.0, 'year']] | F | {'15266156': 1, '22011505': 2, '28508245': 1, '1302139': 1, '7934281': 1, '17308965': 1, '2771351': 1, '25233822': 1, '11001823': 1, '13909760': 1, '27492731': 1, '24251139': 2} | {'3830285-2': 2, '3214431-1': 1} |
164,216 | 3830285-2 | 24,251,139 | noncomm/PMC003xxxxxx/PMC3830285.xml | Epiphora and proptosis as a presenting complaint in acromegaly: Report of two cases with review of literature | A 28-year-old female patient presented with the complaints of watery discharge from both the eyes for the past 6 years. Watering from the eyes increased when she was exposed to sunlight and wind. This was associated with upper eyelid pain and a gradual increase in eye enlargement (right > left). She consulted an Ophthalmologist who gave her frequent courses of antibiotics and acetazolamide, but the complaint persisted. For the past 1½ years, she also experienced diminution of vision and a constant headache throughout the day, which was not even relieved by analgesics. She underwent an MRI brain and was diagnosed with pituitary macroadenoma. She was referred to neurosurgery, where a diagnosis of GH secreting tumor was made and surgery performed. She developed transient diabetes perioperatively while on steroids. After the surgery, she was referred to our endocrine unit. Interrogation revealed that she had noticed a gradual weight gain, enlargement of feet (left > right) and coarsening of facial features over past few years. She had been amenorrheic for the past 8 years, after the last child birth. She had been taking thyroxine and steroid supplements post-surgery.\nExamination revealed a 156.5 cm tall, 52.4 kg female with a muscular built and blood pressure-150/80 mm Hg. There was frontal bossing, prominent jaw and bulbous lips. Bilateral hand and feet enlargement along with increased heel pad thickness was noted. Galactorrhea was present. There was swelling of both the upper eyelids and right lower eyelid and proptosis of the right eye []. Investigations revealed normal hemogram, liver and kidney function tests. Her TFTs were normal on thyrox 75 μg. Morning cortisol after stopping steroids for 1 day was 3.6 μ/dl. LH/FSH and estradiol levels (0.07 mIU/ml, 0.50 mIU/ml and 4.1 pmol/l (respectively) were suggestive of hypogonadism. Prolactin levels were 21.7 ng/ml. Post-operative GH levels were high (301 ng/ml). Post-operative MRI brain revealed a sellar mass sized 3 cm × 3 cm × 40 cm with suprasellar extension and B/L cavernous sinus involvement. | [[28.0, 'year']] | F | {'15266156': 1, '22011505': 2, '28508245': 1, '1302139': 1, '7934281': 1, '17308965': 1, '2771351': 1, '25233822': 1, '11001823': 1, '13909760': 1, '27492731': 1, '24251139': 2} | {'3830285-1': 2, '3214431-1': 1} |
164,217 | 3830286-1 | 24,251,140 | noncomm/PMC003xxxxxx/PMC3830286.xml | Transient central diabetes insipidus following ischemic stroke | A 35 years old male, presented with sudden onset left hemiparesis. Over the next 24 h, he developed generalized tonic-clonic seizure and progressive obtundation of sensorium. There was no history of preceding transient ischemic attack, headache, fever, trauma, hypertension or diabetes mellitus. On examination, he was normotensive, stuporous and pupils were equal in size and reaction. He had left sided hemiparesis and extensor plantar reflex bilaterally. Computerised tomography (CT) scan of the brain revealed bilateral frontal, temporopareital and occipital ischemic infarcts with hemorrhagic transformation. Magnetic resonance imaging (MRI) of brain confirmed these findings. [] MR Arteriography (MRA) and venography (MRV) did not show any evidence of vascular thrombosis.\nHe was managed with anti-cerebral edema measures (Mannitol), statins, antiplatelets and supportive care. Over the next two days, he developed worsening level of consciousness due to increasing mass effect. As a life saving measure, decompressive craniectomy with expansile duroplasty was done. Subsequently, he developed increasing urine output (volume 6900 ml, 5525 ml, 5500 ml in 24 h) with corresponding fluid intake of 3000-4000 ml over the next three days and serum sodium levels increased from 136 mMol/l to 145 mMol/l (N 135-144 mMol/l). Urinary spot sodium was 243 mMol/l. Plasma osmolality (calculated) was 294 mOsm/kg (285-295 mOsm/Kg).\nIn view of his neurological status, he was subjected to a limited water deprivation test. Over three hours of absolute water deprivation, all IV and oral fluids were withheld with a close watch over his BP and Urine output. During the test, he passed 775 ml of urine and developed hypotension (BP 90/60 mmHg), due to which the test was aborted and serum and urine samples were taken for osmolality. At the termination of test, he had serum sodium 145 mMol/l, calculated plasma osmolality of 305 mOsm/kg with corresponding Urine osmolality of 357 mOsm/kg (expected >600 mOsm/kg) which confirmed DI. He was started on Desmopressin nasal spray at a dose of 10mcg twice a day. Over the next two days, his daily urine output had reduced to 2 to 3 litres, commensurate with fluid intake. Urine osmolality increased to 685 mOsm/kg with normalization of sodium levels and plasma osmolality. After 5 days of starting Desmopressin, his urine output decreased to 1050 ml and serum sodium levels decreased to 131 mMol/l, when dose of desmopressin was reduced to 10 mcg once a day and subsequently withdrawn in view of persistent hyponatremia. Following withdrawal of desmopressin, he continued to have normal urine output and serum sodium levels. Urine osmolality was 762 mOsm/kg. He regained full consciousness, but had persistent aphasia, facial paresis and bilateral limb weakness (L > R) with bilateral extensor plantars. Other hormone evaluation including thyroid, cortisol, gonadotropins and testosterone were normal. MRI brain did not show any pituitary haemorrhage or necrosis. Posterior pituitary hyperintense (bright spot) was normally seen []. | [[35.0, 'year']] | M | {'22969261': 2, '10536907': 1, '15070961': 1, '24251140': 2} | {'3429832-1': 1} |
164,218 | 3830287-1 | 24,251,141 | noncomm/PMC003xxxxxx/PMC3830287.xml | An unusual cause of progressive quadriparesis | A 55-year-old lady presented with complaints of neck pain for past 1 year and progressive quadriparesis of 2 months duration and was bed ridden at presentation. There was no history suggestive of lower cranial palsies or sphincteric abnormalities. She underwent surgery for multinodular goiter 15 years ago. Clinically, her vital signs were stable and general physical examination was non-contributory. Neurologically she was conscious, alert with involvement of lower cranial nerves (absent gag reflex and wasting of sternocleidomastoid and trapezius). However, there was no facial sensory loss or Horner's syndrome. Motor examination revealed spasticity of all four limbs. Power was grade 2/5 power proximally and 1/5 distally in left upper limb; whereas, it was grade 0/5 in all other limbs and there was weakness of neck and trunk muscles. Graded loss of all modalities of sensation was noted from C3 dermatome downward without sacral sparing. Examination of neck showed a pulsatile swelling in the right retromastoid region, well-healed scar of previous surgery and solitary nodule in the right lobe of the thyroid. Investigations revealed normal hemogram, biochemistry, normal thyroid function with 2.5 cm × 1 cm nodule in the right lobe of thyroid on ultrasonography. Computed tomography of neck revealed a large tumor destroying C1 and part of C2 vertebrae, occupying craniovertebral junction and encroaching into the cervical canal causing severe compromise [Figure and ]. Through posterolateral approach to the craniovertebral junction, decompression with occipito C3 and C4 vertebrae fusion using Magerl's technique was carried out []. Histopathologically, biopsied tissue showed thyroid follicles filled with colloid within skeletal muscle and connective tissue. There were no papillae giving a diagnosis of metastatic follicular carcinoma of thyroid []. She later underwent completion total thyroidectomy and I131 Radioiodine ablation along with external beam radiotherapy of residual neck mass. Histopathological examination of thyroidectomy specimen also confirmed finding of follicular carcinoma of the thyroid in a solitary nodule. At follow-up after 3 months, her spastic quadriparesis still persisted though the power had improved to 4/5 power proximally and 2/5 power distally in all four limbs. | [[55.0, 'year']] | F | {'18310274': 1, '11035572': 1, '20203334': 1, '26623201': 2, '28694601': 2, '24251141': 2} | {'5490351-1': 1, '4641720-1': 1} |
164,219 | 3830290-1 | 24,251,144 | noncomm/PMC003xxxxxx/PMC3830290.xml | Three cases of thyrotoxic periodic paralysis due to painless thyroiditis | A 21-year-old male presented with sudden onset flaccid quadriparesis with no preceding history of fever, dysphagia, dysphonia, diplopia, bladder, or bowel involvement. There was no relation with heavy carbohydrate meal, exercise or diarrhea, and no past history of similar episode.\nExamination revealed lower limb proximal muscle power of 3/5, diminished deep tendon reflexes (DTR) in all four limbs, bilateral flexor plantar responses, no cranial nerve palsy, and no respiratory muscle involvement. Goiter and clinical feature of thyrotoxicosis were absent. Serum potassium was 2.2 mmol/l (normal [nl.] –3.5-5), and ESR 38 mm/h (nl.–1-25). Thyroid function tests (TFT) showed TSH 0.06 μU/l (nl. –0.5–5), free T4 2.4 ng/dl (nl. 0.7–2.0), T3 210 ng/dl (normal –70–190), and TPO antibody 54 IU/ml (nl. <35). 99mTc pertechnetate thyroid scan uptake was 0.15% (nl.–0.4–1%). | [[21.0, 'year']] | M | {'11228188': 1, '17897330': 1, '15666258': 1, '3550012': 1, '16608889': 1, '15166747': 1, '24251144': 2} | {'3830290-2': 2, '3830290-3': 2} |
164,220 | 3830290-2 | 24,251,144 | noncomm/PMC003xxxxxx/PMC3830290.xml | Three cases of thyrotoxic periodic paralysis due to painless thyroiditis | A 35-year-old male presented with sudden onset quadriparesis with a history identical to that of case 1. He had upper limb proximal muscle powers MRC 3/5, distal muscles 4/5, lower limbs proximal, and distal muscles 2/5. Mild respiratory muscle involvement was evidenced by reduced single breath count of 11 seconds. DTR on all limbs were diminished with bilaterally flexor plantar responses and no cranial nerve palsy. He had a grade 1 goiter and no signs of toxicity. His serum potassium was 1.5 mmol/l, ESR 42 mm/h, TSH 0.005 μU/l, free T4 2.5 ng/dl, TPO antibody 68 IU/ml, and decreased uptake (0.1%) on 99mTc scan. | [[35.0, 'year']] | M | {'11228188': 1, '17897330': 1, '15666258': 1, '3550012': 1, '16608889': 1, '15166747': 1, '24251144': 2} | {'3830290-1': 2, '3830290-3': 2} |
164,221 | 3830290-3 | 24,251,144 | noncomm/PMC003xxxxxx/PMC3830290.xml | Three cases of thyrotoxic periodic paralysis due to painless thyroiditis | A 32-year-old male presented with acute onset flaccid paraparesis, tremors of both hands and palpitations. He had a history of transient proximal weakness 6 weeks back which recovered spontaneously. He had no dysphagia dysphonia, bladder, or bowel involvement.\nHe had power 2/5 in proximal muscles, depressed jerks on all four limbs, bilateral flexor plantar responses, and no signs of cranial nerve palsy. He had tachycardia, fine tremors of both hands, and grade1 diffuse goiter. His serum potassium was 1.8 mmol/l, ESR 30 mm/h, TSH 0.03 μU/l, free T4:3.2 ng/dl, TPO antibody 117 IU/ml (nl < 35), and there was decreased uptake (0.21%) on 99mTc scan.\nAll three cases had normal TSH receptor antibodies, serum creatine kinase (CK) and collagen vascular profile. Blood gas analysis in all three patients excluded acidosis. NCV was normal but EMG showed a myopathic pattern with no decremental muscle action potential. In all three cases fine-needle aspiration cytology (FNAC) was consistent with lymphocytic thyroiditis. Based on clinical features and investigations our diagnosis for each patient was thyrotoxic periodic paralysis secondary to painless or silent thyroiditis.\nCase 1 was managed with oral potassium chloride (KCl) at the rate of 0.2-0.4 mmol/kg and propanolol 120 mg/day. Cases 2 and 3 initially required intravenous KCl at 10 meq/h. All showed marked improvement of paralysis within a week of treatment. All patients were discharged after a week with oral propranolol (80-120 mg/day). After 4 weeks of mean follow-up none had any residual paralysis. At the end of 2 months case 1 presented with normal thyroid profile and propranolol was completely withdrawn. At 3 months the thyroid profile became completely normal in cases 2 and 3 and propanolol was stopped. There was no relapse in any of the three cases even at 6-month follow-up. | [[32.0, 'year']] | M | {'11228188': 1, '17897330': 1, '15666258': 1, '3550012': 1, '16608889': 1, '15166747': 1, '24251144': 2} | {'3830290-1': 2, '3830290-2': 2} |
164,222 | 3830291-1 | 24,251,145 | noncomm/PMC003xxxxxx/PMC3830291.xml | Huge bilateral ovarian cysts in adulthood as the presenting feature of Van Wyk Grumbach syndrome due to chronic uncontrolled juvenile hypothyroidism | A 24-year-old woman presented to us with history of secondary amenorrhea, galactorrhea, abdominal pain, and distension of 6 months duration. Detailed inquiry revealed history of prolonged neonatal jaundice, delayed developmental milestones, short stature, and poor scholastic performance since childhood. She attained menarche at age of 7.5 years. She had irregular cycles with duration varying from 30 to 45 days with 4-6 days flow till 6 months back when she developed secondary amenorrhea. Examination was significant for short stature (height: 114.2 cm; <3rd percentile, standard deviation score (SDS)), weight 25.3 kg (<3rd percentile; SDS), subnormal intelligence, facial puffiness, pallor, pedal edema, dry coarse skin, and cold extremities. Thyroid was not palpable. She had spontaneous galoctorrhea from her left breast. Heart sounds were muffled. Abdominal examination revealed a painless palpable cystic mass sized 11 cm × 10 cm involving the whole abdomen []. She had delayed relaxation of deep tendon reflexes.\nInvestigations revealed microcytic hypochromic anemia, elevated serum TSH (>75 μIU/ml), elevated prolactin (>150 ng/ml) with low free thyroxine (T4) and luteinizing hormone (LH). FSH levels were normal. Serum for tumor markers revealed elevated CA-125 levels, normal beta human chorionic gonadotropin (HCG), and alpha fetoprotein []. Blood glucose, liver function tests, renal function tests, and electrolytes were normal. Abdominal ultrasonography and computed tomography showed a large uniloculor cystic SOL in right adnexa measuring 119 × 81 × 90 mm and a multicystic SOL in left adnexa measuring 55 × 45 × 49 mm suggestive of ovarian cysts []. The uterus was bulky with thickened heterogeneous cervix. Moderate pericardial effusion was noted on echocardiography. Levothyroxine was started at 50 μg per day which was gradually increased to 100 μg per day over 4 weeks. Last evaluated 12 weeks after the initial diagnosis, there was resolution of pericardial effusion, reduction in size of bilateral ovarian cysts along with normalization of CA-125 levels. | [[24.0, 'year']] | F | {'7829625': 1, '16278261': 1, '7386433': 1, '933529': 1, '3931416': 1, '2483831': 1, '8159386': 1, '19017414': 1, '6434588': 1, '31641642': 1, '24251145': 2} | {} |
164,223 | 3830293-1 | 24,251,147 | noncomm/PMC003xxxxxx/PMC3830293.xml | Restoration of sinus rhythm following levothyroxine treatment in a case of primary hypothyroidism presenting with atrial fibrillation and pericardial effusion | A 72-year-old male presented with palpitations, dyspnea, and chest discomfort. He had episodes of “fast heart beats” for 3 months. He complained of chest pain which was substernal, nonradiating, and throbbing in nature. He had no other positive history suggestive of any other disorder. He smoked 10 cigarettes per day for past 25 years, and denied use of alcohol, caffeine, or drugs. Physical examination was unremarkable except for the irregular heart rate (approximately 130 beats per min) and muffled heart sounds on auscultation. Electrocardiogram [] confirmed AF with rapid ventricular rate, which responded to initial treatment with metoprolol [].\nThyroid function tests revealed a sensitive thyroid stimulating hormone (TSH) concentration of 34.70 μIU/ml (normal: 0.40-4.70 μIU/ml), and thyroxine (T4) of 5.57 μg/dl (normal: 8-12 μg/dl) confirming primary hypothyroidism.\nAnti-thyroperoxidase antibodies were negative. His blood counts, serum electrolytes, and serial cardiac enzymes were normal. Chest X-ray revealed mild cardiomegaly. Transthoracic echocardiography showed normal left ventricular systolic function (ejection fraction of 63%), decreased left ventricular diastolic compliance, and massive pericardial effusion (posterior 17 mm, anterior 13 mm). Right atrial and right ventricle showed 30% collapse during diastole, mild left ventricular hypertrophy was present with no regional wall motion abnormalities.\nPatient was treated with levothyroxine which lead to resolution of symptoms and restoration of normal sinus rhythm. Repeat echocardiography showed no collapse of right atrium and right ventricle during diastole) and mild pericardial effusion (11 mm circumferential). | [[72.0, 'year']] | M | {'17923583': 1, '6133415': 1, '3723796': 1, '9470888': 1, '8885821': 1, '11172193': 1, '24251147': 2} | {} |
164,224 | 3830294-1 | 24,251,148 | noncomm/PMC003xxxxxx/PMC3830294.xml | Subclinical hypothyroidism unmasked by preeclampsia and ascites | The patient was a 39-year-old G4P2 +1 at GA29 +3 who was referred to our center from a private hospital. She presented on account of poorly controlled hypertension, generalized edema, and deranged thyroid function test (TFT). She was admitted to the Obstetrics Department with a blood pressure (BP) of 210/130 mmHg from the referring hospital. There was a history of headache and generalized body swelling of a month's duration but no history of proteinuria. There was no history of seizures or previous history of pregnancy induced hypertension. The diagnosis at admission was severe preeclampsia with intrauterine growth restriction and anhydraminios. She was commenced on intravenous magnesium sulfate and oral antihypertensives.\nEndocrinology review was requested on the same day on account of a deranged TFT result from the referring hospital []. Patient had a TFT done because she was noticed to have an anterior neck swelling at a gestational age of 24 weeks. There was also a history of anterior neck swelling 6 years before presentation which had resolved spontaneously. There were no symptoms suggestive of hypothyroidism or hyperthyroidism in the past or at the time of review neither was there goiter at presentation.\nExamination revealed a conscious young woman who was not pale, anciteric, and acyanosed with periorbital edema and bilateral pitting pedal edema up to the knee. There was no anterior neck swelling. Pulse rate was 84 beats per min, BP was 140/100 mmHg, jugular venous pulse was not raised, and heart sounds were 1 and 2 only. The abdomen was distended with gross ascites demonstrable and uterus was difficult to palpate.\nObstetric ultrasound scan confirmed maternal ascites and anhydramnios with the fetus compressed. There was gross ascites of 2 litres with kidneys and liver being normal in size and echogenicity. No intra-abdominal mass lesion was seen. Intrauterine fetal death was confirmed and the patient was delivered of a macerated stillbirth following induction of labor. Broad spectrum antibiotics were added while urinary protein, her weight, and vital signs were monitored closely.\nReexamination on the third postpartum day revealed generalized edema, generalized sluggishness, slurred speech, and gross ascites. Blood pressure remained elevated and was managed with oral nifedipine retard and alpha methyldopa while diuretics (frusemide and aldactone) were prescribed for generalized edema and ascites. Investigations in the course of admission are reported in []. Ascitc fluid was exudative.\nShe had a repeat TFT, 6 weeks after the first, which was still in keeping with subclinical hypothyroidism []. She was subsequently commenced on levothyroxine at 100 μg per day. Follow-up reviews showed marked reduction in abdominal girth and weight despite significant reduction in the dosage of diuretics prescribed [].\nShe was discharged home on the 20th day of admission with no pedal edema and minimal ascites. Medications at discharge included oral levothyroxine 100 μg daily, nifedipine 40 mg b.d, alpha-methyldopa 500 mg b.d and slow k on account of persistent hypokalemia.\nShe was reviewed at the medical outpatient clinic 34 days after discharge with history of poor adherence to her medications for a few days prior to that visit and poor BP control. Ascites had completely resolved clinically and radiologically, while TFT result showed reduction in TSH value. She however did not return for follow-up visits. | [[39.0, 'year']] | F | {'16891828': 2, '460364': 1, '28083456': 2, '17220693': 1, '12915662': 1, '19121255': 1, '1918846': 1, '22270283': 1, '15416907': 1, '14722150': 1, '24251148': 2} | {'5215814-1': 1, '2729906-1': 1} |
164,225 | 3830295-1 | 24,251,149 | noncomm/PMC003xxxxxx/PMC3830295.xml | Cerebral venous sinus thrombosis with autoimmune thyroiditis | 45-year-old female presented in emergency with complaints of headache since 1 month, vomiting since 1 day, and weakness with numbness and tingling in right half of body since 12 h. Her weakness progressed to quadriparesis overnight. She had no history of fever, head injury, seizures. No history of oral contraceptive use and prolonged immobilization. Her menstrual and obstetric history was unremarkable. On examination she was drowsy and disoriented. On neurological examination, reflexes were present and muscle tone was normal but power was 1/5 on right side and 3/5 in left half of body. Fundoscopy showed papilledema.\nNormal hemogram and renal and liver function tests. Thyroid function tests were suggestive of subclinical hypothroidism T3 - 0.94 ng/ml, T4 - 8.36 μg/dl, TSH - 13.92 mIU/ml. TPO antibodies were elevated (>1,300 IU/ml). Thrombophilia profile including prothrombin time index/international normalized ratio, serum homocysteine (5.6 mol/l), ANA, lupus anticoagulant, IgM and IgG cardiolipin antibodies, and APLA antibodies were negative. USG of thyroid showed bilateral bulky lobes with altered echotexture s/o thyroiditis. FNAC of thyroid nodule showed lymphocytic infiltration consistent with a diagnosis of Hashimoto thyroiditis. CT head showed hyperdensity in the region of superior sagittal sinus. MRI brain showed loss of flow void of superior sagittal and left transverse sinuses with altered signal appearing hyperintense on T1W and fluid-attenuated inversion recovery (FLAIR) images suggesting thrombosis.\nShe was put on heparin and warfarin. Her headache improved after 4 days of treatment and patient was discharged after 7 days with no residual neurological deficit. | [[45.0, 'year']] | F | {'17440013': 1, '18958631': 1, '11158038': 1, '12760187': 1, '28228636': 1, '29026409': 1, '16060915': 1, '11223442': 1, '33999384': 1, '8457331': 1, '16968790': 1, '22616347': 1, '16006731': 1, '14611707': 1, '12535752': 1, '24251149': 2} | {} |
164,226 | 3830296-1 | 24,251,150 | noncomm/PMC003xxxxxx/PMC3830296.xml | Juvenile hypothyroidism presenting with hypertrichosis, multicystic ovaries, and pituitary adenoma | A 6-year-old girl was referred for growth of excessive body hair. She was also suffering from poor height gain for 3 years with gradually increasing dryness of skin and lethargy.\nShe was born at full term, her birth weight was 2.25 kg, and she had normal development milestones and average scholastic performance. She did not have excessive somnolence, cold intolerance, constipation, or headache. There was no history of intake of any medication.\nHer height was 104 cm (5th centile target height 159 cm), her weight was 18 kg, and she had normal body proportions. Her pulse rate was 68/min and blood pressure 84/52 mmHg. She had pallor, dry scaly skin and cold extremities. There was a grade1 goiter. Hypertrichosis was particularly noticeable over the lateral aspects of the limbs, the upper back, and forehead []. Her Tanner's sexual maturation score was B1 and P1 for breast and pubic hair, respectively. External genitalia was unambiguously female.\nShe had normocytic normochromic anemia, hemoglobin 10.8 g/dl (normal 12-14 g/dl). TSH was 146 μIU/ml (normal 0.35-5.5), T342 pg/ml (normal 60-181), T40.6 ng/ml (normal 4.5-12.6). The anti-TPO antibody level was 223.05 IU/ml (normal <5.61 IU/ml) and antithyroglobulin level 135.17 (normal <4.17 IU/ml). Testosterone was 0.11 ng/ml (normal <1 ng/ml), 17-hydroxyprogesterone 0.9 ng/ml (normal <2), dehydroepiandrosterone sulfate (DHEAS) 46 μg/dl (normal 16-96), FSH 0.8 mIU/ml (normal 0.3-2.0), LH 0.39 mIU/ml (normal 0.1-6.0), Prolactin 21.2 μg/l (normal 4.7-23.3).\nRadiological investigations revealed a bone age of 4 years (Greulich and Pyle's atlas). Ultrasonography of the pelvis showed a prepubertal uterus of size 2.2 × 1.1 × 0.9 cm with bilaterally enlarged multicystic ovaries (right ovary measuring 2.03 × 1.29 cm and left ovary 2.75 × 1.5 cm with increased ovarian volume) []. Magnetic Resource Imaging scan of sella revealed a sellar mass of 1.5 × 1.3 × 1.0 cm size. Technetium 99 m thyroid scan showed poor and patchy uptake of radiotracer suggestive of thyroiditis.\nA diagnosis of juvenile hypothyroidism due to autoimmune thyroiditis was made and she was started on a levothyroxine in a dose of 50 μg daily. Dose was uptitrated to 75 μg daily and euthyroid status was established. At 6-month follow-up hypertrichosis had nearly regressed. A repeat USG of pelvic organs showed significant reduction in ovarian size. MRI could not be repeated due to financial constraints. | [[6.0, 'year']] | F | {'11518117': 1, '7829625': 1, '4037863': 1, '14523827': 1, '21966653': 2, '21600802': 1, '13232994': 1, '2919516': 1, '6352766': 1, '8986704': 1, '24251150': 2} | {'3169870-1': 1} |
164,227 | 3830301-1 | 24,251,155 | noncomm/PMC003xxxxxx/PMC3830301.xml | Milk alkali syndrome induced by calcitriol and calcium bicarbonate in a patient with hypoparathyroidism | A 56-year-old male patient was consulted in our polyclinic with a 1 week history of fatigue and general weakness. In medical history, he had been taking calcium carbonate (3.0 g/daily) and calcitriol (1 μg/daily) for idiopathic hypoparathyroidism for 5 years. In his physical examination, pulse rate was 70/min and blood pressure was 130/75 mmHg. Patient's general physical status was well and pathological finding was not found on physical exam. Urinalysis was normal. The pertinent laboratory tests revealed severe hypercalcemia, acute kidney injury and metabolic alkalosis []. Calcium carbonate and vitamin D treatment were stopped. Intravenous normal saline was administered. After 3 days, his symptoms such as fatigue and weakness resolved and serum levels of calcium, blood urea nitrogen and creatinine regressed. | [[56.0, 'year']] | M | {'11464680': 1, '33748167': 1, '8667442': 1, '18334075': 1, '1763670': 1, '17699269': 1, '20453404': 1, '11981051': 1, '7049033': 1, '27184240': 1, '17685088': 1, '24251155': 2} | {} |
164,228 | 3830302-1 | 24,251,156 | noncomm/PMC003xxxxxx/PMC3830302.xml | Resolution of “salt and pepper” appearance of the skull with vitamin D therapy | A 27-year-old male patient, presented with the complaint of pain in legs and difficulty while walking for past 4 months. He also complained of pain and stiffness in the lower back for the same time. Patient could walk only with support for the past 1 month. There was no history of any trauma to the back. No history suggestive of bladder involvement, no positive or negative sensory symptoms. Patient was on antidepressant medication for the last few years and housebound for the past few months. Patient's examination revealed no features suggestive of spinal cord involvement; however, power in both lower limbs was grade four out of five in the proximal and distal muscles. No features suggestive of sensory involvement were seen. His systemic examination was unremarkable.\nInvestigations revealed hemoglobin 14.9 g/dl, total leucocyte count 6800/μl, platelets 212,000/μl, blood urea 20 mg/dl, serum creatinine 0.73 mg/dl, serum sodium 142 mEq/l, serum potassium 3.4 mEq/l, serum chloride 108 mEq/l, serum calcium 9.5 mg/dl, serum phosphorus 2.7 mg/dl, serum alkaline phosphate 2347 U/L, serum albumin 5.1 g/dl. Urine examination was unremarkable. Plasma parathyroid hormone (PTH) was 754.0 pg/ml and serum 25-hydroxyvitamin D3 (25[OH] D3) was 4.60 (normal > 20). His X-ray skull showed salt and pepper appearance [], X-ray pelvis showed loosers zones with marked subperiosteal resorption in the region of pubic rami [], X-ray hand showed resorption of the terminal phalanges with the presence of a cortical cyst in the metacarpal []. X-ray lumbosacral spine showed osteoporotic changes with central collapse of lumbar vertebrae and biconvex disc spaces []. His computerized tomography (CT) neck with contrast was normal, sestamibi scan showed diffuse uptake in the bones, with no evidence of parathyroid adenoma discernible in the parathyroid scan.\nA diagnosis of vitamin D deficiency with a secondary hyperparathyroidism with normocalcemia was made. He was given vitamin D and calcium supplementation and his general condition improved over the next few months. Power in musculature improved with resolution of pain. His serum showed PTH levels, after 9 months, of 59.0 pg/ml and calcium 8.9 mg/dl. X-rays skull, hand and pelvis showed remarkable improvement with resolution of salt and pepper appearance, regression of osteopenic changes and cortical cyst in a span of 11 months [Figures –]. | [[27.0, 'year']] | M | {'22525844': 1, '16608887': 1, '9504937': 1, '16087996': 1, '23365170': 1, '22461123': 1, '11493580': 1, '10919943': 1, '19597681': 1, '22928075': 1, '24251156': 2} | {} |
164,229 | 3830304-1 | 24,251,158 | noncomm/PMC003xxxxxx/PMC3830304.xml | Adult primary hypoparathyroidism: A rare presentation | A 77-year-old female hypertensive and diabetic patient came with complaints of cough with purulent expectoration, shortness of breath (MMRC Grade II), and difficulty in swallowing since 2 days. She had long standing generalized weakness. She was, otherwise, in good general condition and vital signs were Pulse-80 beats/min, regular, BP-130/70 mmHg, RR-30/min, SpO2-96% on room air and Temperature 98.4 degree F. She had mild pallor, and an audible inspiratory and expiratory stridor. All other systems were normal on examination.\nBlood investigation showed low Hb counts (9.8 gms%), raised ESR (102 mm/hr), raised serum creatinine (2.01 mg/dl). Chest radiograph showed mild cardiomegaly with normal lung fields. Bronchoscopy and CT scan showed no intrabronchial obstruction, extraluminal compression of airway or other abnormalities.\nWe evaluated Serum Calcium, Phosphorus, PTH levels in view of age and long standing generalized weakness with non-specific complaints. Investigations revealed parathyroid hormone PTH-3.83 pg/ml(↓) [15-65 pg/ml], Serum Calcium-3.2 mg/dl (↓) [8.4-10.2 mg/dl], Sr. Phosphorus-11.8 mg/dl (↑) [2.4-4.5 mg/dl], S.Mg-1.6 mg/dl [1.5-2.5 mg/dl]. Serum Albumin and Vitamin D levels were normal. No nutritional, familial, congenital, infiltrative or autoimmune cause of hypoparathyroidism was obvious. Patient never had surgery or irradiation of neck.\nIn view of laboratory values showing severe hypocalcemia, hypoparathyroidism, and hyperphosphatemia, we considered the possibility of hypocalcemia induced stridor secondary to idiopathic hypoparathyroidism. Patient was treated with high dose intravenous calcium (Calcium Gluconate) and Vitamin D (Calcitriol) in addition to receiving all supportive treatments. Intake of milk and milk products was restricted in view of hyperphosphatemia. She showed immediate response to above treatment with stridor and dysphagia abating on second day of IV calcium therapy. She was discharged in a stable haemodynamic condition. On discharge, Serum calcium was 8.3 mg/dl, Serum phosphorus was 6.5 mg/dl. | [[77.0, 'year']] | F | {'16548867': 1, '4132913': 1, '1995202': 1, '8456263': 1, '18395169': 1, '20339692': 1, '24251158': 2} | {} |
164,230 | 3830306-1 | 24,251,160 | noncomm/PMC003xxxxxx/PMC3830306.xml | Two unusual cases of severe recalcitrant hypocalcemia due to aminoglycoside-induced hypomagnesemia | A 34-year-old male, diagnosed case of MDR-TB on second line ATT including kanamycin for six months, came to hospital with tingling sensation of both lower limbs and cramps of hand. He had no history of vomiting, diarrhea or oliguria. On examination, he was emaciated, pale, and had bilateral extensive lung parenchymal disease []. His investigation [] revealed hypocalcemia, hypomagnesemia, and hypermagnesuria. After detail study, kanamycin was stopped and magnesium and calcium supplementation was started. Within two weeks of treatment, patient showed improvement both biochemically and clinically. | [[34.0, 'year']] | M | {'5489186': 1, '4340029': 1, '4116993': 1, '1722865': 1, '12189007': 1, '1137260': 1, '31001341': 1, '33535401': 1, '10668849': 1, '24251160': 2} | {'3830306-2': 2} |
164,231 | 3830306-2 | 24,251,160 | noncomm/PMC003xxxxxx/PMC3830306.xml | Two unusual cases of severe recalcitrant hypocalcemia due to aminoglycoside-induced hypomagnesemia | A 46-year-old male, a case of MDR-TB who has stopped treatment twice and now on second line ATT including kanamycin for past one year, came to hospital with generalized tonic-clonic convulsion and altered sensorium. He had no history of headache, vomiting or fever at time of admission. On examination, patient was drowsy; however, rest of neurological examination was normal. He also had bilateral pleural effusion with bilateral lower lobe consolidation []. His investigation [] revealed hypocalcemia, hypomagnesemia, and hypermagnesuria. His treatment was modified, kanamycin was stopped, and magnesium and calcium supplementation was started. Within four weeks of treatment, patient showed improvement both biochemically and clinically. | [[46.0, 'year']] | M | {'5489186': 1, '4340029': 1, '4116993': 1, '1722865': 1, '12189007': 1, '1137260': 1, '31001341': 1, '33535401': 1, '10668849': 1, '24251160': 2} | {'3830306-1': 2} |
164,232 | 3830308-1 | 24,251,162 | noncomm/PMC003xxxxxx/PMC3830308.xml | Diabetes due to recurrent pancreatitis secondary to hypercalcemia due to primary hyperparathyroidism | A 21-year-old woman, presented with acute onset of abdominal pain over epigastric region radiating towards back with vomiting.\nThe patient was overweight with a body mass index (BMI) of 24.8 kg/m2. General physical examination was noncontributory apart from a nodule in the lower pole of right lobe of thyroid gland. No acanthosis nigricans and hirsutism were seen. Her menstrual history was normal. Systemic examinations revealed mild hepatomegaly. However, serum amylase and lipase were high []. Abdominal ultrasonography revealed features suggestive of acute pancreatitis along with left renal calculus. There was no evidence of gall stones. The patient was diagnosed with acute pancreatitis and managed conservatively.\nThe patient's past history shows repeated episodes of abdominal pain over last 3 years, which required hospitalization. There was recurrent history of pain in the flanks and on two occasions she had passed stones while passing urine. Straight X-ray of kidney, ureter, and bladder region showed the presence of renal stones in both the kidneys. There was no history of polyuria and polydipsia. She had a history of constipation. She however did not have any behavioral or mood disorders. The patient was then diagnosed with recurrent pancreatitis and nephrolithiasis.\nDuring the course of pancreatitis she never had any hypocalcemia. On repeated occasion her serum calcium was around 10 mg/dL. Her serum albumin was within normal range. She was detected to have diabetes mellitus with HbA1c 6.9% and was put on insulin.\nLipid profile, liver function, renal function, and thyroid function tests were normal. Prothrombin time was 11.6 s (control 11.5 s) with international normalized ratio (INR) 1.01. Routine urine analysis was also normal. CT scan did not reveal any growth. Further investigation of laboratory parameters, such as serum calcium, albumin, and PTH was abnormal [].\nThyroid ultrasonography showed small, well defined, oval shaped hypoechoic structure just inferior to the lower pole of right lobe of thyroid gland suggestive of parathyroid adenoma or small lymph node [].\nAbdominal contrast-enhanced computed tomography (CECT) showed features suggestive of mild acute pancreatitis with left renal calculus. Magnetic resonance cholangiopancreatography showed chronic pancreatitis with no evidence of biliary obstruction or choledocholithiasis [].\nPatient was diagnosed with PHPT causing hypercalcemia which resulted in nephrolithiasis and recurrent pancreatitis further leading to pancreatic diabetes. | [[21.0, 'year']] | F | {'7499184': 1, '28487796': 2, '5657432': 1, '10222803': 1, '15775837': 1, '21584170': 2, '19335036': 1, '24251162': 2} | {'3079873-1': 1, '5405398-1': 1} |
164,233 | 3830315-1 | 24,251,169 | noncomm/PMC003xxxxxx/PMC3830315.xml | All Madelung deformities are not endocrine | A 13-year-old girl referred to us with a history of deformity of bilateral forearm from the age of 5 to 6 years. There was no history of pain in the joint of hands, trauma to the wrist and no history of similar illness in the family.\nPatient was moderately built and significantly short for her age []. With height of 130 cm (less than 3rd percentile). Upper segment was 69 cm, lower segment was 61 cm, weight of 35 kg and body mass index of 20.71 kg/m2. The arm forearm ratio was 1.78 suggestive of mesomelia. Secondary sexual characteristic Tanner-Whitehouse staging - B4 (breast), P4 (pubic hair), A3 (axillary hair) her elder brother had normal height for age and no any hand deformities and so were her parents.\nInvestigation showed hemoglobin of 12.5 g/dl, liver function test and renal function test were normal Ca++= 9.0 mg/dl alkaline phosphates 260 IU and phosphorus = 3.5 mg/dl. X-ray bilateral wrist showed malformed medial radial epiphysis with dorsal and ulnar shift and with increased length of phalanges suggestive of Madelung deformity []. Patient was evaluated for other causes of Madelung deformity. Her ultrasound abdomen showed no hepatomegaly or splenomegaly and had normal sized uterus and ovary X-ray spine and X-ray elbow were normal []. Her luteinizing hormone = −1.1 mIU/ml follicle stimulating hormone = 2.4 mIU/ml and karyotype was normal as was urine mucopolysaccharide screening.\nBased on the history, clinical examination, and investigations findings, the final diagnosis of LWD as a cause of Madelung deformity was made. | [[13.0, 'year']] | F | {'1402266': 1, '14344358': 1, '3361203': 1, '10749976': 1, '16650979': 1, '17922307': 1, '24251169': 2} | {} |
164,234 | 3830316-1 | 24,251,170 | noncomm/PMC003xxxxxx/PMC3830316.xml | An unusual case of episodic quadriparesis | A 29-year-old male, presented with the complaint of sudden onset weakness of all four limbs since last night. History was negative for unusually high carbohydrate intake, excessive exertion or alcohol intake in the previous night. He also denied symptoms of unexplained sweating, tremors, heat intolerance, prolonged vomiting or any drug intake over a prolonged period of time. He had a preceding history of muscle cramps and paresthesia for about a month. Past history dates back in the year 2002, which revealed that the patient had similar mode of presentation. Subsequently, he had been admitted in a local hospital and improved symptomatically with conservative therapy. This episode repeated 1 year back and he was treated in the similar way. However, the details of further treatment history could not be gathered. Neurological examination revealed bilaterally symmetrical weakness (Gr 2/5) of all four limbs and generalized hyporeflexia with bilaterally flexor plantar response. Eyes, face, tongue, pharynx, larynx, diaphragm and sphincters were not involved. Higher functions, cranial nerves and sensory system were intact.\nThe present investigations revealed serum potassium: 4.3 mEq/L (reference range: 3.5-5), corrected calcium: 13 mg/dl (8.5-10.5), phosphate: 2.6 mg/dl (3-5) and alkaline phosphatase: 216 U/L (80-306). All other electrolytes were within the normal limit. Routine blood examinations, complete hemogram, creatinine, thyroid function tests, serum creatine phosphokinase, serologic viral markers and serum protein electrophoresis did not reveal any abnormality. Further evaluation of muscular weakness by electromyography was normal. Nerve conduction velocity study was also normal. However on examination of the abdomen by ultrasonography, multiple renal calculi were found in both kidneys. X-ray abdomen reassured the evidence of bilateral nephrolithiasis. On further plan, serum immunoassay for parathyroid hormone value was found to be 147 pg/ml (reference range: 10-69) and 25-hydroxy vitamin D value was 25 ng/dl (reference range: 11.1-42.9). T score at wrists had evidence of osteopenia (~1.0). His serum calcitonin was normal (7.4 pg/ml) (reference range: <5) and 24 h urinary calcium excretion reported as high (396 mg) (reference range <300). Though, Technetium 99m (99m TC) sestamibi scan [] could not confirm the possible etiology but ultrasound and computed tomography (CT) scan of neck the evidence of bilaterally enlarged parathyroids [Figures and ]. He was treated with volume correction and supportive measures. He improved dramatically again within 24 h and with the diagnosis of PHPT, he has been planned for surgery. | [[29.0, 'year']] | M | {'2935672': 1, '15256632': 1, '6732192': 1, '7677469': 1, '7875801': 1, '16150247': 1, '527609': 1, '3190071': 1, '24251170': 2} | {} |
164,235 | 3830317-1 | 24,251,171 | noncomm/PMC003xxxxxx/PMC3830317.xml | Rhabdomyolysis: A rare presentation of aldosterone-producing adenoma | A 42-year-old woman presented with acute onset lower limb paralysis associated with severe proximal muscle pain. These symptoms were not associated with respiratory difficulty, dysphagia, dysarthria or sensory symptoms and there was no associated backache, fever, rash or constitutional symptoms. She had a 2 year history of hypertension, which was poorly controlled despite treatment with a combination of nifedipine, atenolol and losartan. She was treated by a general practitioner and at initial diagnosis of hypertension had undergone biochemical evaluation including serum electrolyes, which had been within normal limits. She experienced two similar, but short lasting episodes of weakness in the preceding year, but had not been investigated. Three days prior to admission she had been given Frusemide as add on therapy by her general practitioner due to uncontrolled hypertension. Her blood pressure on admission was 160/100 mmHg. Clinical examination favored an acute onset myopathy with symmetric flaccid paralysis of lower limbs (muscle power - 3/5) with normal muscle power (5/5) in the upper limbs.\nInitial work-up revealed severe hypokalemia (potassium - 2.0 mmol/l) with an elevated creatine kinase (CK) of 11347 IU (16-190) and increased lactic dehydrogenase of 856 IU/l (240-480). Patient's urine was positive for myoglobin with a high urinary myoglobin 4,170 μg/l. Serum creatinine was 130 μmol/l. In addition, patient had high urinary potassium of 19.45 mmol/24 h with metabolic alkalosis (pH - 7.540, HCO3-38 mmol/l, base excess - 15 mmol/l and PCO2-44 mmHg).\nThe other biochemical values on initial evaluation were as follows; serum aspartate aminotransferase - 244 IU/l (up to 35 IU/l); alanine aminotransferase - 193 IU/l (2-40); Sodium - 145 mmol/l; blood urea - 45 mg/dl; calcium - 0.9 mmol/l (1.12-1-32); phosphorus - 2.7 mg/dl (2.7-4.5); magnesium - 1.4 mg/dl (1.58-2.55); fasting blood glucose 110 mg/dl and the total protein was 7.6 g/dl with albumin 3.2 g/dl. Thyroid function tests were normal with a free T4 level of 1.02 ng/dl and thyroid-stimulating hormone 3.2 μIU/ml.\nBased on the above findings, patient was diagnosed as having hypokalemic paralysis and rhabdomyolysis. Treatment was initiated by oral and intravenous supplementation of potassium and after 10 days, muscular strength and CK levels had returned to normal. Conduction studies and electromyography, which were performed after the correction of hypokalemia, were normal.\nThe coexistence of hypertension, hypokalemia with high urinary potassium loss in association with metabolic alkalosis raised the possibility of primary aldosteronism (PA), which lead to further hormonal evaluation. Aldosterone levels were 22,600 ng/dl (normal, 3.6-24.0 ng/dl) and the plasma renin activity (PRA) value was below the detection limit of our method (0.2 ng/ml/h). Aldosterone/renin ratio (ARR) was 113,000 ng/ml per ng/ml/h (<10). Abdominal ultrasound did not reveal adrenal lesions, but abdominal computed tomography scan showed a 20 mm × 16 mm hypodense mass in the medial limb of the right suprarenal gland []. She underwent right sided adrenalectomy and pathological examination of the gland confirmed a 20 mm adrenal adenoma. Post-operatively the patient was normokalemic without spiranolactone and the PRA was 0.52 ng/ml/h; aldosterone was 1.3 ng/dl with a reduced ARR of 2.5 (<20) ng/ml per ng/ml/h. After 4 weeks of discharge, her BP was normal without any antihypertensives and she was normokalemic with normal muscle strength. | [[42.0, 'year']] | F | {'12920439': 1, '17215661': 1, '5032523': 1, '12746276': 1, '33838028': 1, '26413177': 1, '19218772': 1, '15001583': 1, '18552288': 1, '24251171': 2} | {} |
164,236 | 3830318-1 | 24,251,172 | noncomm/PMC003xxxxxx/PMC3830318.xml | Acute adrenal insufficiency due to primary antiphospholipid antibody syndrome | A 44-year-old female patient presented to us with acute abdominal pain associated with giddiness and vomiting. She had a very low blood pressure (80/50 mm of Hg). Systemic examination was normal. Her initial serum cortisol was 20 μg/dl (normal 5-25 μg/dl) [].\nRepeat serum cortisol done 24 h later was 1.3 μg/dl and concurrent plasma adrenocorticotropin hormone was 698 pg/ml (normal 45 pg/ml). These feature confirmed the diagnosis of evolving acute adrenal insufficiency (AAI).\nComputed tomography (CT) scan of the abdomen revealed, bilateral enlarged adrenal glands, the right adrenal showed good enhancement with contrast, whereas the left adrenal showed no contrast enhancement suggesting acute ischemia []. CT Angiography repeated at 48 h showed that the previously enhancing right adrenal also failed to enhance with intravenous (IV) contrast. These findings indicated venous infarction of both adrenal glands [].\nIn view of the acute onset of adrenal insufficiency in an otherwise healthy female we initially considered the possibility of underlying vasculitis. This was however ruled out on subsequent evaluation. Thrombotic work-up revealed prolonged activated thromboplastin time, which didn’t correct with the addition of normal plasma, indicating the presence of a circulating anticoagulant. Her prothrombin time was normal, lupus anticoagulant was positive and anti-cardiolipin antibody level was mildly elevated, 30 GPL units (normal <25 GPL units). Protein C and protein S levels were normal. Based on the above clinical and laboratory findings, this patient was diagnosed to have APS with bilateral infarction of the adrenal glands leading to AAI.\nShe was initially treated with IV steroids and heparin infusion. She was subsequently started on the oral warfarin and the dose was titrated to maintain the international normalized ratio between 2.5 and 3.0. At discharge, her abdominal pain had subsided and her blood pressure had stabilized. She was advised to continue tab. hydrocortisone, tab. fludrocortisone and tab. warfarin. At 3 month follow-up, she remained well. | [[44.0, 'year']] | F | {'12892401': 1, '11953980': 1, '16189171': 1, '10651763': 1, '33738556': 1, '12050123': 1, '22701015': 1, '18932000': 1, '11882732': 1, '24251172': 2} | {} |
164,237 | 3830320-1 | 24,251,174 | noncomm/PMC003xxxxxx/PMC3830320.xml | Adrenal incidentaloma: A case of pheochromocytoma with sub-clinical Cushing's syndrome | A 42-year-old female patient was admitted under Department of Gastroenterology with abdominal pain for 1 week. Physical examination was unremarkable. Routine biochemical evaluation including complete blood count, renal function tests (including serum electrolytes) and liver function tests were normal. Abdominal computed tomography (CT) revealed a right supra-renal mass (40 mm × 39 mm × 40 mm), which was heterogeneously enhancing with multiple cystic areas and a homogenously enhancing solid component within the anterior limb of the right adrenal gland. Left adrenal gland was normal []. As per the CT findings, right-sided adrenal adenoma with the possibility of pheochromocytoma was suspected.\nOn endocrine assessment, she had a complaint of intermittent palpitations and headache for 4 years. There was no history of fractures, muscle weakness, easy bruisability, menstrual irregularity and hirsutism. She was on treatment for hypertension and diabetes for 4 years with an adequate control. She was not on any exogenous steroids. On examination, her height was 155 cm, weight was 60 kg, body mass index was 24.97 kg/m2, blood pressure was 130/80 mmHg and pulse rate was 82/min. There were no cushignoid features and hyperpigmentation of skin [].\nHer endocrine investigations revealed raised 24-h urinary metanephrines and nor-metanephrines with value of 3268 μg/24-h (normal range 52-341) and 4591 μg/24-h (normal range 88-444), respectively; raised 8 a.m. serum cortisol with value of 80 μg/dl (normal range 5-25); and normal plasma aldosterone level of 32.84 pg/ml (normal range 34-273). She had non-suppressible serum cortisol of 56.91 μg/dl and 25.86 μg/dl after 1 mg-overnight dexamethasone suppression test (DST) and 48 h - 2 mg/day DST, respectively.\nAfter pre-operative management with alpha and beta blockers, she underwent laparoscopic right adrenalectomy. During the post-operative period, she was watched for hypotension and hypoglycemia, but the entire course remained uneventful. Repeat 8 a.m. serum cortisol on 1st post-operative day was 11.20 μg/dl and she was started on intravenous hydrocortisone 50 mg tid.\nThe excised mass measured 4 cm × 3.5 cm × 3 cm with weight of 12 g. The Pathologist concluded that the lesion was pheochromocytoma staining positive for chromogranin and synaptophysin with hyperplastic adrenal cortex [].\nPatient was discharged on oral prednisolone 5 mg bid. Two weeks later, she was re-evaluated and her 24-h urinary fractionated metanephrines came out to be in normal range and fasting 8 a.m. serum cortisol level was 10 μg/dl (prednisolone stopped 2-day prior to testing). Prednisolone dose was tapered slowly over 2-month and presently; she is not on any medication and doing well. | [[42.0, 'year']] | F | {'26446319': 1, '21481011': 1, '33644621': 1, '11598859': 1, '19632967': 1, '11134141': 1, '24251174': 2} | {} |
164,238 | 3830321-1 | 24,251,175 | noncomm/PMC003xxxxxx/PMC3830321.xml | Functioning adrenal myelolipoma: A rare cause of hypertension | A 40-year-old man referred to department of endocrinology with adrenal mass and hypertension. He was diagnosed with hypertension 3 years back, initial BP was 180/110 mm Hg, was started on anti-hypertensive treatment. On examination, there were no neurocutaneous markers or marfanoid habitus, no features of Cushing's syndrome, 24-hour urine metanephrines level was 3000 micrograms/day (normal < 900 micrograms/day, the test was done after stopping all interfering drugs). Ultrasonography revealed 9.8 × 8.5 cms well-defined predominantly hyperechoic lesion, faint hypoechogenicity originating from right suprarenal region abutting the upper pole of right kidney and lower surface of right lobe of liver suggestive of right adrenal mass. CECT of abdomen showed 9.8 × 8.5 cm well-defined, well-circumscribed heterogenous hypoattenuated mass lesion noted in right suprarenal region and minimal enhancement on contrast with −80 to −100 HF units of attenuation suggestive of myelolipoma of right adrenal gland []. Baseline hematological and biochemical investigations and urinalysis were normal. Low-dose dexamethasone suppression test was normal.\nIn view of hypertension, adrenal mass, and elevated 24-hour urine metanephrines (>3 times), possibility of pheochromocytoma was considered. Hypertension was brought under control. Patient underwent surgery, and well encapsulated right adrenal tumor (weight: 500 gm) was excised []. Biopsy of specimen was suggestive of adrenal myelolipoma []. Immuno-histochemistry of specimen revealed positive for chromogranin A, suggestive of catecholamine-secreting granules in the tissue [].\nThe patient had remission in hypertension. Metanephrine levels became normal after surgery. The patient is normal at the 3-month follow-up. | [[40.0, 'year']] | M | {'34568440': 1, '23032842': 1, '16864921': 1, '18366886': 1, '19918428': 2, '21740587': 2, '14999547': 1, '32774233': 1, '24251175': 2} | {'3142232-1': 1, '2769438-1': 1} |
164,239 | 3830323-1 | 24,251,177 | noncomm/PMC003xxxxxx/PMC3830323.xml | Primary adrenal insufficiency in case of antiphospholipid syndrome | A 44-year-old lady presented with hemoptysis, cough and shortness of breath. She had a 3-month history of progressive darkening of skin along with weakness, anorexia, nausea and weight loss of 3 kg over 1 month. She had a past history of a first trimester abortion. History of deep vein thrombosis, pulmonary embolism, connective tissue disorder was ruled out. Her body mass index was 18, goiter was absent, she had tachycardia (pulse rate 110/min) and blood pressure was 108/76 mm Hg with postural drop of 26. Pallor and skin and mucosal pigmentation were present.\nOn investigations: Hb 11.6 g%, total cholesterol 10,100 (N 72%, L 23%, E 5%), erythrocyte sedimentation rate:62 (1st h), platelets 86,000, urine R/E normal, Cr 1.1 mg/dl, liver function tests normal, echo normal.\nChest X-ray showed right middle zone opacity. Computed tomography (CT) scan of lungs revealed subpleural consolidation in mid and lower zones of the right lung with ground glass opacity and areas of hemorrhage and filling defect in right descending pulmonary artery. CT pulmonary angiography confirmed right descending pulmonary artery embolism. Duplex scan revealed right superficial femoral vein thrombosis. Renal and adrenal veins were normal in Duplex scan and magnetic resonance angiography (MRA).\nProthrombin time was 13.8 (normal [N] 11.2-14.2), activated partial thromboplastin time 142 s (N 31-42), fibrin/fibrinogen degradation products was raised, lupus anticoagulant and anticardiolipin antibody were markedly positive. Anti-nuclear antibodies, double-stranded deoxyribonucleic acid, anti-neutrophil cytoplasmic antibody and rheumatoid factor were negative. Human immunodeficiency virus and hepatitis serology was negative. Sputum and blood for Bactec culture for acid-fast bacteria and fungus was negative.\nBaseline 8 A.M. cortisol was 2.3 mcg/dL with an adrenocorticotropic hormone (ACTH) of 306 pg/ml. 250 mcg ACTH stimulation test showed a 1-h cortisol level of 2.5 mcg/dL. Thyroid function test was normal, but thyroid peroxidase antibody was 590 mU/ml (normal <35). Follicle-stimulating hormone was 7 mIU/ml CT of adrenals was normal.\nBased on clinical features and investigations our diagnosis was PAI probably of autoimmune nature in a case of pulmonary thromboembolism due to APS along with autoimmune thyroid disease. Our limitations: Antiadrenal antibody not estimated.\nShe was started on hydrocortisone 100 mg three times daily and heparin. She was subsequently discharged on replacement dose of hydrocortisone and warfarin. After 6 months follow-up, the patient did not have further thrombotic episodes and requires replacement hydrocortisone. | [[44.0, 'year']] | F | {'20716147': 1, '20848817': 1, '16189171': 1, '16941999': 1, '28217529': 1, '12640187': 1, '10651763': 1, '31523539': 2, '24251177': 2} | {'6741395-1': 1} |
164,240 | 3830325-1 | 24,251,179 | noncomm/PMC003xxxxxx/PMC3830325.xml | Topical-steroid-induced iatrogenic Cushing syndrome in the pediatric age group: A rare case report | A 5-month-old female was admitted in our hospital for complaint of fever, cough, increased rate of breathing since 1 month. The patient also had a complaint of swelling over face and all over the body since last 2 month.\nOn examination the patient was febrile; tachycardia and tachypnea were also there. Anemia, generalized anasarca, and hepatomegaly were the other significant findings. There were fading rashes present all over the body. Blood pressure in supine position was 84/66 mm Hg, which was above the 95th centile for this age group.\nIn the past the patient had a history of skin infection at 2 months of age after which mother took treatment from a quack who prescribed betamethasone for topical application. Since then she was applying betamethasone ointment on the whole body.\nIn laboratory findings the patient found to have decreased hemoglobin (8 g%), raised total leukocyte count (12,000) with raised polymorphs (80%), abnormal liver function (SGPT-1100, SGOT 700), hyperglycemia (serum glucose 164 mg%), abnormal coagulation profile (INR 1.7), normal renal function and urinalysis.\nSerum cortisol was raised [34.95 mcg/dl (normal 3-5 mcg/dl)] eight times the baseline value for this age;[] a dexamethasone test was negative.\nUltrasound abdomen showed hepatomegaly with minimal ascite; no suprarenal mass was reported. Transcranial ultrasound and neuroimaging of the brain were within normal limits. Dermatology opinion was taken and the patient was diagnosed as seborrhic dermatitis. Treatment was started but unfortunately the child could not be saved. | [[5.0, 'month']] | F | {'31275149': 1, '31334078': 1, '15461763': 1, '34840742': 1, '29606814': 1, '29259830': 2, '33619779': 1, '24251179': 2} | {'5702924-1': 1} |
164,241 | 3830326-1 | 24,251,180 | noncomm/PMC003xxxxxx/PMC3830326.xml | Aromatase inhibitors in male sex | A 15-year-old male presented with macromastia. He had delayed puberty.\nWt - 62.7 kg; Ht - 155 cm; Sexual Maturation Rate (SMR) - G1P1, testes - 3 ml, stretched penile length (SPL) - 5 cm.\nLH - 6.3 IU/L, follicle-stimulating hormone (FSH) - 2.9 IU/L, prolactin (PRL) - 5.1 ng/ml, normal thyroid-stimulating hormone (TSH) and T4.\nTestosterone (T) - 43.8 ng/dl and estradiol (E2) - 9.79 pg/ml. T/E2 = 4.4:1. He was prescribed letrozole 2.5 mg - 3 times/week.\nAfter 6 months of AI therapy:\nWt - 68.8 kg; Ht - 158.5 cm; SMR - G3P3, testes 10 ml, SPL - 6 cm. There was insignificant change in breast enlargement.\nT - 331.62 ng/dl; E2-8.05 pg/ml. T/E2 = 41.2.\nThere was 650% increase in T and 17.9% decrease in E2. | [[15.0, 'year']] | M | {'18426834': 1, '16649968': 1, '33901434': 1, '11792932': 1, '16189252': 1, '17940445': 1, '22579129': 1, '24251180': 2} | {'3830326-2': 2, '3830326-3': 2, '3830326-4': 2} |
164,242 | 3830326-2 | 24,251,180 | noncomm/PMC003xxxxxx/PMC3830326.xml | Aromatase inhibitors in male sex | A 14-year-old male was referred for obesity. He had delayed puberty.\nWt - 66.6 kg; Ht - 158 cm; SMR - G1P1, SPL - 4 cm.\nLH - 3.59 IU/L; FSH - 2.48 IU/L; PRL - 13.8 ng/ml, normal TSH and T4.\nT - 25.81 ng/dl; E2 - 141.3 pg/ml; T/E2 = 0.18:1.\nHe was prescribed injection T - 100 mg monthly and letrozole 2.5 mg - 3 times/week for 4 months. After 3 weeks of last dose of injection T and 3 days of last dose of letrozlole: Wt - 68.9 kg; Ht - 159.5 cm; SMR-G2P2, SPL ~5 cm.\nT - 310.6 ng/dl; E2 - 13.15 pg/ml; T/E2 = 23.6:1.\nThere was ~1100% increase in T and 90% decrease in E2. | [[14.0, 'year']] | M | {'18426834': 1, '16649968': 1, '33901434': 1, '11792932': 1, '16189252': 1, '17940445': 1, '22579129': 1, '24251180': 2} | {'3830326-1': 2, '3830326-3': 2, '3830326-4': 2} |
164,243 | 3830326-3 | 24,251,180 | noncomm/PMC003xxxxxx/PMC3830326.xml | Aromatase inhibitors in male sex | A 23-year-old male was referred for management of hypogonadism.\nWt - 55.9 kg; Ht - 161 cm; body mass index - 21.6; no anosmia; SMR - G1P1, SPL - 4 cm. LH <0.07 IU/L, FSH - 0.032 IU/L, PRL - 4.93 ng/ml, T - 13 ng/dl.\nHe was prescribed injection T - 100 mg every 3 weeks along with letrozole 2.5 mg - 2 times/week. After 3 weeks of last (4th) injection T and 3 days of last letrozole dose: T - 74 ng/dl.\nThere was 469% increase in T. | [[23.0, 'year']] | M | {'18426834': 1, '16649968': 1, '33901434': 1, '11792932': 1, '16189252': 1, '17940445': 1, '22579129': 1, '24251180': 2} | {'3830326-1': 2, '3830326-2': 2, '3830326-4': 2} |
164,244 | 3830326-4 | 24,251,180 | noncomm/PMC003xxxxxx/PMC3830326.xml | Aromatase inhibitors in male sex | A 27-year-old male was referred for poor semen quality. His total functional sperm fraction (TFSF), denoted by sperm count (×106) by normal morphology (%) by normal motility (%), was 70 × 106/ml × 30% × 30% =6.3.\nT - 257.9 ng/dl; E2 - 35.8 pg/ml; T/E2 = 7.2:1.\nHe was prescribed letrozole - 2.5 mg - 2 times/week.\nAfter 1 month of therapy: T - 754.9 ng/dl; E2 - 28.5 pg/ml; T/E2 = 26.5:1.\nThere was 200% increase in T and 20% decrease in E2.\nTFSF - 80 × 106 × 70% × 30% =16.8. | [[27.0, 'year']] | M | {'18426834': 1, '16649968': 1, '33901434': 1, '11792932': 1, '16189252': 1, '17940445': 1, '22579129': 1, '24251180': 2} | {'3830326-1': 2, '3830326-2': 2, '3830326-3': 2} |
164,245 | 3830327-1 | 24,251,181 | noncomm/PMC003xxxxxx/PMC3830327.xml | Steroid cell tumor not otherwise specified of bilateral ovaries: A rare cause of post menopausal virilization | A 54-year-old gravida two, para two post menopausal woman presented with a 6 month history of progressively worsening facial hair growth and receding hairline. She required daily shaving and was troubled by the excessive loss of scalp hair. There was no history of bleeding per vagina, abdominal pain, or distension. On examination, she had hirsutism with a Ferriman-Gallwey score of 13/36. She had greasy skin and although post-menopausal she had non-atrophic breasts. Pelvic examination revealed clitoromegaly. There were no striae, acne, and bruising or proximal muscle weakness.\nHormonal assessment revealed an inappropriately high serum follicle-stimulating hormone (FSH) level of 1.1 mIU/mL (post menopause >30 mIU/mL), serum luteinizing hormone (LH) level of 3.2 mIU/mL (post menopause >30 mIU/mL), and a serum testosterone level of 7.31 ng/ml (normal 0.4-0.76 ng/mL). Additionally, she had a serum dehydroepiandrosterone sulfate (DHEA-S) level of <15 μg/dL (normal 35-430 μg/dL) and a serum testosterone after dexamethasone suppression of 6.32 ng/ml (not suppressed). The hormone profile demonstrated normal values for serum prolactin, cortisol, thyroid-stimulating hormone, and human chorionic gonadotrophin. Tumor marker CA-125 was 0.55 u/ml (1.9-16.3). Other hematological and biochemical parameters were normal. Imaging by transvaginal ultrasound and computed tomography of abdomen and pelvis revealed no ovarian masses. Thus, ovarian venous sampling was carried out under radiological guidance, but the left ovarian vein cannulation was technically difficult and the procedure was relatively unsuccessful except for revealing that the right ovary was a source of testosterone in this patient [].\nThe patient, therefore, underwent hysterectomy and bilateral salpingo-oophorectomy. During the laparotomy, straw-colored ascitic fluid was evacuated but found to be negative for malignant cells. The right ovary was slightly enlarged (4 × 1.5 × 1.3 cm) showing a slightly elongated, nodular appearance. Left ovary was normal in appearance (3 × 1.6 × 1.4 cm) []. The cut surface of both ovaries showed multiple white spots. There were no peritoneal lesions. Microscopic sections of both ovaries revealed infiltrating islands and cords of tumor cells exhibiting round to oval nuclei and abundant eosinophilic cytoplasm [Figures and ]. There were no features to suggest malignant behavior such as nuclear atypia, hemorrhage, necrosis or increased mitotic activity. Reinke's crystals were not observed. Immunohistochemically, tumor showed intense reactivity to alpha inhibin. Brown-colored pigment was also noted in the cytoplasm []. The final diagnosis was bilateral ovarian steroid cell tumor NOS. Histologically, the tumor exhibited benign characteristics. Tumor was confined to both ovaries whereas bilateral tubes and parametrial tissue were normal. Sections of the uterus revealed inactive endometrium with adenomyosis.\nBy 3 weeks post surgery, her serum testosterone had returned to normal range: 0.38 ng/mL and the clinical signs of hyperandrogenism resolved. She currently remains asymptomatic with normal testosterone levels and imaging at 6 months and 12 months after surgery. | [[54.0, 'year']] | F | {'2823622': 1, '17980097': 1, '24251181': 2} | {} |
164,246 | 3830329-1 | 24,251,183 | noncomm/PMC003xxxxxx/PMC3830329.xml | A rare case report of 46XY mixed gonadal dysgenesis | A 16-year-old person, reared as female, born out of nonconsanguineous marriage, presented to our clinic with complaints of genital ambiguity and primary amenorrhoea along with lack of secondary sexual characters. She underwent reduction clitoroplasty and vaginoplasty on 22/03/2000. There was no h/s/o crisis or cyclical abdominal pain in the past. However, the patient was taking 5 mg of prednisolone after being labeled as a case of congenital adrenal hyperplasia (CAH). No history of recent onset change in sexual identity. Other past history, family history, antenatal history, perinatal history, and developmental history were noncontributory. On earlier evaluations, a small uterus was found on ultrasonogrphy (USG) studies but no gonads were visualized.\nOn examination, anthropometric measurements were appropriate for her age. She was normotensive for her age group. General and systemic examinations were unremarkable. No Turner's stigmata were visualized. Genital examination revealed a single perineal opening, phallic length of 5 cm, with a well-formed glans and a well-formed scrotal sac. Prader staging was 3/5. Sexual maturity rating was A0P1B2. The mucosa above the perineal opening was pink in color.\nRoutine biochemical and hematological investigations were normal. A karyotype analysis revealed 46XY karyotype. There was no evidence of hypocortisolemia (cortisol 9.08 μg/dl, adrenocorticotropic hormone [ACTH] 82.5 pg/ml) or elevated level of 17-OH- progesterone (0.16 ng/ml). Basal testosterone level was 588 ng/dl with basal androstenedione level of 1.83 ng/ml (male: 0.7-3.6, female: 0.3-3.5). Pooled luteinizing hormone (LH) was 11.79 mIU/ml and follicle-stimulating hormone (FSH) was 66.37 mIU/ml. Serum estradiol level was 25 pg/ml (21-251). Basal and 72 h post beta-human chorionic gonadotropin (hCG) levels of androstenedione and testosterone levels were done (basal testosterone of 652 ng/dl and basal androstenedione of 1.17 ng/ml; 72 h post hCG testosterone of 896 ng/dl and androstenedione of 1.34 ng/ml).\nMRI pelvis [] revealed uterus didelphys with obstructed right moiety and bilateral ovarian-like structures.\nThe patient was managed in collaboration with Department of Gynecology and Obstetrics and discussions with patient party and a decision was taken to remove the gonads and Mullerian structures laparoscopically. However at the time of surgery, only right sided gonads and adjacent tubal structures were visualized and removed. However, left sided Mullerian remnants could not be removed due to adhesion to sigmoid colon.\nHistopathological examination [] revealed presence of testicular tissue showing atrophic seminiferous tubules with hyperplasia of Leydig cells. Epididymal tissue and an epididymal cyst are also present. However, no ovarian tissue was seen.\nThe patient is still admitted with us as on the day of writing this manuscript and is being managed with oral estrogens. | [[16.0, 'year']] | F | {'1094776': 1, '34485063': 2, '11305285': 1, '12422582': 1, '2699336': 1, '24581244': 1, '24251183': 2} | {'8384022-1': 1} |
164,247 | 3830330-1 | 24,251,184 | noncomm/PMC003xxxxxx/PMC3830330.xml | All males do not have 46 xy karyotype: A rare case report | A 26-year-old male presented with bilateral gynecomastia for last 6 years with poor development of secondary sexual characters. He was fourth of the siblings and born out of nonconsanguineous marriage with male external genitalia.\nOn examination height was 161 cm, arm spam = 164 cm, upper segment/lower segment (US/LS) ratio = 1.06, weight = 60 kg, midparental height (MPH) =172 cm with a body mass index (BMI) of 23.14 kg/m2, stretch penile length (SPL) = 6 cm, testicular volume (TV) = 2 ml bilaterally, firm in consistency and with Tanner stage IV public hairs, sparse axillary, facial hairs, and gynecomastia.\nOn investigation liver and renal function test were within normal limits. Gonadotrophins (luteinizing hormone (LH) and follicle stimulating hormone (FSH)) value were elevated with low serum testosterone, normal estradiol and thyroid hormones, and ultrasonography (USG) did not reveal any Mullerian derivatives but had small size testis. Semen analysis showed azoospermia and testicular biopsy revealed seminiferous tubules without spermatogenic activity []. Chromosomal analysis of peripheral blood using 72 h stimulated culture with GTG banding revealed 46 XX pattern. Fluorescent in situ hybridization (FISH) by multicolor DNA probe kit (CEP X/Y) showed presence of sex determining region of Y chromosome (SRY) gene locus on X chromosome [ and ]. | [[26.0, 'year']] | M | {'26855499': 1, '16769064': 1, '17579198': 1, '17986281': 1, '16200839': 1, '31650121': 2, '14154995': 1, '22814614': 1, '24251184': 2} | {'6790926-1': 1} |
164,248 | 3830331-1 | 24,251,185 | noncomm/PMC003xxxxxx/PMC3830331.xml | Coexistence of gonadal dysgenesis and Mayer-Rokitansky-Kuster-Hauser syndrome in 46, XX female: A case report and review of literature | A 21-year-old female was evaluated in our clinic because of primary amenorrhea and poor breast development. She is a child of non-consanguineous parents. Her birth event, perinatal and neonatal period were uneventful. Her growth and development were normal with normal intelligence. At the time of presentation, her height was 160 cm and weight 47 kg. On examination, there was no facial dysmorphism, no features suggestive of Turner syndrome like webbing of the neck or wide carrying angle. No skeletal deformity was found. Her blood pressure was 110/70 mmHg in both arms. Her pubic hair and breast development were in tanner 3 stage and there was scanty axillary hair. Genital examination revealed blind vaginal pouch. She had history of seizure at the age of 19 years and she is on antiepileptic medications. Her hemoglobin was 11.2 g/dl with normal differentials. Her renal function tests and liver function tests were normal. Hormonal evaluation showed elevated follicle-stimulating hormone (100 IU/L) and luteinizing hormone (32 IU/L) with undetectable estradiol (<5 pg/ml) and testosterone (<0.1 ng/ml). Her serum thyroid stimulating hormone (2.3 mIU/ml) and cortisone (10 μg/dl) levels were normal. Ultrasound of pelvis did not show uterus or ovaries. Laparoscopy revealed absent of uterus, normal fallopian tubes and streak ovaries. Her computed tomography scan of the brain revealed bilateral periventricular and corona radiata hypointensity with undulation of both lateral ventricles suggestive of ischemic insult, rest of brain parenchyma and pituitary were normal. Her karyotype, obtained from peripheral blood lymphocytes by G-staining, was 46XX (20 cell lines). We obtained ovarian samples during laparoscopy and histopathology of ovarian tissues revealed streak ovaries. We confirmed coexistence of two disorder namely, gonadal dysgenesis and MRKHS in this patient. She was put on ethinyl estradiol 10 μg/day, daily for development of secondary sexual characteristics and bone health. | [[21.0, 'year']] | F | {'19757710': 1, '17718797': 1, '8298739': 1, '28216916': 2, '15550498': 1, '27625567': 2, '14686026': 1, '12433033': 1, '18074363': 1, '12552332': 1, '18182450': 1, '6700887': 1, '30878957': 1, '19213530': 1, '17093891': 1, '10554753': 1, '15037423': 1, '11779614': 1, '6829638': 1, '19213036': 1, '21253547': 2, '27207981': 1, '1271429': 1, '12749067': 1, '7855016': 1, '15550889': 1, '3158739': 1, '4061495': 1, '24251185': 2} | {'5007921-1': 1, '5296832-1': 1, '3021861-1': 1} |
164,249 | 3830332-1 | 24,251,186 | noncomm/PMC003xxxxxx/PMC3830332.xml | Invasive cranial mycosis our experiences | A 56yr old male[], recently detected to have diabetes was admitted in our institute in Hyperglycaemic Hyperosmolar State (serum osmolarity - 347meq/dl) with septicaemia and renal insufficiency. He was treated with intravenous insulin infusion and injectable antibiotics. Within 48 hrs, he became well hydrated and his sensorium improved. His sugars were well controlled. After 3 days, he complained of pain in right eye and right maxillary region. He also developed ptosis [] with complete ophthalmoplegia with dilated fixed pupil on the right side. CT scan head & orbit showed granulomas at right orbital apex. Some destruction of contiguous bone was also reported. He then developed black necrotic area adjacent to nose on right side and there was necrotic mass in right nasal cavity. Patient was taken for emergency surgery and debridement of necrotic mass was done. Mass showed broad, non-septated, ribbon like hyphae with wide angled branching on fresh KOH mount []. Culture later grew mucormycosis. Inj. amphotericin B was started.\nFinal impression was Hyperglycaemic Hyperosmolar State with Mucormycosis. Despite good control of sugars, adequate debridement and antifungal therapy, patient succumbed. | [[56.0, 'year']] | M | {'15523194': 1, '25205894': 1, '20007402': 1, '22408650': 1, '24251186': 2} | {'3830332-2': 2, '3830332-3': 2, '3830332-4': 2} |
164,250 | 3830332-2 | 24,251,186 | noncomm/PMC003xxxxxx/PMC3830332.xml | Invasive cranial mycosis our experiences | A 50yr old male[], who had Type2 Diabetes for last 4yrs was admitted in our institute in 2009. He was very irregular with his treatment and was on indegenous medications for past few days. He had history of frontal headache, dizziness, slurred speech and weakness on left half of body. Ten days back, he became inattentive. He was in Hyperglycaemic Hyperosmolar state with septicaemia. CT scan head revealed large (5-6cm) discrete, irregular peripheral ring- enhancing necrotic lesion in right frontoparietal region of brain causing mass effect & midline shift with perifocal edema []. Neurosurgical intervention was done and 8ml of thick viscous black fluid, which was mainly caseous, was aspirated. The material was analysed. Microscopic examination revealed Langerhans giant cells with moniliform septated hyphal elements and tentative diagnosis of chronic granulomatous inflammation with super added fungal infection was made. On culture growth was observed after 1 week & morphologically classified as Rhinocladiella Mackenzie []. For the management of the case,\ninsulin infusion was given along with injectable amphotericin B and Antitubercular drugs. Despite this therapy patient's condition continued to deteriorate & he sucummed within 2 weeks of diagnosis. | [[50.0, 'year']] | M | {'15523194': 1, '25205894': 1, '20007402': 1, '22408650': 1, '24251186': 2} | {'3830332-1': 2, '3830332-3': 2, '3830332-4': 2} |
164,251 | 3830332-3 | 24,251,186 | noncomm/PMC003xxxxxx/PMC3830332.xml | Invasive cranial mycosis our experiences | A 55yr old male who was known case of T2DM, was admitted in our institute in 2011. He had history of trauma to face on left side. CT scan brain and face was done, which revealed fracture of whole left maxillary sinus, left ethmoid sinus & bilateral sphenoid sinus with left peri-orbital edema. His lab investigations showed high blood sugars and leucocytosis. Renal function and urine routine were normal. After some days, patient developed swelling over face which specially involved left side. Black area was present around left eye. Scraping was done, sent for KOH 10% mount. It showed fungal hyphae, which were non - septate. Culture grew Mucormycosis. He was put on insulin infusion and injectable Amphotericin B. Later, extensive surgical debridement including enucleation of left eye ball and facial reconstruction of left side was done [ and ]. Patient responded to treatment and was discharged after 6 weeks. | [[55.0, 'year']] | M | {'15523194': 1, '25205894': 1, '20007402': 1, '22408650': 1, '24251186': 2} | {'3830332-1': 2, '3830332-2': 2, '3830332-4': 2} |
164,252 | 3830332-4 | 24,251,186 | noncomm/PMC003xxxxxx/PMC3830332.xml | Invasive cranial mycosis our experiences | A 27yr old non-diabetic male was admitted in our institute in 2013 with chronic kidney disease (urea- 172.5mg% & creatinine- 8.5mg%), metabolic acidosis, septicemia and normocytic normochromic anaemia. He had noticed ptosis in right eye since one day []. On examination, Ocular movements were restricted in right eye suggestive of involvement of 3rd, 4th and 6th cranial nerve and papilledema was present. Black discoloration was present over right nasal region. His right palate showed a white patch which later turned to black []. MRI brain and orbit showed mucosal thickening in right maxillary and ethmoid sinus. Tissue was sent for culture and biopsy. Immediate 10% KOH mount was done, which came positive for fungal filaments []. Culture report later confirmed Mucormycosis. Patient was put on haemodialysis. He did not give consent for debridenment and further management. Unfortunately, the attendents took the patient home against medical advice []. | [[27.0, 'year']] | M | {'15523194': 1, '25205894': 1, '20007402': 1, '22408650': 1, '24251186': 2} | {'3830332-1': 2, '3830332-2': 2, '3830332-3': 2} |
164,253 | 3830333-1 | 24,251,187 | noncomm/PMC003xxxxxx/PMC3830333.xml | Re-emergence of a rare syndrome: A case of mauriac syndrome | A 15-year-old Type 1 diabetic boy was referred to us for evaluation of short stature. He was diagnosed to have T1DM, following an episode of diabetic ketoacidosis (DKA) 8 years back, and was started on premix (30/70) insulin. He was irregular with the treatment, with 4 hospitalisations for DKA till date.\nExamination showed that he was significantly short for his age, height 131 cms (less than 3rd percentile), weight 28 kg (less than 3rd percentile) and body mass index of 16.31. Secondary sexual characteristic A1, P1, testicular volume less than 4 ml bilaterally. He had abdominal fat deposition [Figures and ] and liver was palpable clinically 5 cms below costal margin [] with no splenomegaly or free-fluid. There were no signs of chronic liver failure.\nInvestigations showed haemoglobin of 13.5 gm/dl. Liver function tests, renal function tests, and urine routine examination were normal. Ultrasound abdomen showed liver enlargement 15.5 cms with increased echotexture, with normal spleen and portal vein and no free-fluid. On evaluation for diabetic status, he had an HbA1c of 10.3%, urine microalbumin 70 μg/gm of creatinine, and fundus showing background diabetic retinopathy. He had a bone age of 10.2 years, (Tanner Whitehouse 2) thyroid-stimulating hormone (TSH) of 2.4 mIU/ml and T4 of 8.8 microgm/dl. His growth hormone (GH) stimulation test and overnight dexa methasone suppression test were normal (after blood glucose control and testosterone priming).\nBased on the clinical history and investigations, the final diagnosis of Mauriac syndrome was made and the patient was advised tight control of sugars. He was switched over to basal bolus regime, with Glargine in the night and three doses of short-acting insulin before meals. He was follow-up for 6 months. He had shown reduction in hepatomegaly and a height gain of 3 cms. After that he was lost to follow-up. | [[15.0, 'year']] | M | {'30013788': 2, '7047112': 1, '33867669': 1, '30616577': 2, '22689598': 1, '14456773': 1, '29527255': 1, '33927961': 2, '874671': 1, '24251187': 2} | {'6041848-1': 1, '6322227-1': 1, '8076427-1': 1, '8076427-2': 1} |
164,254 | 3830335-1 | 24,251,189 | noncomm/PMC003xxxxxx/PMC3830335.xml | Erroneous glucose recordings while using mutant variant of quinoprotein glucose dehydrogenase glucometer in a child with galactosemia | A 2-month-old male child was admitted to our hospital for jaundice and failure to thrive. The child was the first child born of a third degree consanguineous marriage. His birth weight was 3.5 kg. At 1 month of age, the child was noticed to have a yellowish green discoloration of the conjunctiva. The parents reported feeding difficulties and poor weight gain. His current weight was 2.8 kg. He was anemic, icteric and had hepatomegaly. The liver function tests revealed a cholestatic pattern. Admission arterial blood gas was suggestive of compensated metabolic acidosis with a high anion gap. His urine examination revealed ketonuria. Upon admission, random capillary glucose was performed, which revealed a value of 310 mg/dL [].\nSubsequent readings taken every hour for the next 6 h were above 250 mg/dL. Capillary glucose testing was performed using Accu-Check\n® Performa (Roche diagnostics, Mannheim, Germany) glucometer. In view of suspected diabetic ketoacidosis, an endocrinology consultation was sought and hydration and insulin infusion were considered. However, the corresponding random venous plasma glucose was 67 mg/dL (performed using glucose oxidase method) and there was an absence of glucosuria. Hence, it was decided to withhold insulin infusion and potentially fatal hypoglycemia was avoided. In view of a possible cross reaction of high galactose with the glucometer, which employs a MutQ-GDH chemistry further testing was not performed using the same glucometer. A Benedict's test of urine showed the presence of reducing sugars. A quantitative test for galactose-1-phosphate uridyl transferase in whole blood showed a value of 3.85 U/g Hb (normal range 11-41.0 U/g Hb).\nQuantitative test for galactose 1-phosphate in red blood cell was 1.8 mg/dL (normal range 0-1 mg/dL). A liver biopsy revealed macrovesicular steatosis with bile duct proliferation and a fibrosis score of 4/6 [].\nThe child was started on a galactose free formula. He showed steady improvement with resolution of jaundice and weighed 4.0 kg on repeat examination 1 month later. | [[2.0, 'month']] | M | {'20351227': 1, '30032338': 1, '28500115': 1, '20879959': 1, '29736696': 1, '15053381': 1, '25519295': 1, '22872934': 1, '24251189': 2} | {} |
164,255 | 3830339-1 | 24,251,193 | noncomm/PMC003xxxxxx/PMC3830339.xml | Yellow palms and soles: A rare skin manifestation in diabetes mellitus | A 41-year-old male presented to the outpatient department with a 1-month history of yellow discoloration of both palms and soles []. He was a known case of diabetes for the last 18 years on oral hypoglycemic agents. On examination he was normotensive and his conjunctiva was not icteric. His lab investigation reveals FBS 187 mg/dl; glycocylated hemoglobin value was 10.6%. The serum bilirubin and thyroid function tests were within normal limits. He did not report ingesting excessive amounts of carotene-rich fruits or vegetables, such as carrots, squash, and green beans. The patient was treated with insulin and metformin medication, and followed up after 2 months. The yellow discoloration of his palms and soles has improved after 2 months []. | [[41.0, 'year']] | M | {'29035185': 1, '20316821': 1, '1224904': 1, '17021324': 1, '24251193': 2} | {} |
164,256 | 3830343-1 | 24,251,197 | noncomm/PMC003xxxxxx/PMC3830343.xml | A change for good may not be always good! An interesting case of recurrent hypoglycaemia | A 62-year-old man presented with fever, cough, dyspnoea, and unintentional weight loss of 3 kgs within 3 months. Chest X-ray revealed some scattered pulmonary shadows for which a CT scan of chest was planned. During the hospital stay patient developed documented symptomatic and asymptomatic hypoglycaemia almost daily especially in morning hours including two episodes of severe hypoglycaemia for which endocrine opinion was taken.\nOn reviewing the history, the patient was on metformin 500 mg and glimepride 1 mg, each twice a day after meals since 8 yrs. His blood glucose and other metabolic parameters were well controlled on this medication and he was very regular with regards to his diabetic diet and physical exercise. He did regular self blood glucose monitoring with a periodically calibrated glucometer and maintained a good record of his data. He had never been hospitalized for hypoglycaemia or ketoacidosis, so far. The patient had never recorded any severe hypoglycaemic events, so far. However, he noticed that his blood glucose values started to follow a downward trend since last 6 months with an appreciable drop of his fasting capillary blood glucose values by an average of 10-15 mg/dl, despite of regular and relatively liberal diet. Patient also confirmed some of these relatively low values with laboratory plasma glucose values. At this point of time the patient self adjusted his medications by gradually reducing the doses of Oral Hypoglycaemic Agent (OHA) or oral antidiabetic agents. Due to persistent low blood glucose values despite of liberalized diet, he stopped all OHA after 3 months. There was no history suggestive of any renal, hepatic disorder, alcohol consumption, diabetic retinopathy or any other underlying autoimmune disorder. The patient was not on angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) ACEI or ARBs, fluoroquinolones, sulphonamides. He was receiving paracetamol and cefuroxime for his current illness.\nOn examination, patient had a BMI of 23.5 kg/m2. He had no stigmata of chronic kidney disease. However, he had a palpable liver of two finger breadths below the costal margin which was non-tender but there were no other features suggestive of chronic liver disease.\nOn investigation, liver function tests were normal and his serum creatinine was 1.04 mg/dl with a clearance of 88 ml/min. CT scan of the chest performed to diagnose his chest pathology revealed right lower lobe consolidation with multiple pulmonary densities with pleural effusions in both lobes along with a large hypodense mass occupying almost entire right lobe of liver consistent with the provisional diagnosis of hepatocellular carcinoma with pulmonary metastasis, which was confirmed with biopsy [].\nBiochemical tests done during hypoglycaemia (blood glucose 44 mg/dl) showed a serum cortisol level of 36.5 μg/dl, suppressed serum insulin 0.6 IU/ml (3-35 μIU/ml, RIA) and C-peptide level 0.2 ng/ml (0.85-3.3 ng/ml, RIA) with negative serum ketones [], which ruled out endogenous hyperinsulinism. IGF-1 done was normal. In the given clinical scenario, ectopic secretion of big IGF-2 from the tumor mass was suspected but big IGF-2 assay was not available. Hence, a provisional diagnosis of non-islet cell hypoglycaemia as a part of paraneoplastic syndrome due to IGF-2 secreted by hepatocellular carcinoma was made. | [[62.0, 'year']] | M | {'18045950': 1, '16518997': 1, '16909744': 1, '3185662': 1, '24251197': 2} | {} |
164,257 | 3830350-1 | 24,251,204 | noncomm/PMC003xxxxxx/PMC3830350.xml | Conservative management of severe bilateral emphysematous pyelonephritis: Case series and review of literature | A 38-year-old lady with 10 years type 2 diabetes mellitus (T2DM) presented with pain abdomen, fever, nausea, and vomiting for 2 weeks and decreased urine output for 2 days. Investigations revealed pyuria, renal failure, and leukocytosis []. Piperacillin-tazobactam plus linezoid was started empirically. Computerized tomography (CT) abdomen following initially suggestive ultrasonography (USG) revealed severe bilateral EPN (left > right) [] with gas in bilateral renal parenchyma extending into left perinephric and paranephric areas. Urine culture was positive for Klebsiella sensitive to piperacillin. She became afebrile after 3 days. General well-being improved with increase in urine output, reduction in serum urea, and creatinine. Repeat USG done weekly showed improvement in EPN. She was discharged after 5 weeks. Last evaluated, she was doing well 8 months after diagnosis. | [[38.0, 'year']] | F | {'25246841': 1, '34796256': 1, '3289424': 1, '10743706': 1, '9228098': 1, '28242985': 2, '9123695': 1, '2649332': 1, '18203942': 1, '30002786': 1, '10737279': 1, '9112478': 1, '8254788': 1, '2661615': 1, '11096052': 1, '26692672': 1, '3976120': 1, '9165586': 1, '4057396': 1, '26715900': 1, '24251204': 2} | {'3830350-2': 2, '3830350-3': 2, '5317070-1': 1} |
164,258 | 3830350-2 | 24,251,204 | noncomm/PMC003xxxxxx/PMC3830350.xml | Conservative management of severe bilateral emphysematous pyelonephritis: Case series and review of literature | A 36-year-old lady with 8 years of poorly controlled T2DM and three episodes of urinary tract infection in last 18 months presented with high grade fever, vomiting, burning micturation, and prostration for 1 week. Investigations revealed pyuria, renal failure, and leukocytosis []. CT abdomen revealed bilateral EPN (left >> right) with extension of gas into bilateral perinephric and paranephric tissues []. Piperacillin-tazobactam plus linezoid was started, later changed to imipenem-cilastatin as per the culture (E. coli) and antibiogram report. PCD with drain in situ of left kidney was done on day-3 admission leading to drainage of 300 ml pus. She showed rapid clinical improvement. Improvement in EPN was documented by repeated USG. The drain was removed after 6 weeks and patient discharged a week later. | [[36.0, 'year']] | F | {'25246841': 1, '34796256': 1, '3289424': 1, '10743706': 1, '9228098': 1, '28242985': 2, '9123695': 1, '2649332': 1, '18203942': 1, '30002786': 1, '10737279': 1, '9112478': 1, '8254788': 1, '2661615': 1, '11096052': 1, '26692672': 1, '3976120': 1, '9165586': 1, '4057396': 1, '26715900': 1, '24251204': 2} | {'3830350-1': 2, '3830350-3': 2, '5317070-1': 1} |
164,259 | 3830350-3 | 24,251,204 | noncomm/PMC003xxxxxx/PMC3830350.xml | Conservative management of severe bilateral emphysematous pyelonephritis: Case series and review of literature | A 52-year-old lady with 14 years T2DM presented to emergency with fever, nausea, vomiting, decreased urine output, and left flank pain and swelling for 2 weeks. Examination was significant for anasarca, hypotension, and palpable swelling in the left lumbar region. X-ray abdomen was suggestive of EPN of left kidney []. CT abdomen revealed enlarged left kidney with irregular margins, presence of gas, and necrotic tissue which extended into the paranephric areas. Few foci of gas in the collecting system of right kidney were noted []. Fluid resuscitation, ionotropic support, and piperacillin-tazobactam plus linezoid were administered. Investigations [] revealed pyuria, culture from which revealed Klebsiella. She received two sittings of hemodialysis on day-2 and 7. PCD with drain in situ of left kidney was done on day-2 leading to drainage of 200 ml of pus, culture from which revealed E. coli. Both the organisms were sensitive to piperacillin and aminoglycosides. Amikacin was added on day-12 once renal function improved (creatinine: 1.2 mg/dl). The drain was subsequently removed after 8 weeks and patient discharged a week later. | [[52.0, 'year']] | F | {'25246841': 1, '34796256': 1, '3289424': 1, '10743706': 1, '9228098': 1, '28242985': 2, '9123695': 1, '2649332': 1, '18203942': 1, '30002786': 1, '10737279': 1, '9112478': 1, '8254788': 1, '2661615': 1, '11096052': 1, '26692672': 1, '3976120': 1, '9165586': 1, '4057396': 1, '26715900': 1, '24251204': 2} | {'3830350-1': 2, '3830350-2': 2, '5317070-1': 1} |
164,260 | 3830351-1 | 24,251,205 | noncomm/PMC003xxxxxx/PMC3830351.xml | Diabetic neuropathic cachexia in a young female | A 42-year-old house wife (P2 + 0, last child birth 24 years ago) was admitted with complaints of generalized body ache of 1 year duration. It was more at night and progressively increasing in severity. The patient had numbness and severe burning sensation over her feet, ascending rapidly to involve her legs and thighs. It was associated with loss of weight (approximately 8 kg), loss of appetite, nausea, frequent vomiting, and altered bowel habits without history of fever or pain abdomen. She was detected to have diabetic 1 year ago and put on oral hypoglycemic agents (OHAs). There was no history suggestive of any acute diabetic complication. Past medical history was nonsignificant. She had undergone cholecystectomy 2 months back (Histopathological examination (HPE) suggestive of chronic cholecystitis without malignant change). She was amenorrhoic for last 2 months. On admission, she was biochemically euthyroid with normal creatinine phosphokinase (CPK) level, negative antinatriuretic factor (ANF), rheumatoid factor, anti-double stranded deoxyriobonucleic acid (dsDNA), and poor glycemic status (HbA1C 16.9%).\nWeight: 36.5 kg, body mass index (BMI): 15.7 kg/m2, blood pressure (BP): 100/70 mmHg, pulse: 70/min, regular, all peripheral pulses palpable, pallor: +, icterus: nil, edema: nil, goiter: Gr I, acanthosis: absent, muscle function test (MFT): 6/6 b/l, ankle brachial pressure index (ABPI): left 0.9, right 1.0. Fundus was normal. Profound symmetrical wasting was noted in all extremities with associated bilateral weakness more in proximal muscle groups of the lower extremities. Reflexes were symmetrically decreased in all extremities with absent ankle jerks. The gait was unsteady due to muscle weakness and paresthesias. Otherwise, systemic examination was normal.\nHemoglobin (Hb): 9.4; total leukocyte count (TLC): 12,400; differential leukocyte count (DLC): neutrophils (N)-78, lymphocytes (L)-18, monocytes (M)-2, eosinophils (E)-2; erythrocyte sedimentation rate (ESR): 86; adequate platelet.\nRenal and hepatic profile was normal except hypoproteinemia (albumin/globulin (Alb/Glb):2.6/2.2) and hypokalemia. Human immunodeficiency virus (HIV) was nonreactive. Serum protein electrophoresis did not show any monoclonal band. Whole body bone scintigraphy and bone marrow aspiration study were normal. Nerve conduction velocity (NCV) revealed symmetrical distal axonal and demyelinating type of sensorimotor polyneuropathy involving lower limbs more than upper limbs. Computed tomography (CT) scan abdomen suggested hepatomegaly with mildly dilated common bile duct (CBD) (post cholecystectomy) along with suspected stricture ileum along with proximal narrowing. Chest X-ray, CT scan brain, ultrasonography (USG) abdomen, upper gastrointestinal (GI) endoscopy, colonoscopy, Ba meal follow through, CT enteroclysis were normal. | [[42.0, 'year']] | F | {'1563256': 1, '30497111': 2, '3509122': 1, '6625793': 1, '4364389': 1, '24251205': 2} | {'6536903-1': 1} |
164,261 | 3830360-1 | 24,251,214 | noncomm/PMC003xxxxxx/PMC3830360.xml | Can a faulty injection technique lead to a localized insulin allergy? | Patient is a 38-year-old female diagnosed as a case of diabetes mellitus (DM) presented with neuropathic symptoms in a clinic outside our hospital with an initial fasting plasma glucose (FPG): 256 mg/dl, postprandial plasma glucose (PPG): 426 mg/dl. She was put onto inj. premixed insulin (30/70) 12 IU before breakfast and 6 IU before dinner along with metformin 500 mg twice daily after meals (BDPC). A standard 1,200 kCal/day, diabetic diet, and exercise were also advised. She presented to our outpatient department (OPD) 2 months later with a complain of redness and itching at the injection site after administration of insulin (noticed for last 3-4 month after she changed her insulin brand), and burning sensation in both feet specially during the night. She had no family history of DM, no significant past illness (including bronchial asthma), no history of any drug/food allergy. Insulin was administered by her 20-year-old daughter, and she never practiced self-monitoring of blood glucose (SMBG). On examination, her body mass index (BMI) was 22.37 kg/m2, she had no acanthosis nigricans/skin tag. Other general and systemic examinations revealed no abnormality. She had no sensory loss on 10-g monofilament test and normal ankle brachial index (ABI) values. But her insulin injection sites (over abdomen and thighs) showed multiple pigmented areas with small scars and few urticarial patches [Figures and ]. She had no lipoatrophy or lipohypertrophy at the injection site.\nHer investigations revealed complete blood count (CBC) within normal limit, serum (Sr.) creatinine 0.9 mg/dl, Sr. lipid parameters within normal limit, ultrasonography (USG) abdomen was normal, and present glycemic status: FPG = 201 mg/dl and PPG = 310 mg/dl. When her daughter was enquired about the insulin injection technique, she demonstrated a faulty technique. She used to insert the needle horizontally (not vertically) with the plane of skinfold making an intradermal injection instead of a subcutaneous one []. | [[38.0, 'year']] | F | {'2196303': 1, '16375762': 1, '29805817': 2, '3276478': 1, '12974781': 1, '29333459': 1, '28969185': 1, '26843018': 2, '18186805': 1, '24251214': 2} | {'5899865-1': 1, '4801812-1': 1} |
164,262 | 3830975-1 | 24,255,764 | noncomm/PMC003xxxxxx/PMC3830975.xml | Inflammatory Myofibroblastic Tumor of the Urinary Bladder Managed by Laparoscopic Partial Cystectomy | A 17-year-old unmarried nonsmoking female presented with burning micturition, increasing urinary frequency, suprapubic pain, and occasional hematuria for the past 1 year. The patient had no history of fever, pyuria, or flank pain. The results of general and systemic physical examinations were unremarkable. The results of routine hemogram and blood chemistry profiles were within normal limits. Ultrasonography of the abdomen and pelvis revealed a large heteroechoic mass arising from the dome and anterior wall of the urinary bladder. Contrast-enhanced computerized tomographic scans revealed a large, eccentric lobulated heterogeneously enhancing mass sized 8 cm×5 cm×5 cm and arising in the midline from the dome and anterior wall of the urinary bladder (). Cystoscopy showed a broad-based, lobulated growth arising from the dome and anterior bladder wall. Biopsy of the lesion revealed oval to spindle-shaped cells accompanied by lymphocytes, neutrophils, and plasma cells on a myxoid stroma. The spindle cells had a high nuclear: cytoplasm ratio, a scant to moderate amount of eosinophilic cytoplasm, and oval to elongated hyperchromatic nuclei with frequent mitoses. Immunohistochemistry was positive for vimentin, smooth muscle actin, muscle-specific actin, cytokeratin, and anaplastic lymphoma kinase-1 (ALK-1) and negative for desmin (). A diagnosis of IMT was made and LPC was planned.\nThe bowel was prepared 1 day before surgery. A standard transperitoneal four-port technique was used with the patient in a modified lithotomy and 20-degree Trendelenburg position. First, a 12-mm camera port was placed 3 cm above the umbilicus. Two working ports 10 mm on the right side and 5 mm on the left side were placed at the midclavicular line 2 cm below the level of the umbilicus. Another 5-mm port was placed midway between the umbilicus and the symphysis pubis. The bladder was mobilized starting from just above the peritoneal reflection on the anterior abdominal wall and was extended down on both sides in an inverted-V shaped manner. Dissection was carried down to Retzius' space with mobilization of the bladder from all sides. With simultaneous cystoscopic guidance and transillumination, the tumor outline was defined (). Cystotomy was done about 2 cm away from the tumor margin and was carried circumferentially around the tumor leaving a 2-cm healthy margin (). The bladder was closed in two layers with 2-0 polyglactin suture and the specimen was retrieved in an EndoCatch bag (USCC, Norwalk, CT, USA). A Foley catheter and tube drain were placed in the bladder and Retzius' space, respectively. Operative time was 130 minutes and blood loss was 200 mL with no intraoperative complications. The drain was removed on the second postoperative day and the patient was discharged on the fourth day. The catheter was removed on the 10th postoperative day after a cystogram revealed no leaks.\nOwing to the uncertain malignant potential of the IMT, the patient was kept on 3 monthly cystoscopic surveillance and has been free from any recurrence after 22 months of surgery. | [[17.0, 'year']] | F | {'8469507': 1, '16450787': 1, '26566481': 1, '27974989': 2, '30203811': 1, '7445316': 1, '26137047': 1, '16819319': 1, '26880824': 1, '17122505': 1, '32189076': 1, '18707729': 1, '9606801': 1, '28710194': 1, '11473460': 1, '11598176': 1, '10208459': 1, '24255764': 2} | {'5126425-1': 1} |
164,263 | 3830976-1 | 24,255,765 | noncomm/PMC003xxxxxx/PMC3830976.xml | Psoas Abscess Secondary to Renal Tuberculosis in a Middle-aged Woman | A 45-year-old woman presented with dull aching abdominal pain in the right upper quadrant over the past 2 months. The pain was vague in character and nonradiating. She did not complain of fever or chills. There were no gastrointestinal or urological complaints. She had a history of mycobacterial cervical lymphadenitis in her twenties, which had been treated with antituberculous medications for 2 years.\nHer initial blood pressure was 120/70 mmHg and her body temperature was 36.6℃. A physical examination revealed a palpable mass in the right upper quadrant below the lower costal margin without obvious tenderness. No costovertebral angle tenderness was elicited. Initial hematological and biochemical tests showed no remarkable findings, except a decreased hemoglobin level (10.9 g/dL). Neither pyuria nor hematuria was shown in the urinalysis.\nAbdominal plain radiography showed extensive lobulated calcifications on the right renal shadow, suggestive of a tuberculous kidney (). Abdominal computed tomographic (CT) scan better demonstrated calcifications of the right kidney, right upper ureter, and retroperitoneal lymph nodes. There was no functioning parenchyma in the right kidney, and the dilated calyceal spaces were filled with low-attenuation contents. These abscess-like intrarenal collections extended to the right psoas muscle through the right posterior pararenal space. A CT scan showed apparent thick-walled collections measuring 6 cm×4 cm×8 cm in the right psoas muscle (). A percutaneous catheter was placed in the right posterior pararenal space to obtain contents for culture and to drain the abscess. A purulent, light gray material was drained from the catheter; however, no acid-fast bacilli were seen in the pus, and the pus culture yielded no bacteria. The results of polymerase chain reaction (PCR) for Mycobacterium tuberculosis in the pus were also negative. The patient was explored and subjected to a right nephrectomy to surgically remove the infectious source. The remaining psoas abscess, which had degenerated into a hard mass, was also removed. The histopathological examination of the nephrectomized specimen and the specimen from the remaining psoas abscess revealed chronic granulomatous inflammation with caseous necrosis, consistent with tuberculosis (). No acid-fast bacilli were detected by Ziehl-Neelsen staining of the specimens. Postoperatively, the patient took antituberculous drugs for 6 months. The patient is now asymptomatic at 2 years of follow-up. | [[45.0, 'year']] | F | {'7594368': 1, '9002579': 1, '1532700': 1, '4089725': 1, '18836557': 1, '21461285': 1, '12580563': 1, '24255765': 2} | {} |
164,264 | 3830992-1 | 24,255,633 | noncomm/PMC003xxxxxx/PMC3830992.xml | ALK-Positive Renal Cell Carcinoma in a Large Series of Consecutively Resected Korean Renal Cell Carcinoma Patients | The patient was a 44-year-old male. The RCC was incidentally found by ultrasonography during a routine health check-up and radical nephrectomy was done. The patient had no history of sickle cell trait. He was alive, without evidence of disease, 12 years after surgery. | [[44.0, 'year']] | M | {'22343386': 1, '26337274': 1, '31627758': 2, '31905821': 1, '22743654': 1, '33850785': 1, '29415665': 1, '31936678': 1, '11684952': 1, '23196275': 1, '21587085': 1, '32020234': 1, '21076462': 1, '15837991': 1, '23613665': 1, '32102128': 2, '8122112': 1, '31393373': 1, '21494621': 1, '21945349': 1, '21855232': 1, '21213368': 1, '17185414': 1, '19636007': 1, '33526874': 1, '22252991': 1, '20979469': 1, '20979472': 1, '21258247': 1, '27041925': 1, '27225638': 1, '22129856': 1, '21773754': 1, '18923524': 1, '24255633': 2} | {'6798478-1': 1, '7044692-1': 1} |
164,265 | 3830995-1 | 24,255,636 | noncomm/PMC003xxxxxx/PMC3830995.xml | Abdominal Fibromatosis in a Young Child: A Case Study and Review of the Literature | A 15-month-old boy was referred to our surgical department because of a growing mass in the epigastric area. He had no history of trauma prior to the time that the mass was noticed by the parents. The pregnancy, birth, and neonatal history were uneventful, and there was no history of hospitalization or surgery. The child's developmental milestones were within normal limits. Ultrasonography demonstrated a solid and relatively well-circumscribed mass with mild heterogeneous echogenicity, measuring 1.9×0.9 cm. A fine needle biopsy showed proliferation of bland-looking spindle-shaped cells with collagen. A histological diagnosis of benign mesenchymal tumor, such as a neurofibroma, was made. During follow-up, the mass increased rapidly in size, and was excised one year after it was first detected. On gross examination, the tumor was 4.3×4.1 cm and partly circumscribed. The cut surface of the mass was solid and grayish-white without hemorrhage or necrosis (). The tumor was microscopically composed of parallel long fascicles of spindle-cells with a uniform appearance (). The tumor cells had a pale eosinophilic cytoplasm and small, elongated nuclei that were embedded in a variable collagen network, consistent with abdominal fibromatosis (). The edges of the resected mass were infiltrative, and the surgical margins were positive (). Mitotic figures were <1/10 high power fields. No cellular atypia or necrosis was present. Most of the tumor cells were positive for nuclear β-catenin staining (). S-100 protein, estrogen receptor, and progesterone receptor expressions were negative. The patient could not undergo reoperation to remove the remnant tumor because of a difficult abdominal wall reconstruction. One month after the operation, the patient underwent chemotherapy including vinblastine plus methotrexate (MTX) by intravenous bolus infusion. Postoperative ultrasonography at three months showed a suspected recurrence at the abdominal wall, but this was not pathologically demonstrated. Additional chemotherapy and a rework-up were planned. The patient is currently alive and healthy at seven months after the operation. | [[15.0, 'month']] | M | {'10889380': 1, '18778992': 1, '11843943': 1, '9738571': 1, '9486614': 1, '16015632': 1, '3675193': 1, '9336146': 1, '10573349': 1, '10071306': 1, '7595743': 1, '21478276': 1, '2790427': 1, '28819469': 1, '15832090': 1, '3331192': 1, '19950127': 1, '3616218': 1, '24255636': 2} | {} |
164,266 | 3830996-1 | 24,255,637 | noncomm/PMC003xxxxxx/PMC3830996.xml | Cotyledonoid Dissecting Leiomyoma of the Uterus with Intravascular Luminal Growth: A Case Study | A 43-year-old Korean female (gravida 2, para 2) with a three-year history of a palpable abdominal mass was admitted to the gynecology outpatient department. She had a history of two caesarian sections. The patient had been followed up for 12 months. A recent evaluation showed a marked increase in tumor size (up to approximately 8.0 cm) and the presence of abdominal pain. Abdominopelvic computed tomography showed a large enhancing mass measuring 13.0 cm that encased the left adnexa, the uterus, and the left iliac vein (). Omental haziness and small seeding nodules suggested the possibility of seeding carcinomatosis peritonei. Intraoperatively, no collection of pelvic cavity fluid was found. Total abdominal hysterectomy and bilateral salpingo-oophorectomy were performed with removal of the parametrially extended tumor. Grossly, the multinodular mass was dark red, congested and spongy with bulbous protuberances over the extrauterine surface and bilateral broad ligaments (). Contrary to the dark red color of the external surface, the cut surface showed a homogeneous, grayish tan-colored, multinodular, firm trabeculated appearance (). No intravascular growth or invasion was identified on gross examination. Leiomyosarcoma was initially suspected. Microscopically, the excised mass was composed of variably sized multiple nodules, which were surrounded by perinoudular widened hydropic degeneration (). The nodules consisted of fascicles of spindle cells with no cellular pleomorphism, mitotic activity, or coagulation necrosis (). The mass encased the bilateral ovaries and salpinges, which were free from tumor invasion. Intravascular protruding growth was also found (). Immunostaining for CD34 highlighted the endothelial cells of the blood vessels surrounding the foci of the intravascular growth of the leiomyoma (). The spindle cells were positive for muscle-specific actin (IA4, prediluted, Dako, Glostrup, Denmark) and desmin (D33, prediluted, Dako). They were negative for CD10 (56C6, prediluted, Dako). CDL with an intravascular growth pattern was diagnosed. | [[43.0, 'year']] | F | {'22247805': 1, '12483013': 1, '17123108': 1, '22710314': 1, '8944038': 1, '21331771': 1, '27073566': 1, '11205711': 1, '18382364': 1, '11895490': 1, '9176406': 1, '19856670': 1, '34444270': 1, '20402679': 1, '24255637': 2} | {} |
164,267 | 3830997-1 | 24,255,638 | noncomm/PMC003xxxxxx/PMC3830997.xml | Fine-Needle Aspiration Cytology of Low-Grade Cribriform Cystadenocarcinoma with Many Psammoma Bodies of the Salivary Gland | A 90-year-old man presented with a palpable mass on his left postauricular region that had been present for three years. The mass was hard, fixed, and recently increased in size. These symptoms were not accompanied by pain, tenderness, local hotness, or recent weight loss. The patient was healthy for his age and had an unremarkable medical history.\nMagnetic resonance imaging revealed a well-enhanced 5 cm solid mass including a cystic component in the left parotid gland. The margin of the mass was partly ill-defined. Neither regional nor distant metastasis was found on positron emission tomography-computed tomography scan. The initial diagnosis from clinical and radiologic evidence was a metastatic lymph node or a malignant tumor of the parotid gland. FNA of the tumor was performed.\nPapanicolaou-stained smears revealed that tumor cells were arranged both in tight clusters and individually dispersed (). The tumor cells had round or oval nuclei with mild atypia. Most of the tumor cells had fine chromatin without prominent nucleoli, but some had inconspicuous small nucleoli (). The cytoplasm was scant in most of the tumor cells, and numerous naked cells were identified (). Some tumor cells had a polygonal shape with dense opaque cytoplasm, which suggested squamoid differentiation even though no obvious keratin material was noted (), and a few had cytoplasmic vacuoles of various sizes (). Cytoplasmic granules were not found. Inflammatory cells, including lymphocytes, neutrophils, and some macrophages were scattered across the background, and characteristically, numerous psammoma bodies were identified throughout the smears. Most psammoma bodies were present in the background and not connected to the tumor cells, but some of them were surrounded by tumor cells (, inset). Necrosis, mucin, and myxoid stromal components were not found in the background, and only one mitotic figure was noted. In view of these cytologic findings, we considered the possibility of either a malignant tumor of the parotid gland or a metastatic tumor of some other organs, most likely the thyroid gland. The possibility of a metastatic thyroid carcinoma could not be excluded because of the presence of many psammoma bodies, which are unusual findings in FNA of salivary glands. No other findings suggesting a specific type of thyroid carcinoma were identified, and no intra-thyroidal lesion was found in radiological examination. Therefore, we diagnosed a low-grade malignancy of the parotid gland and recommended complete excision of the mass.\nWe surgically removed the parotid gland, which measured 8.5 cm×6 cm×5 cm. On a cut section, a tan to gray solid tumor with a cystic area measuring 5.3 cm×4.5 cm×4 cm was seen. It was relatively well demarcated from the surrounding parotid gland but was nonencapsulated. In the cystic area of the tumor, an intracystic papillary-growing pattern was noted (). Microscopically, the tumor was composed of multilocular cystic lumens in the periphery and solid or papillary proliferation of tumor cells with fibrous stroma in the cystic area (). The cystic lumens were lined by two or more bland tumor cells. In the intracystic solid area, the tumor cells were arranged in papillary, cribriform, and solid patterns (). The cystic lumens were filled with pink secretory materials, including some macrophages. The tumor cells had round to oval nuclei with inconspicuous nuclear atypia and eosinophilic or clear cytoplasm. Mitotic figures were very rare (<1/10 high power fields), and necrosis was absent. Cellular pleomorphisms and prominent nucleoli were not observed, but some small nucleoli were present. Neither perineural nor vascular invasion were present, but focal stromal invasion of the tumor cells into the fibrotic stroma was noted. Numerous psammoma bodies were observed in fibrotic stroma and between the tumor cells (). All these microscopic findings in the surgical specimen were similar to the cytologic findings from preoperative FNA. Immunohistochemically, most tumor cells were positive for S-100 protein (). Smooth muscle actin (SMA) () and p63 () were positive only in the periphery of the cystic lumens and the rims of papillary, cribriform, and solid tumor cell nests, which suggests intracystic or intraductal growth. The Ki-67 proliferation index was less than 5%. Thyroid transcription factor-1 (TTF-1) and thyroglobulin were negative. | [[90.0, 'year']] | M | {'23406647': 1, '8780532': 1, '15252310': 1, '21319326': 1, '20410810': 1, '19697733': 1, '30555776': 1, '32596656': 1, '23042752': 1, '34055815': 1, '23419146': 2, '24255638': 2} | {'3598350-1': 1, '3598350-2': 1} |
164,268 | 3830998-1 | 24,255,639 | noncomm/PMC003xxxxxx/PMC3830998.xml | A Primary Malignant Rhabdoid Tumor in Adult Liver | A 50-year-old male had admitted for further evaluation of large hepatic mass. The hepatic mass was found accidently in ultrasonography. His major symptom was a 7-kg weight loss in one month. No gastrointestinal symptoms were present. He had no history of hypertension or diabetes. The serologic markers for hepatitis were negative. His mother had died due to cholangiocarcinoma. On physical examination of the patient, a spider angioma was detected. In the laboratory tests, aspartate aminotransferase/alanine aminotransferase/alkaline phosphatase were increased at 148/54/1,215 U/L, alpha-fetoprotein (AFP) 166 ng/mL, and carcinoembryonic antigen (CEA) 8.19 ng/mL, but cancer antigen 19-9 was in the normal range at 26.6 U/mL. Computerized tomography (CT) showed a very large multinodular hypoattenuating mass with rim enhancement in the whole left lobe and anterior segment of the right lobe (). Also the common hepatic lymph nodes were increased in size. There was no abnormality in each right of left kidney. On positron emission tomography-CT, a large hypermetabolic mass was seen, encompassing the whole left lobe and the anterior segment of the right lobe ().\nFor diagnostic confirmation, CT-guided needle biopsy was performed. The biopsy cores were composed of hypercellular areas alternating with necrosis and hemorrhage. The cellular lesion showed loosely cohesive tumor cell clusters separated by intermediate fibrous septa. The large round tumor cells showed abundant eosinophilic cytoplasm and eccentric vesicular nuclei with prominent nucleoli (). Abnormal mitoses were frequent. Mucicarmine staining was negative for abundant cytoplasm. The immunohistochemical stains showed diffuse cytoplasmic-positive staining for cytokeratin (CK) 19 and vimentin () and focal positivity for epithelial membrane antigen and CK7. The immunohistochemical stains for hepatocyte antigen, alpha-fetoprotein, CK20, CD34, CD117, actin, desmin, S100, and human melanoma black 45 (HMB45) showed no reaction in tumor cells. Also the tumor cells showed partial loss of positivity for integrase interactor-1 (INI-1) (). | [[50.0, 'year']] | M | {'1700599': 1, '12378463': 1, '9100795': 1, '12518355': 1, '21139471': 1, '24982576': 1, '20035421': 1, '206343': 1, '28427232': 1, '10640148': 1, '16791124': 1, '24255639': 2} | {} |
164,269 | 3830999-1 | 24,255,640 | noncomm/PMC003xxxxxx/PMC3830999.xml | Nesidioblastosis and Pancreatic Non-functioning Islet Cell Tumor in an Adult with Type 2 Diabetes Mellitus | A 43-year-old woman was hospitalized due to fever and right flank pain with a 2-year history of type 2 DM treated with oral hypoglycemic agents. Physical examination indicated right flank knocking tenderness. All laboratory findings were within normal limits, except for an increased white blood cell count in blood and urine, and elevated blood sugar level (201 mg/dL). Abdominal computed tomography showed a right ureteral stone with pyelonephritis. A 3.6 cm-sized cystic lesion in the pancreatic head was found incidentally (). After treating the pyelonephritis, the patient underwent a pylorus-preserving pancreatico-duodenectomy and double Roux-en-Y reconstruction based on a pancreatic cystic tumor, such as a solid pseudopapillary neoplasm or serous cystadenoma. Grossly, the cut surface of the pancreas head revealed a well-demarcated, solitary cystic mass that measured 5.6×3.7 cm and was dark red in color, with a soft cut surface and extensive hemorrhage (). On serial-sectioning, adjacent non-tumor pancreatic tissue appeared normal in gross examination. Histologically, the pancreatic mass was surrounded by a fibrous capsule consisting of nests or trabecular cords of neoplastic cells with extensive hemorrhage and coagulation necrosis (). The neoplastic cells were relatively uniform, with round or irregular nuclei and abundant eosinophilic cytoplasm, and revealed a centrally located round to oval nucleus. The chromatin pattern was characteristically coarsely clumped. Mitoses were very difficult to find. Lymphovascular invasion of the tumor cells was not observed. The neoplastic cells stained diffusely positive for synaptophysin and chromogranin (), but were negative for insulin and glucagon. The proliferation index was very low on the Ki-67 immunohistochemistry stain. Based on the histological and immunohistochemical findings, the tumor was diagnosed as a non-functioning pancreatic neuroendocrine tumor. There were a number of irregularly distributed hyperplastic islets throughout the uninvolved pancreatic parenchyma, and their contour and size were markedly variable (). Many islets were closely associated with pancreatic duct structures (). Hyperplastic islets were characterized by the presence of islet cells showing enlarged hyperchromatic nuclei with pleomorphism (). The majority of these dysplastic islet cells were positive for insulin, but negative for glucagon (). The histology of the non-tumoral pancreatic tissue was compatible with diffuse nesidioblastosis. She remained free of any sign of recurrent tumor and her diabetic symptoms were controlled with oral hypoglycemic drugs for 40 months after surgery. | [[43.0, 'year']] | F | {'15517495': 1, '6257459': 1, '18437091': 1, '18070631': 1, '11570912': 1, '15581742': 1, '17131493': 1, '8388173': 1, '31967075': 1, '11126710': 1, '18931647': 1, '24255640': 2} | {} |
164,270 | 3831000-1 | 24,255,641 | noncomm/PMC003xxxxxx/PMC3831000.xml | Primary Extraskeletal Mesenchymal Chondrosarcoma of the Anterior Mediastinum | A 21-year-old woman visited an outside hospital with the chief complaint of intermittent chest discomfort and respiratory difficulty for 2 months. In the medical history, the patient had taken medication for schizophrenia for several years. On the chest computed tomography (CT) scan, the patient had a 13-cm heterogeneous enhancing mass with multifocal calcification in the anterior mediastinum that invaded the pericardium and was associated with massive left pleural effusion. The mass encased the aortic arch and branch along with the left and main pulmonary arteries, but did not appear to be originating from the osteocartilaginous structures of the thoracic region (). The patient then underwent a CT-guided needle biopsy, for which a diagnosis of solitary fibrous tumor was suggested on a biopsy. Then, the patient was referred to the Dong-A University Medical Center to confirm the diagnosis and undergo further treatment. Although the tumor could not be resected completely due to the extensive invasion into the main vessels, a surgical excision of the mass along with wedge resection of the left upper lung and partial resection of the pericardium was performed. The tumor at the time of surgery was found to invade the pericardium and to be tightly adhered to the left upper lung. However, it could be easily separated from the adjacent ribs. The resected tumor, measuring 13×7.5 cm, was solid, lobulated, and partially covered by a thin fibrous capsule. On the cut section, the tumor was tan white, and soft to fish-flesh, while the lobulated cut surface exhibited focal areas of irregularly sized glistening cartilage and coarse calcification (). Microscopically, the lesion was composed of a highly cellular proliferation of undifferentiated round, oval, or spindle-shaped cells with an abrupt transition with small islands of well-differentiated hyaline cartilage, frequently associated with central calcification and ossification (). In some areas, the undifferentiated cells were separated by branching, sinusoidal vascular channels imparting the lesion with a hemangiopericytoma-like pattern (). Immunohistochemically, the cartilaginous portion of the tumor showed S100 protein positivity, but the undifferentiated cells showed negative immunoreactivity for the S100 protein (). Undifferentiated cells showed strong membranous immunoreactivity for CD99, whereas only isolated cells in the cartilaginous portion stained for CD99 (). The tumor cells exhibited negative immunoreactivities for cytokeratin and CD34. The patient made an uneventful postoperative recovery and was discharged on postoperative day 5 with advice to undergo chemotherapy and local radiotherapy. However, the patient refused any further treatment. The patient is still alive with a residual tumor at the time of writing this report (8 months postoperatively). | [[21.0, 'year']] | F | {'26358060': 1, '9158707': 1, '2242853': 1, '21308446': 1, '26413313': 2, '24255641': 2} | {'4568935-1': 1} |
164,271 | 3831001-1 | 24,255,642 | noncomm/PMC003xxxxxx/PMC3831001.xml | Neuroendocrine Dysplasia Combined in a Tubular Adenoma of Rectum: A Case Report | A 56-year-old female had a chief complaint of frequent loose stools and visited the local clinic in September 2012. The patient did not have any prior gastrointestinal problems. She had a previous surgical history for stress urinary incontinence in 2006, and had received re-operation for small bowel perforation that occurred in the sling operation. She was referred to the Kunkuk University Medical Center, Seoul, Korea for further evaluation. A colonoscopic examination was performed and revealed a large, laterally spreading circumferential mass at the rectum. The mass was greater than 5 cm in size. Due to the clinical suspicion of malignancy, a low anterior resection with extensive lymph node dissection was performed.\nUpon gross examination, a well-circumscribed, slightly elevated circumferential mass was identified in the rectum, measuring 6.0×5.0 cm (). Grossly, the mass was extending to the submucosa, exhibiting a fibrotic appearance with blurring of the muscularis mucosae. The lesion was entirely embedded and fully evaluated.\nHistologically, the elevated lesion was a typical tubular adenoma with low grade dysplasia, showing nuclear stratification and elongation (). Beneath the adenomatous polyp, multiple small cellular nests were observed at the base of the adenomatous polyp (). The cellular nests were clustered forming micronodules, and some of them fused together. At higher magnification, the cellular nests were composed of monotonous cells with eosinophilic, finely granular cytoplasm and stippled chromatin with central nuclei, reminiscent of neuroendocrine cells (). Prominent nucleoli or mitosis were absent or inconspicuous. These cell nests were infiltrating the lamina propria and muscularis mucosae, and some of the cell nests seemed to intermingle with the adenomatous polyp. A desmoplastic reaction was not observed. The endocrine cell clusters were scattered multifocally along the polyp, measuring 3 cm in total diameter. The largest individual neuroendocrine cell nest measured up to 220 µm in its greatest dimension. Twenty-three regional lymph nodes were dissected, but metastatic tumor cells were not identified.\nFor confirmative diagnosis, immunohistochemical staining of the chromogranin, synaptophysin, p53, and Ki-67 labeling index were performed. The cells were diffuse, strongly positive in chromogranin (), and weakly positive in synaptophysin. The chromogranin staining was not only positive in the neuroendocrine cell nests, but also focally positive in the basal cells of the adenomatous polyp. The p53 staining and Ki-67 labeling index were both negative in the neuroendocrine cell nests (). The patient recovered well without any complications, and follow-up colonoscopic examination 3 months after surgery found no evidence of recurrence. | [[56.0, 'year']] | F | {'2871146': 1, '3522394': 1, '32981102': 1, '9647591': 1, '9659277': 1, '3544888': 1, '7731741': 1, '14991503': 1, '17122508': 1, '24255642': 2} | {} |
164,272 | 3831002-1 | 24,255,643 | noncomm/PMC003xxxxxx/PMC3831002.xml | Intravascular Papillary Endothelial Hyperplasia of the Chest Wall Misdiagnosed as a Malignancy on Fine Needle Aspiration | A 75-year-old male underwent a subtotal gastrectomy at 62 years of age. He was diagnosed as a well-differentiated adenocarcinoma confined to the gastric mucosa. He remained in good health until 3 years ago, at which time he noticed a 2 cm asymptomatic mass on the chest wall. The mass was situated 10 cm apart from the previous surgical scar. One week before hospital admission, he experienced pain at the site of the mass and was referred for further evaluation.\nThe clinical condition of the patient was good. Physical examination revealed a firm, smooth, round mass on the anterior chest wall. The size of the mass had not changed since initial presentation. The mass was initially presumed to be a lipoma or epidermal inclusion cyst on physical palpation. However FNA was necessary to rule out a metastatic adenocarcinoma originating from the stomach.\nThe FNA cytology showed low cellular smears containing a few cohesive sheets of polygonal pleomorphic cells with vesicular chromatin, prominent nucleoli, abundant dense cytoplasm, and cytoplasmic vacuoles. Scattered individual polygonal cells were also present in a hemorrhagic background (). Some fibrins were intermingled, and some of the cells showed long cytoplasmic processes suggestive of spindling. Pleomorphic polygonal cells were arranged in alveolar or glandular patterns that were suspected to be metastatic adenocarcinoma.\nThe pathologic findings of the excised mass showed a well-demarcated vascular lesion within the skeletal muscle associated with a hematoma. There was an anastomosing papillary core lined by plump endothelial cells. The papillae contained fibrin-like materials and the endothelial cells were pleomorphic with vesicular nuclei and prominent nucleoli (). Mitotic figures were not observed. The overall cellular features were similar to those observed in the aspirate smears. The cells showed diffuse strong cytoplasmic immunoreactivity for CD34 and factor VIII-related antigen, and were negative for cytokeratin, confirming the diagnosis of intravascular papillary endothelial hyperplasia. | [[75.0, 'year']] | M | {'12827709': 1, '2108526': 1, '21385237': 1, '10086561': 1, '10432892': 1, '16470861': 1, '23661940': 2, '8442671': 1, '22378085': 1, '16299742': 1, '24255643': 2} | {'3643361-1': 1} |
164,273 | 3831016-1 | 24,255,654 | noncomm/PMC003xxxxxx/PMC3831016.xml | A Case of Three Consecutive Events of Acute Myocardial Infarctions in Three Different Vessels | On September 25, 2012, a 51-year-old man visited the emergency room for acute retrosternal squeezing chest pains for the past twelve hours. He had no history of diabetes mellitus, hyperlipidemia, and nor a familial history of coronary artery disease. However, he was a current smoker (30 pack years). He had hypertension and history of two consecutive acute MI.\nThe first acute MI was on February 21, 2000. The electrocardiogram (ECG) showed ST-segment elevations in the inferior leads (II and aVF) and the anterior (V 2-4) leads (). The peak levels of creatine kinase-MB (CK-MB) and troponin T were 31.71 and 2.51 ng/mL. The coronary angiography was performed. The coronary angiography showed a total occlusion with thrombus and Thrombolysis in Myocardial Infarction (TIMI) 0 distal flow in the proximal portion of the left anterior descending from the coronary artery (LAD), which was successfully treated with a bare metal stent (3.0×15 mm, NIR Royal® stent, Boston Scientific Corporation, Natick, MA, USA). In addition, he had taken aspirin 100 mg, atenolol 25 mg, captopril 37.5 mg and simvastatin 10 mg once daily and cilostazol 100 mg twice daily, on a regular basis after the first MI event.\nThe second acute MI was on December 30, 2007. The ECG showed ST-segment elevation in the inferior (II, III, and aVF) leads (). The peak levels of CK-MB and troponin T were 164.7 and 4.01 ng/mL. Emergent coronary angiography was performed. The coronary angiography showed total occlusion with thrombus, with TIMI 0 distal flow in the mid portion of the right coronary artery (RCA), which was successfully treated with a paclitaxel eluting stent (4.0×24 mm, TAXUS®, Boston Scientific Corporation, Natick, MA, USA) (), and a 95% restenosis in a stent with thrombus, and TIMI 0 distal flow in the proximal portion of the LAD, which was successfully treated with a zotarolimus eluting stent (2.75×30 mm, ENDEAVOR®, Medtronic Inc., Minneapolis, MN, USA) and overlapping a sirolimus eluting stent (3.0×23 mm, CYPHER®, Cordis Corporation, Warren, NJ, USA) (). There were no other stents for appropriate lesion lengths and sizes, except ENDEAVOR and CYPHER stents at that time.\nHe had taken aspirin 100 mg, clopidogrel 75 mg, ramipril 2.5 mg and simvastatin 10 mg once daily and molsidomine 2 mg twice daily, on a regular basis after a second MI event.\nAt the third acute MI, physical examination showed that his blood pressure was 90/60 mm Hg, the heart rate was 64/min, and respiratory rate was 20/min. He had a regular heart beat and clear heart sounds without murmurs.\nElectrocardiogram showed Q-wave and ST elevation in the V 1-5 and T-inversion in V 4-6 (). The peak levels of CK-MB and troponin T were 17.84 and 0.741 ng/mL.\nEchocardiographic evaluation revealed aneurysmal changes at the apicoseptal wall in the left ventricle, and ischemic insult in the LAD and the RCA territory. An ejection fraction of 40% was observed.\nEmergent coronary angiography showed a total occlusion with thrombus and TIMI 0 distal flow in the proximal portion of the left circumflex coronary artery and collateral flow from RCA, which was successfully treated with a zotarolimus eluting stent (3.5×22 mm, RESOLUTE INTEGRITY®, Medtronic Inc., Minneapolis, MN, USA) (). After primary percutaneous interventions, the patient became stable without chest pains and was discharged on the fourth hospital day.\nHematological analyses were performed and showed the following results: D dimer 0.38 ug/mL (<0.5 ug/mL), antithrombin III 107% (80-120%), protein C activity 131% (70-130), and protein S activity 90% (70-130). In addition, immunological analyses were performed and indicated the following results: lupus anticoagulant titer 1.01 (0.8-1.2), anti-beta2-glycoprotein1 immunoglobulin G/M titer negative/negative, anti-cardiolipin antibody immunoglobulin G/M titer negative/negative and homocystein 12.33 umol/L (5.08-15.4 umol/L). Further, the platelet drug response assay was also performed and displayed the following results [The results of the assay are reported as absolute P2Y12-Reaction-Units (PRU), as well as percent inhibitions (% inhibition), the latter calculated as 100-(TEST/BASE×100) or {(BASE-TEST)/BASE}×100]: PRU 215 (0-240), % inhibition 31% (20-80). He was discharged after uneventful recovery with triple anti-platelet therapy using aspirin 100 mg and clopidogrel 75 mg once daily and cilostazol 100 mg twice daily. He had also been treated with ramipril 2.5 mg, bisoprolol 2.5 mg and rosuvastatin 10 mg once daily and molsidomine 2 mg twice daily. The patient has been followed-up at the outpatient department without further symptoms. | [[51.0, 'year']] | M | {'10807742': 1, '19949590': 1, '19182293': 1, '19352331': 1, '11152415': 1, '18810723': 1, '10078489': 1, '19419580': 1, '23006996': 2, '22323330': 1, '16610572': 1, '20946992': 1, '16364973': 1, '24255654': 2} | {'3508820-1': 1} |
164,274 | 3831017-1 | 24,255,655 | noncomm/PMC003xxxxxx/PMC3831017.xml | Very Early Onset of Amiodarone-Induced Pulmonary Toxicity | A 54-year-old man was admitted to the hospital with chest pain and ST elevation myocardial infarction. He had no medical history, except for a 60 pack-year smoking history and that he was current smoker. A cardiac catheterization showed total occlusion with Thrombolysis in Myocardial Infarction 0 flow at the proximal left anterior descending artery. He had percutaneous coronary intervention with stenting at the proximal left anterior descending coronary artery. On the night of the catheterization, ventricular tachycardia developed. He was electrically cardioverted, which resulted in sinus rhythm, and amiodarone therapy was started at an initial loading dose of 150 mg intravenously (i.v.), followed by a daily dose of 730 mg i.v. for 2 days. A transthoracic echocardiogram demonstrated anterior and anteroseptal hypokinesis of the left ventricle with an ejection fraction of 35%. After 2 days of amiodarone therapy - a total of 1635 mg of amiodarone - low-grade fever developed with mild dyspnea. Pulse oximetry was 88% in oxygen saturation on room air. Compared with the initial chest X-ray finding, a follow-up chest radiography demonstrated bilateral diffuse infiltration (). Blood tests showed a leukocyte count of 15800/mm3 and a serum creatinine value of 1.2 mg/dL. Pneumonia was suspected and intravenous therapy with piperacillin, tazobactam and levofloxacin was started. The results of blood and sputum culture were negative. Gram's stain and a smear for tuberculosis organisms were also negative, as were serologic tests for Legionella and Chlamydia trachomatis. Mycoplasma pneumoniae polymerase chain reaction tests were also negative. Values for antinuclear antibody, double-stranded deoxyribonucleic acid antibodies, rheumatoid factor, as well as C'3 and C'4 were all within normal limits. Pulmonary edema was also suspected and intravenous diuretics therapy (Lasix 100 mg/day for 3 days) was started; however, no interval change was noted on chest radiography after 3 kg of weight loss. A high resolution computed tomography scan of the chest showed bilateral diffuse consolidation, ground glass opacity and underlying emphysema (). Owing to a high suspicion of amiodarone pulmonary toxicity (APT), amiodarone was discontinued after a total dose of 4035 mg over more than 8 days. Steroid therapy was not started due to mild respiratory symptoms. Pulmonary function tests showed mild obstructive impairment and carbon monoxide diffusing capacity (DLCO) was checked as 16.1 L (79%). As the clinical status was stabilized, bronchoscopy was performed. Bronchoalveolar lavage revealed a cell count of 200 cells/µL with prominent eosinophilia (8%) and foamy macrophages (). No bacteria or fungi were identified via microscopic examination or culture of the lavage fluid. Ten days after amiodarone was discontinued, the patient was discharged with mild dyspnea. Three months later, APT appeared to be reversible with the resolution of chest radiography findings () and recovery of symptoms. | [[54.0, 'year']] | M | {'33331164': 2, '31853440': 1, '18460037': 1, '2364524': 1, '20553056': 1, '27574388': 1, '20356785': 1, '3286141': 1, '3282816': 1, '24255655': 2} | {'7745655-1': 1} |
164,275 | 3831018-1 | 24,255,656 | noncomm/PMC003xxxxxx/PMC3831018.xml | Isolated, Broad-Based Apical Diverticulum: Cardiac Magnetic Resonance Is a "Terminator" of Cardiac Imaging Modality for the Evaluation of Cardiac Apex | A 30-year-old woman was referred to our center with complaints of headache and right side weakness. Her medical history was unremarkable except for intermittent migraine attacks. She had no clinical risk factors for cerebrovascular disease. Small multifocal cerebral infarctions were found in her brain through brain magnetic resonance imaging. With suspicion of a cardiac source of embolism, transthoracic echocardiography was performed, which revealed apical akinetic movement with a band-like structure (arrow in ) in the LV. LV opacification with echocardiographic contrast showed no evidence of apical thrombi (). Initial electrocardiogram did not suggest any sign of apical aneurysm, like ST elevation in anterior leads (). Computed tomographic thoracoabdominal angiography revealed normal findings, including no atherosclerosis (). In addition, she was young and had no risk factors for coronary artery disease, suggesting the impression that the chance for myocardial infarction was not high. For further evaluation of LV apex, CMR was ordered. The CMR identified a broad-based apical diverticulum (2.6×3.0 cm-sized) with mechanical activity, nearly synchronous with LV activity (), along with an LV ejection fraction of 43%. Interestingly, delayed enhancement of CMR (DECMR) conveyed high signal intensity in some parts of diverticulum (). She was finally diagnosed with a huge, isolated LV apical diverticulum with mixed muscular and fibrous type. On anticoagulation with warfarin, she was given permission to leave the hospital. | [[30.0, 'year']] | F | {'21757159': 1, '16612072': 1, '15282470': 1, '26191396': 2, '10556226': 1, '15193690': 1, '24255656': 2} | {'4492182-1': 1} |
164,276 | 3831019-1 | 24,255,657 | noncomm/PMC003xxxxxx/PMC3831019.xml | A Case of Unusual Visceral Heterotaxy Syndrome with Isolated Levocardia | A 19-year-old male was referred to the Pediatric Cardiology Clinic of Chonbuk National University Hospital for the evaluation of abnormal chest X-ray films showing the position of the stomach gas as being discordant with the location of the heart. The patient had no cardiac symptoms and was a normal developed adolescent. Family and past histories were negative. Physical examination revealed this young man to be acyanotic and was in no distress. Cardiac examinations revealed a grade 1/6 ejection systolic murmur at the upper left sternal border. The liver dullness was presented in the upper left quadrant of the abdomen. The remaining part of the physical examination was entirely normal.\nPlain X-ray films of the chest and abdomen showed a normally located heart and a right-sided stomach (). The electrocardiogram was normal with sinus rhythm. Trans-thoracic echocardiographic study demonstrated no intra-cardiac lesions. The IVC was seen on the left side, crossed the midline at the level of the hepatic dome, and connected directly to the right atrium. Spiral computed tomography of the thorax and abdomen showed situs inversus with levocardia and multiple spleens in the right upper quadrant of the abdomen (), a midline liver, a midline positioned gall bladder, hepatic veins with unusual drainage into the IVC (), and a prominent pancreatic head with associated absence of body and tail of the pancreas. The stomach was located on the right side. Most of small bowel loop was located in the right-lateral portion of the abdomen along the left side ascending colon, with some intestinal malrotation. The splenic artery originated from the celiac trunk of the left sided descending aorta with tortuosity coursing to the spleens. There was a discrete aneurysmal dilatation (2.0×2.6 cm in diameter) in the proximal portion of the artery (). The IVC ran on the left side (), and connected directly to the right atrium (). Azygos and hemiazygos veins, and lumbar veins on both sides were slightly dilated. The ascending aorta, main pulmonary artery, pulmonary veins, and superior vena cava were all normally positioned. The structure of right lung was a mirror to the normal left lung, i.e., bilateral bi-lobed lungs (). | [[19.0, 'year']] | M | {'6050934': 1, '9569265': 1, '22056515': 1, '31258874': 2, '25737490': 1, '6878069': 1, '26629295': 1, '1893555': 1, '10464794': 1, '1191445': 1, '12438031': 1, '4682005': 1, '10024407': 1, '10917309': 1, '17324986': 1, '25917470': 1, '25926924': 1, '22103459': 1, '24255657': 2} | {'6586116-1': 1} |
164,277 | 3831305-1 | 24,265,653 | noncomm/PMC003xxxxxx/PMC3831305.xml | Polypoidal Choroidal Vasculopathy – A Type I Polypoidal Subretinal Neovasculopathy | A 47 year old Filipino female presented with the sudden onset of decrease in vision in the right eye in 1998. Visual acuity was: OD 20/70 OS 20/20. Fundus exam showed large orange subretinal vascular structures in the extrafoveal region with serous detachment in the fovea (Fig. ). ICG angiography showed a temporal branching vascular network with extrafoveal polyps (Fig. ). This eye underwent macular laser and has maintained 20/20 vision after 14 years. The ICG angiogram of the left eye showed a completely normal choroidal vasculature without a PCV complex (Fig. ).\nThirteen years later in 2011 the patient noted the sudden onset of a black and grey spot in the left eye for 2 weeks. ICG angiography confirmed the presence of a new peripapillary polypoidal vascular complex (Fig. ), that was not present on ICG angiography 13 years earlier. Optical coherence tomography corresponding to the polyps showed that the subretinal neovascular complex lies above Bruch’s membrane and below the retinal pigment epithelium (Fig. ). This patient was treated with intravitreal 2.0 mg ranibizumab in the PEARL2 study with remarkable resolution of the large vascular polyps, the retinal pigment epithelial detachment, the serous retinal detachment, and the branching vascular network (BVN) (Fig. ). | [[47.0, 'year']] | F | {'20924258': 1, '19726427': 1, '25416513': 1, '25646029': 1, '34109282': 1, '9109756': 1, '1693009': 1, '19854291': 1, '27465105': 1, '24265653': 2} | {} |
164,278 | 3831768-1 | 24,104,711 | noncomm/PMC003xxxxxx/PMC3831768.xml | Donor disc attachment assessment with intraoperative spectral optical coherence tomography during descemet stripping automated endothelial keratoplasty | A 72-year-old female patient with corneal edema due to Fuchs corneal dystrophy, after 2 years, uneventful phacoemulsification surgery with intraocular lens implantation was scheduled for DSAEK. The visual acuity was 20/200. The following eye had visual acuity of 20/25 (correction + 1,0 Dsph) and underwent Descemet's stripping endothelial keratoplasty (DSEK) combined with phacoemulsification surgery 3 years earlier. Spectral-domain optical coherence tomography (SD OCT) examination revealed corneal edema with Descemet membrane folds on posterior corneal surface and fluid spaces under the corneal epithelium. Central corneal thickness was 843 μm.\nThe DSAEK procedure was performed under local, peribulbar anesthesia with additional intravenous sedation. The donor cornea was dissected with a Moria microkeratome (350 μm keratome plate). After fashioning the clear corneal incision, the Descemet membrane was stripped with reverse Sinskey hook. The surgery was discontinued and the optical coherence tomography (OCT) exam with commercially available SD OCT device (IVue; Optovue, Fremont; USA) was performed. The OCT device was held by the surgeon. Acquiring of the image was gained by pressing the foot pedal after focusing the anterior eye segment structures within the OCT scan []. After making sure that all of Descemet membrane was removed, the donor disc was inserted into the anterior chamber with Busin glide spatula. The corneal incisions were sutured with 10-0 nylon. The air was injected into the anterior chamber with following eye surface sweeping in order to remove fluid from the graft interface. The graft seemed to be attached when analyzing in the surgical microscope. After performing SD OCT, multiple fluid micro-spaces were revealed in the area of the graft interface []. Due to that, we performed corneal stab incisions in the four main clock hours. After incisions, SD OCT revealed a proper graft adhesion to the posterior corneal surface []. At the end of the surgery, the anterior chamber was left filled with quarter of the volume of injected air. The whole procedure lasted for 35 min, which increased the time of the surgery by approximately 15 min. | [[72.0, 'year']] | F | {'19643492': 1, '27702622': 1, '18061268': 1, '20098306': 1, '27491407': 1, '33489322': 1, '20307045': 1, '25055146': 1, '19631129': 1, '29942817': 1, '20591396': 1, '16631048': 1, '17466845': 1, '24104711': 2} | {} |
164,279 | 3831772-1 | 24,104,715 | noncomm/PMC003xxxxxx/PMC3831772.xml | Reverse masquerade syndrome: Fungal adnexal infection mimicking carcinoma in a HIV-positive patient | A known HIV-positive, 48-year-old male patient on Highly Active Anti Retroviral (HAART) therapy for the last 4 months and anti-tubercular therapy (ATT) since the last 3 months, presented with a painless, rapidly progressive ulcerated lesion involving the conjunctiva, lids, and anterior orbit of the right eye for past 3 weeks. According to the patient, the lesion started as a small boil over the right upper lid, which rapidly increased in size. Then, he developed a swelling over the medial canthal area. Both the lesions bled to touch. The patient gave history of decrease in vision in the right eye over the last 10 days. Best corrected visual acuity in the right eye was perception of light with inaccurate projection of rays and that of the left eye was 6/6; N6 (Snellen). The anterior segment examination of the left eye was within normal limits. Fundus examination of left eye revealed cotton-wool-spots and flame-shaped hemorrhages in the periphery suggestive of AIDS-related retinal microvasculopthy.[] The right eye conjunctiva was congested with a sloughed-out area measuring 1 × 0.5 cm with underlying scleral thinning. The cornea showed an epithelial defect and thinning with extensive keratinization. The upper lid showed a 2.5 × 1 cm full-thickness defect with an overlying black eschar and a medial canthal ulcerative lesion []. Ultrasound B scan of the right eye was within normal limits. Routine blood investigations were within normal limits, except mild decrease in hemoglobin levels (8.6 mgm/dl). Erythrocyte Sedimentation Rate was raised to 128 mm/h. CD4 lymphocyte count was 100 cells/μl and viral load of 101 copies of RNA/ml.\nMagnetic resonance imaging (MRI) revealed a soft tissue lesion in the right supero-medial extra-conal space associated with thickening of extra-ocular muscles []. Considering the above findings in this immuno-compromised patient, the differential diagnoses were squamous cell carcinoma of the lid with extension into the orbit and zygomycosis. The patient was accordingly taken up for incisional biopsy of the periocular lesion for definitive histopathological diagnosis. Surprisingly, no malignant cells were found in the biopsy specimen. Gomori methenamine silver stain (GMS) staining showed plenty of fungal filaments []. Part of the specimen was also sent for microbiological analysis that showed presence of numerous budding yeast cells on KOH/Calcofluor-white stain []. Culture confirmed it as Candida albicans. The patient was started on IV fluconazole 600 mg once daily for 14 days after discussion with an infectious disease specialist. Topical antibiotic drops and lubricants were continued. HAART therapy and ATT were continued.\nOn his next follow-up visit, the patient had responded significantly to this therapy. The lid defect had healed. There were symblepharon and lagophthalmos of 7 mm. Cornea was opaque and keratinized []. Temporary tarsorrhaphy was performed, and he was advised to undergo symblepharon release with amniotic membrane transplantation with full thickness skin graft of right upper lid. Repeat MRI revealed significant resolution of the lesion []. | [[48.0, 'year']] | M | {'18711264': 1, '15765601': 1, '27380972': 1, '16107193': 1, '18711265': 1, '19617805': 1, '20859237': 1, '24104715': 2} | {} |
164,280 | 3831775-1 | 24,104,718 | noncomm/PMC003xxxxxx/PMC3831775.xml | One day wonder: Fast resolution of macular edema following intravitreal ranibizumab in retinal venous occlusions | A 60-year-old hypertensive man presented with decreased vision in the left eye since 6 months. Patient had been diagnosed with ischemic CRVO and secondary glaucoma in the left eye. He had undergone trabeculectomy in the left eye and was previously treated with intravitreal bevacizumab followed by intravitreal Ozurdex for persistent macular edema. Anterior segment evaluation of left eye showed well-formed bleb, no neovascularisation in iris or angle. Intra-ocular pressure was within normal limits. Fundus evaluation of the left eye was suggestive of old CRVO with diffuse macular edema []. Fundus fluorescein angiography (FFA) showed leakage within the foveal avascular zone (FAZ) in the late phase, there was no leakage related to neovascularization []. 3D spectral domain optical coherence tomography (OCT) (Optovue) showed gross cystoid macular edema [].\nPatient was treated with intravitreal ranibizumab (0.5 mg) in the left eye and 3D OCT was repeated the next day. A significant reduction in macular edema was demonstrated on OCT with reduction in central foveal thickness []. | [[60.0, 'year']] | M | {'20417567': 1, '7526212': 1, '32617913': 1, '12470137': 1, '21684606': 1, '24492507': 1, '21283055': 1, '21715011': 1, '16086947': 1, '24104718': 2} | {'3831775-2': 2, '3831775-3': 2} |
164,281 | 3831775-2 | 24,104,718 | noncomm/PMC003xxxxxx/PMC3831775.xml | One day wonder: Fast resolution of macular edema following intravitreal ranibizumab in retinal venous occlusions | A 70-year-old hypertensive “man presented with gross decrease in vision in the right eye since 1 month. Anterior segment examination and intra-ocular pressure were within normal limits, fundus evaluation of the right eye showed CRVO with retinal haemorrhages and cystoid macular edema. [] FFA showed blocked fluorescence corresponding to retinal haemorrhages with leakage within the FAZ []. 3D OCT showed gross cystoid macular edema [].\nPatient was administered intravitreal ranibizumab (0.5 mg) in the right eye. 3D OCT demonstrated a dramatic overnight reduction in macular edema with reduction of central foveal thickness []. | [[70.0, 'year']] | M | {'20417567': 1, '7526212': 1, '32617913': 1, '12470137': 1, '21684606': 1, '24492507': 1, '21283055': 1, '21715011': 1, '16086947': 1, '24104718': 2} | {'3831775-1': 2, '3831775-3': 2} |
164,282 | 3831775-3 | 24,104,718 | noncomm/PMC003xxxxxx/PMC3831775.xml | One day wonder: Fast resolution of macular edema following intravitreal ranibizumab in retinal venous occlusions | A 50- year-old man presented with blurring of vision in the left eye since 6 months. Anterior segment evaluation and intra ocular pressure were within normal limits. Fundus evaluation of the left eye showed old inferotemporal BRVO with macular edema. Sectoral PRP marks were visible inferotemporally. Colour fundus photography [] and 3D OCT was performed. OCT showed diffuse macular edema [].\nPatient was treated with intravitreal ranibizumab (0.5 mg) in the left eye. 3D OCT after 1 day showed a significant reduction in macular edema with a decrease in central foveal thickness []. | [[50.0, 'year']] | M | {'20417567': 1, '7526212': 1, '32617913': 1, '12470137': 1, '21684606': 1, '24492507': 1, '21283055': 1, '21715011': 1, '16086947': 1, '24104718': 2} | {'3831775-1': 2, '3831775-2': 2} |
164,283 | 3831854-1 | 24,319,584 | noncomm/PMC003xxxxxx/PMC3831854.xml | Beyond a prolonged QT interval | A 14-year-old girl was admitted with generalized tonic-clonic convulsions for 2 min along with tongue biting. Her family reported previous recurrent attacks of muscle cramps and carpo-pedal spasms of four months' duration prior to admission but they had never previously sought medical help.\nThe patient had a good appetite and no diarrhea, with no prior history of cardiovascular disease or symptoms. She was not on any regular medications. She lived mainly indoors, avoided sunlight, and wore a veil outdoors mainly due to traditional beliefs. Her family noticed an abnormal gait eight months prior to presenting at our clinic and she usually asked for help to stand from a squatting position. | [[14.0, 'year']] | F | {'20511054': 1, '8735313': 1, '21660912': 1, '660871': 1, '10893393': 1, '15866097': 1, '24319584': 2} | {} |
164,284 | 3831855-1 | 24,319,585 | noncomm/PMC003xxxxxx/PMC3831855.xml | Hypertension, sweating and palpitation in a psychotic patient – don’t miss the somatic cause | A 27-year-old man was admitted from prison because of acute psychosis. He was convinced of being part of a conspiracy system, he was not adequate in time and place, but there were no optical or auditory hallucinations.\nIn his medical history there was a fracture of the right fourth finger, there was no positive family history for hypertension or cancer, he was not under any medical treatment, he was jobless and smoked a lot of cannabis.\nOn admission the patient was hypertensive (164/95 mmHg) and had a systolic murmur. Physical examination was otherwise unremarkable. Routine laboratory test was normal.\nPaliperidone treatment was successfully administered to treat psychosis.\nHe complained about intermittent palpitations and increased sweating during the night. Because of the sinustachycardia and right-sided thoracic pain in combination with elevated d-dimers a pulmonary CT angiogram was performed. No pulmonary embolism was found but a truncated bilateral hypervascular lesion in both adrenal glands. MRI of adrenal glands showed a tumour measuring 3.4 × 3.7 cm on the right side and another one, measuring 1.1 × 1.3 cm on the left side (). Further laboratory tests showed no hypercortisolism or hyperaldosteronism, but catecholamine and vanillin mandelic acid (VMA) levels in the 24-h urine sample (noradrenaline 1438 nmol/mmol Cr (reference <75), normetanephrine 3.48 nmol/mmol Cr (reference <0.18), VMA 17.9 µmol/mmolCr (reference <3.0)) were elevated. Chromogranin A was considerably elevated (475 µg/l, reference 19–98 µg/l). Metaiodobenzylguanidine (MIBG) scintigraphy showed an intense tracer uptake in projection to both adrenal glands. No extraadrenal paragangliomas were detected. The genetic testing neither showed mutations in the SDHB or SDHD (succinate dehydrogenase B and D subunits) gene nor the typical mutations for MEN2 (multiple endocrine neoplasia) or von Hippel–Lindau syndrome (VHLS). After medical pretreatment with phenoxybenzamine the patient had total adrenalectomy on the right side and partial adrenalectomy on the left side without pre-, intra- or postoperative hypertensive crisis. He required glucocorticoid substitution, initially administered IV, later on a maintenance dose of fludrocortisones 0.1 mg/day. The diagnosis of a bilateral pheochromocytoma was histologically confirmed. The increased sweating and the palpitations disappeared after the surgery. The psychiatric treatment continued, the patient had regular sessions and continued the neuroleptic and antidepressant drug therapy as well. According to his psychiatrist, one and a half years later his condition is stable. He does not smoke cannabis and is starting a job. To keep his status he does not want to stop the medication at the moment. | [[27.0, 'year']] | M | {'21128018': 1, '2787623': 1, '17237836': 1, '6850183': 1, '16013915': 1, '11182843': 1, '23493174': 1, '21159286': 1, '24319585': 2} | {} |
164,285 | 3831857-1 | 24,319,587 | noncomm/PMC003xxxxxx/PMC3831857.xml | Bilateral patellar tendon rupture | We present an exceedingly rare case of spontaneous bilateral patellar tendon rupture in a fit and well 38-year-old Afro-Caribbean gentleman regularly participating in recreational long-distance running. Prior to sustaining this injury, he complained of ongoing anterior knee pain, for which he was awaiting an outpatient X-ray arranged by his general practitioner after weeks of anti-inflammatory medications proved ineffective. The patient was jogging and sustained a fall onto his right knee. The patient was unable to return to his feet, requiring assistance to hospital. He presented to the Accident and Emergency department with pain, swelling and lack of active extension at both knees. Clinically, there was swelling at the patellar tendons, with a high-riding patellar bilaterally, confirmed on plain radiography.\nHe was subsequently admitted under the care of the orthopaedic team where he was surgically managed with simultaneous primary repair. Midline incisions were made over both knees, and repair was achieved using Krackow pull-out sutures with fibre wire, ethibond-modified kesseler suture, fibre glass box suture and retinacular repair with vicryl 1-0. The Insol Selvesti ratio was checked as 1:1 on both sides under image intensifier. Finally, cylinder back slabs were applied bilaterally to immobilize both knee joints.\nPostoperatively, the patient was transferred to the ward where he received a week of inpatient physiotherapy. Post-discharge, he was reviewed in the fracture clinic fortnightly where both wounds demonstrated healthy healing with no signs of infection or inflammation. At the seventh postoperative week, his casts were exchanged for hinged braces to initiate movement from 0–40° and he was referred to the physiotherapist for quadriceps strengthening exercises with whom he made good progress. | [[38.0, 'year']] | M | {'9211611': 1, '6778117': 1, '20427222': 1, '9848596': 1, '30765446': 1, '22708324': 1, '8756939': 1, '27439466': 2, '21642599': 1, '8775966': 1, '19690926': 1, '18265971': 1, '24319587': 2} | {'4955213-1': 1} |
164,286 | 3831858-1 | 24,319,588 | noncomm/PMC003xxxxxx/PMC3831858.xml | Retropharyngeal abscess in a six-week-old child: an approach to management | A six-week-old thriving, full term male presented to a peripheral emergency department (ED) with a left anterolateral neck swelling. This was associated with overlying erythema and he was febrile at 38.1°. The parents of the child did not wait for the child to be seen but returned the following day for review. The erythema and swelling had increased and a palpable mass in the left neck with associated cervical lymphadenopathy was present. On initial blood investigations, he had a white cell count (WCC) of 16.6 and a C-reactive protein (CRP) of 69.2. He was admitted and commenced on IV flucloxacillin and cefotaxime. Ultrasound of the neck demonstrated a 3 × 2.7 × 2.1 cm lobulated lesion consistent with an abscess. His antibiotics were subsequently changed from flucloxacillin to vancomycin and arrangements were made to transfer the patient to a tertiary paediatric centre.\nOn arrival, the child had mild stertor but no increased work of breathing. He was saturating at 100% on room air. On examination, a large palpable suprahyoid left neck swelling anterior to the sternocleidomastoid muscle was present with overlying erythema. He had mild trismus and torticollis to the left. There was anterior displacement of the posterior and left lateral pharyngeal wall present on transoral examination. Repeat WCC was 8.6 and CRP was 72. A CT was performed that demonstrated a large RPA with inflammatory and phlegmonous changes into the left parapharyngeal space predominantly and extending inferiorly to the level of the C5 vertebra (). An opinion was sought from the otolaryngology department and theatre was booked to secure the airway and drain the abscess.\nA gaseous induction and a 3.0 oral endotracheal tube were used to secure the airway. A Lindholm laryngoscope was used to visualize the posterior oropharynx and needle aspiration utilizing a spinal needle was performed to confirm the presence of a collection. One millilitre of 1:100,000 xylocaine with adrenalin was used to infiltrate the posterior pharyngeal wall and a 2 cm vertical paramedian incision was made. Blunt dissection into the cavity combined with pressure to the left neck expressed approximately 6–7 ml of pus. Swabs were taken and sent for microscopy, culture and sensitivity. The wound was washed out with hydrogen peroxide and normal saline. A Penrose drain was inserted transorally into the cavity and secured with a 4.0 silk suture to the posterior pharyngeal wall adjacent to the incision.\nPost-operatively, the patient was admitted into the paediatric intensive care unit (ICU) and was continued on IV vancomycin, cefotaxime and metronidazole. The patient remained intubated, while the swelling resolved and was fed via nasogastric tube. The Penrose drain was removed on day 2 post-op in ICU and the child was extubated on day 3. Staphylococcus aureus sensitive to cephalothin, clindamycin and fluxloxacillin was cultured. IV vancomycin and cefotaxime was continued for five days with oral flucloxacillin for a further five days. Feeds were commenced as normal on day 5. He was transferred back to the peripheral hospital the following day without further complication. | [[6.0, 'week']] | M | {'17931262': 1, '18307424': 1, '18312875': 1, '22481424': 1, '14967751': 1, '24319588': 2} | {} |
164,287 | 3831860-1 | 24,319,576 | noncomm/PMC003xxxxxx/PMC3831860.xml | Right lower lobectomy following inhalation of a toy traffic cone | A 46-year-old man presented in early 2012 having a 16-year history of recurrent respiratory tract infections. He had originally presented to the respiratory physicians in 1996, and in 2004, he developed an empyema which required thoracotomy and drainage. Following drainage, he remained relatively well requiring infrequent oral antibiotics for exacerbations of bronchiectasis on a background of repeated episodes of right basal pneumonia. A sputum specimen from the patient cultured positive for Haemophilus influenzae. A high-resolution computed tomography scan (HRCT) in 2004 demonstrated bronchiectasis and this was confirmed on repeat imaging eight years later. His background history included right lower lobe childhood bronchiectasis diagnosed after an episode of haemoptysis. A further HRCT scan demonstrated an area of high attenuation in the right lower lobe bronchus intermedius ( and ). This was intra-luminal and solid in keeping with appearances of a foreign body or simply a calcified secretion: it looked like a toy traffic cone.\nOn enquiry, the patient recalled swallowing a toy traffic cone over 40 years ago when he was six years old. He had choked at the time but assumed it had been swallowed. Ongoing respiratory review resulted in a referral to our thoracic department for surgical assessment. A rigid bronchoscopy showed the right lower lobe bronchus was narrowed to a tiny orifice continually discharging pus. The bronchus intermedius was short and the middle lobe was inflamed. The right main bronchus and upper lobe were both normal as was the apical segment of the right lower lobe.\nFurther surgical management included a flexible bronchoscopy under general anaesthetic to assess the bronchus to the lower lobe. Due to the protracted clinical history, it was doubtful that extraction would be possible and the patient was scheduled for an elective thoracotomy. Preoperative investigations included a chest X-ray which demonstrated obliteration of the right costodiaphragmatic angle and normal pulmonary function tests (). At operation, a bronchoscopy revealed an indurated area at the bifurcation of the middle lobe and right lower lobe bronchi. This area still discharged pus and bronchial lavage and suctioning revealed a yellow foreign body which was extraluminal. The surgical team proceeded to perform a right lower lobectomy and wedge excision of the middle lobe.\nIntraoperatively, multiple inflammatory adhesions were discovered. The right inferior pulmonary vein and right pulmonary artery were both identified and divided. The right apical segmental artery and right basilar artery were also identified and divided enabling the posterior hilar artery to be visualized and the bronchus exposed. During dissection of the bronchus, profuse quantities of pus were aspirated (). The toy traffic cone was identified in the same location as that determined on CT (). Once removed, the right lower lobe bronchus was stapled and oversewn using a 3-0 Vicryl suture. A small section of the middle lobe was excised after dividing the inferior segmental bronchus of the middle lobe.\nThere were no postoperative complications reported and a short course of intravenous antibiotics was given. Histopathological examination revealed a significantly underdeveloped right lower lobe having areas of focal consolidation and changes consistent with bronchiectasis. The right lower lobe bronchi had diffuse dilatation and associated peribronchial fibrosis and scarring. The toy traffic cone was returned to the patient (). | [[46.0, 'year']] | M | {'12151654': 1, '10591564': 1, '15689749': 1, '9750707': 1, '24319576': 2} | {} |
164,288 | 3832319-1 | 24,255,622 | noncomm/PMC003xxxxxx/PMC3832319.xml | Aplastic anemia associated to systemic lupus erythematosus in an AIDS\npatient: a case report | This report describes the clinical course of a 39-year-old woman who was referred to our\ninstitute for evaluation due to persistent pancytopenia with intermittent transfusion\ntreatment (packed red blood cells and platelets). Her medical history indicated HIV\ninfection for 15 years, regular HAART (tenofovir, lamivudine, ritonavir, and atazanavir)\nwith good and prolonged virological control (viral load < 50 copies/mL and CD4\nT-lymphocyte count of 628 cells/ µL), intermittent polyarthritis of the hands,\ntransvaginal bleeding and bacterial pneumococcal meningitis four months earlier. There\nwas no report of fever, rash, photosensitivity, oral or nasal ulcers, or neurological or\nrenal disorders. Her physical examination was normal, except for pallor and petechiae in\nthe lower limbs without adenopathy or hepatosplenomegaly.\nRepeated tests performed within the previous 16 weeks showed anemia (hemoglobin level:\n6.8-9.7 g/dL; mean cell volume, 90.5-110.0 fL), absolute reticulocyte count (8.7-29.1 ×\n109/L), leukopenia (1.71-3.49 × 109/L) with neutropenia\n(0.58-1.53 × 109/L), variable lymphocyte count (0.44-2.79 × 109/L)\nand severe thrombocytopenia (2-10 × 109/L). An extensive laboratory\nevaluation was conducted for vitamin B12, folate, bilirubin, lactate dehydrogenase,\nhaptoglobin, rheumatoid factor, complement components (C3 and C4), prothrombin time,\nactivated partial thromboplastin time, thyroid function, and renal and hepatic tests\nwithout alterations. Serologic markers for hepatitis B and C, cytomegalovirus\n(immunoglobulin M), and parvovirus (immunoglobulin M) were nonreactive. A direct\nantiglobulin test was negative. Urinary protein was 610 mg/24h. Effusions were not\ndetected in imaging studies. A myelogram showed severe hypoplasia of the erythrocytic,\ngranulocytic, and megakaryocytic series with the presence of 40% of typical lymphocytes\nand no evidence of infiltration by parasites or tumor cells. A bone marrow biopsy\nconfirmed hypocellularity with reduced hematopoiesis (5% cellularity) and absence of\nreticular fibrosis or necrosis ( and\n). Analysis of antinuclear antibodies (>\n1:640, coarse speckled nuclear pattern), anti-ribonucleoprotein (1:1600) and anti-Sm\n(1:800) antibodies were reactive at high titers (antiScl70 and anti-native DNA did not\nreact). In accordance with the criteria of the American College of Rheumatology for SLE\nand the International Agranulocytosis and Aplastic Anemia Study Group, the diagnosis of\nSLE-associated AA was proposed.\nThe potential toxic effects of antiretroviral drugs as a cause of AA were tested before\nthe start of immunosuppressive therapy through a temporary eight-week treatment\ninterruption, but no change in the hematological picture or transfusion dependence was\nobserved. Thus, according to the hypothesis of SLE-associated AA, immunosuppression with\nprednisone (1 mg/kg/day) and hydroxychloroquine (400 mg/day) was initiated with\nprogressive and sustained improvement of the cytopenias during the following six weeks\nand total transfusion independence. The patient remained in follow-up with regular use\nof hydroxychloroquine and HAART; the CD4 count > 500 cells/µL and no cytopenias were\nreported after 20 months. | [[39.0, 'year']] | F | {'17039179': 1, '15045634': 1, '24387179': 1, '28286502': 1, '11404825': 1, '22015937': 1, '12076063': 1, '29390513': 2, '16823830': 1, '16079164': 1, '19734415': 1, '9694056': 1, '12848988': 1, '24255622': 2} | {'5758215-1': 1} |
164,289 | 3832320-1 | 24,255,623 | noncomm/PMC003xxxxxx/PMC3832320.xml | Intrachromosomal amplification of chromosome 21 (iAMP21) detected by\nETV6/RUNX1 FISH screening in childhood acute lymphoblastic leukemia: a case\nreport | An 11-year-old girl with a two-month history of joint pain in both hands and shoulders\nthat evolved to arthritis was admitted to the Onco-Hematology Pediatric Service of\nHospital Estadual Bauru, São Paulo, Brazil. A physical examination revealed that the\npatient did not present enlarged palpable lymph nodes in the cervical, submandibular,\naxillary or inguinal regions. No signs of musculoskeletal abnormalities, including\ninflammatory joint arthritic changes, were noted. Examinations of the cardiovascular and\nrespiratory systems were also normal. The hemoglobin level was low (11 g/dL), white\nblood cell count was also low (3 x 109/L) with no blast cells, platelet count\nwas 165 x 109/L and lactate dehydrogenase (LDH) was 23 U/L. The morphologic\nevaluation of the bone marrow showed 95% blast cells with lymphoid characteristics\ncompatible with French-American-British (FAB) classification L1. Flow cytometry revealed\na population with 71% of blast cells that expressed CD79a, CD19, CD20, CD38, CD58, CD66c\nheterogeneously, low expressions for CD10, CD13, CD22, and negative expressions for\ncCD3, sCD3, cCD7, CD45, CD34, CD15, CD33, cIgM, and myeloperoxidase (MPO) thus\ncompatible with BCP-ALL. The patient was initially treated according to the\nALL-IC-BFM2009 protocol for medium risk(. Peripheral blood showed good treatment response to prednisone on\nDay 8, and bone marrow examination at the end of the induction therapy showed complete\nremission. The patient is clinically well without any evidence of disease five months\nafter diagnosis.\nThe patient's bone marrow sample was sent for cytogenetic analysis, at the time of\ndiagnosis, to the Cytogenetics Laboratory of the Bone Marrow Unit, National Cancer\nInstitute (INCA). The 24-hour culture technique was unsuccessful in obtaining metaphase\ncells for chromosome analysis(.\nFluorescence in situ hybridization (FISH) was performed on interphase cells using the\ncommercially available LSI ETV6/RUNX1 ES dual color translocation probe, LSI MLL dual\ncolor break apart rearrangement probe, and the LSI BCR/ABL ES dual color translocation\nprobe (All from Abbott Diagnostics, Maidenhead, United Kingdom), according to the\nmanufacturer's instructions. Two-hundred interphase cells were scored for each probe.\nInterphase FISH (iFISH) analysis revealed no ETV6/RUNX1 fusion signals and 6 to 10\nsignals for the RUNX1 probe in 75% of the analyzed nuclei in this child ( & ). FISH analyses with MLL and BCR/ABL probes showed normal results. | [[11.0, 'year']] | F | {'18565891': 1, '3855285': 1, '22436535': 1, '21822204': 1, '18358930': 1, '22118741': 1, '34706776': 2, '21487021': 1, '31285807': 1, '32010613': 1, '31456164': 1, '21527530': 1, '27393278': 1, '11516105': 1, '17095619': 1, '24255623': 2} | {'8555128-1': 1} |
164,290 | 3832461-1 | 24,255,591 | noncomm/PMC003xxxxxx/PMC3832461.xml | Purtscher’s retinopathy followed by neovascular glaucoma | A 66-year-old Japanese man presented to our hospital with blurred vision and a central scotoma in his left eye 1 month after suffering from a head injury, which was reported to have occurred following a blow received on his left forehead during a fight. The patient initially noticed the ophthalmic symptoms 1 week after the injury. According to his medical records after the injury occurred, there were no contusions or subcutaneous hemorrhages in the facial region. Computed tomography of his head revealed no fracture, brain damage, or intracranial hemorrhage. Furthermore, there was no history of bone fracture, strong compressions to the chest and abdomen, or direct globe contusion. Although he had a history of hypertension and angina pectoris that were satisfactorily controlled by beta-blocker therapy, there was no history of diabetes and hyperlipidemia. He was a chronic smoker (20 cigarettes per day for 40 years).\nAt initial presentation, his best-corrected visual acuity (BCVA) on a decimal chart was 1.5 oculus dexter and 0.6 oculus sinister. The intraocular pressure (IOP) was 12 mmHg in both eyes. The critical flicker frequency was 38 Hz oculus dexter and 24 Hz oculus sinister. A relative afferent pupillary defect was present in his left eye. Fundus examination revealed no distinct abnormalities in the right eye; however, it revealed multiple white lesions surrounding the optic disk of the left eye, without retinal neovascularization (). Goldmann perimetry demonstrated paracentral scotomas in the left eye (). Optical coherence tomography demonstrated retinal edema, particularly in the inner retina of the left eye ( and ). Furthermore, carotid artery ultrasonography was performed to rule out ocular ischemic syndrome. Although there were slight plaques bilaterally, no significant coarctation was observed. On the basis of these findings, a clinical diagnosis of Purtscher’s retinopathy of the left eye was made. The patient was followed up without treatment.\nOne month after the initial examination, visual acuity in the left eye deteriorated, and the BCVA and IOP became 0.01 in decimal chart and 37 mmHg, respectively. Gonioscopy revealed angle neovascularization in all quadrants. The angle was wide open with no peripheral anterior synechiae. In addition, fluorescein angiography demonstrated a delay of 33 seconds in the arm-to-retina circulation time, with a mild leak observed from the peripheral vessels as well as from nonperfused areas in the peripheral retina; however, there was no retinal neovascularization (). A diagnosis of neovascular glaucoma of the left eye was made, and treatment with intravitreal bevacizumab injection (1.25 mg/0.05 mL) and a total of 2,764 shots of panretinal photocoagulation was initiated to rapidly decrease IOP and avoid peripheral anterior synechiae.\nOne month after treatment (3 months after the head injury), BCVA and IOP in the left eye recovered to 0.4 in decimal chart and 8 mmHg, respectively, under latanoprost treatment. Five months after the head injury, BCVA and IOP in the left eye were 0.4 in decimal chart and 7 mmHg, respectively, without hypotensive drugs. The angle neovascularization and white lesions gradually regressed (). The visual field defect partially recovered (). Optical coherence tomography showed retinal thinning in the inner layers ( and ). | [[66.0, 'year']] | M | {'16500213': 1, '22125405': 1, '29234228': 1, '27895936': 1, '17556428': 1, '29643027': 1, '21847341': 1, '24255591': 2} | {} |
164,291 | 3832775-1 | 23,306,947 | noncomm/PMC003xxxxxx/PMC3832775.xml | Aneurysm of the superficial temporal artery following parotid gland surgery-Case report and review of the literature | A 46-year-old male underwent surgery of the left parotid gland due to cystadenolymphoma. After a postoperative interval of 6 weeks free of complications, a pulsating tumor of the preauricular region had developed. Complaints included a feeling of pressure, sharp pain, and recurrent swelling. The lesion was found to be an aneurysm of the superficial temporal artery by using duplex ultrasound (Fig. ) and a contrast enhanced spiral CT scan of the head (Fig. ). The aneurysm was treated by circumscribed revision surgery of the upper parotid region under general anesthesia. Afferent and efferent vessels were identified and ligated. The aneurysm was then excised to prevent any further discomfort (Fig. ). After surgery, no further complications, particularly no facial nerve paralysis, were observed, and the patient was dismissed on the second day after surgery. The following histopathological analysis revealed, as expected, a false aneurysm of approximately 10 mm in diameter. It was almost completely filled-out by a thrombus consisting of layered fibrin and erythrocytes (Fig. ). | [[46.0, 'year']] | M | {'19825227': 1, '15179202': 1, '22302542': 1, '9746094': 1, '34352906': 1, '34557290': 2, '16450773': 1, '33941432': 1, '14576656': 1, '23306947': 2} | {'8453294-1': 1} |
164,292 | 3833462-1 | 24,265,553 | noncomm/PMC003xxxxxx/PMC3833462.xml | Early resorption of an artificial bone graft made of calcium phosphate for cranioplasty: case report | A 24-year-old man noticed a slow growing mass over the left parietal region of his skull. Radiological studies suggested an osteoma. After 3 years of follow-up, the lesion became larger, with an irregular surface. Surgical resection was then indicated.\nThe procedure consisted of an open craniectomy. The bone around the tumor was removed using a pneumatic craniotome, and by drilling away bony matrix over the sagittal sinus bone to the sagittal suture. After complete tumor removal, CP was performed using calcium phosphate bone cement (Bone Plast® Bone Void Filler, Biomet, Warsaw, IN, USA), covering the entire bone gap (22 cm2), and above the inner table close to the sagittal sinus. Pathologic analysis suggested osteoma with low density of Haversian canals and mineralization, without signs of malignancy.\nOne month after the procedure, the patient noticed that the CP was not consolidated. He felt the flap moving while performing the Valsalva maneuver. Radiological investigation was performed and the area covered by the CP was not consolidated to the bone, and fragmentation could be observed ( and ). After 3 months, the patient noticed a sunken area of scalp. Radiological investigation reported that the patient had absorbed the calcium phosphate bone cement ( and ). | [[24.0, 'year']] | M | {'14758944': 1, '22970998': 1, '21119415': 1, '26495204': 1, '27011500': 1, '32556704': 1, '19319064': 1, '20885250': 1, '24265553': 2} | {} |
164,293 | 3833936-1 | 24,265,644 | noncomm/PMC003xxxxxx/PMC3833936.xml | A Case of Mycobacterium kansasii Pulmonary Disease Presenting as Endobronchial Lesions in HIV-Infected Patient | A 39-year-old male presented with cough and blurred vision for 1 month. Six years ago he was diagnosed with HIV infection in another hospital and he was followed regularly at public health care facility. He had no previous history of pulmonary tuberculosis or other pulmonary diseases. He was a nonsmoker and nondrinker. Forty days ago before admission, he visited the other hospital due to blurred vision and cough for 1 month. CD4 cell counts were 3/mm3 and highly active antiretroviral therapy with combivir and kaletra was started with the concurrent treatment for cytomegalovirus retinitis. He was transferred to our hospital for further evaluation of chronic cough with an abnormal chest X-ray.\nThe patient had a chronically ill appearing and vital signs were stable. There were no specific findings in head and neck area. Breathing sounds were clear and there were no signs of abdominal tenderness. A complete blood count showed white blood cell count of 9,390/mm3 (neutrophil 61.0%, lymphocyte 21.0%, eosinophil 7.0%), hemoglobin 11.3 g/dL, and platelet 322×109/L with C-reactive protein of 3.62 mg/dL (normal, <0.5 mg/dL). A blood chemistry analysis was unremarkable. CD4 count was 247/mm3, and HIV viral load was 2,499 copies/mL. Tuberculin skin test revealed a negative result with a positive interferon-gamma release assay result. Initial chest X-ray showed bilateral hilar prominence, raising the possibility of bilateral hilar lymphadenopathy (). Chest computed tomography revealed multifocal nodular consolidations with some surrounding ground glass opacities in both lungs. There were several enlarged lymph nodes with some internal low-attenuated lesions in the paratracheal, subcarinal, and both hilar regions (). Bronchoscopy showed an elevated nodular lesion with central whitish necrosis at apical segment of right upper lobe and luminal narrowing at apical part of apicoposterior segment of left upper lobe (). Bronchial mucosal biopsy was performed at the both above segments. As bronchial washing fluids smear was positive acid fast bacilli, we started with standard antituberculous medication empirically. However, NTM was detected by polymerase chain reaction from the bronchial specimens and histologic findings at bronchial mucosa revealed chronic granulomatous inflammations with positive Ziehl-Neelsen stain (). One month later, M. kansasii was isolated in bronchial washing fluids and bronchial mucosa specimens. Finally, we diagnosed M. kansasii pulmonary disease with bronchial involvement and he was treated with isoniazid at 300 mg, rifabutin at 150 mg, and ethambutol at 1,200 mg. After the medication, his cough improved gradually and a chest X-ray after 18 months of treatment showed complete regression of the bilateral hilar lymphadenopathy (). | [[39.0, 'year']] | M | {'17277290': 1, '8239182': 1, '16085747': 1, '16478850': 1, '12370997': 1, '15942302': 1, '28740687': 1, '24265644': 2} | {} |
164,294 | 3833937-1 | 24,265,645 | noncomm/PMC003xxxxxx/PMC3833937.xml | Intrapleural Corticosteroid Injection in Eosinophilic Pleural Effusion Associated with Undifferentiated Connective Tissue Disease | A 67-year-old man was admitted with a 1-month history of increasing dyspnea of modified Medical Research Council grade 3. The patient had undergone mitral valve replacement 20 years earlier and had been treated for heart failure, diabetes, and hypertension. His medications included warfarin, digoxin, furosemide, losartan, isosorbide mononitrate, glimepiride, and thiotacid. He had no smoking history. At the time of hospitalization, the patient was alert and the following findings were noted in a physical examination: blood pressure, 140/60 mm Hg; pulse rate, 84 beats/min; respiratory rate, 20 breaths/min; and body temperature, 37.6℃. He had no history of chest trauma or any prominent abnormalities on chest, abdominal, and lower-extremity examinations. Other results of the physical examination were non-specific.\nOn a physical examination, decreased breath sounds were auscultated on the left lower thorax. A chest radiograph showed blunting of the left costophrenic angle (). Chest computed tomography images obtained after therapeutic thoracentesis revealed pleural thickening and calcification on the right posterior pleura but no nodule, mass, or lesion in the lung parenchyma showing in connective tissue disease (). Transthoracic echocardiography revealed enlargement of both atria, dilatation of the left-sided ventricle, and concentric left ventricular hypertrophy with left ventricle ejection fraction 57%. Mild mitral regurgitation and tricuspid regurgitation (grade II) were noted, but no definite change could be observed. There was no pericardial effusion or pericardial thickening, and no valvular vegetations were seen. Although a dose of diuretics had been added for several days, the amount of the left pleural effusion increased markedly, and the patient was referred to a pulmonologist. Laboratory examinations showed the following findings: white blood cell count, 9,300/mm3; hemoglobin, 11.7 g/dL; platelet count, 338,000/mm3; aspartate aminotransferase, 29 IU/L; alanine aminotransferase, 24 IU/L; total protein, 7.8 g/dL; blood urea nitrogen, 22 mg/dL; creatinine, 1.4 mg/dL; C-reactive protein, 8.3 mg/dL; and NT-pro B-type natriuretic peptide (BNP), 1,324 pg/mL. Arterial blood gas analysis in room air yielded results within normal ranges. Analysis of the pleural effusion revealed the following findings: color, yellow; pH, 7.4; specific gravity, 1.010; red blood cell count, 13,760/mm3; white blood cell count, 990/mm3 (neutrophils, 2%; lymphocytes, 29%; eosinophils, 34%); protein, 4.2 g/dL; lactate dehydrogenase, 384 U/L; glucose, 117 mg/dL; carcinoembryogenic antigen, 0.2 ng/mL; adenosine deaminase, 31 IU/L; negative acid-fast staining, culture, non-specific cytology, and negative results in real-time polymerase chain reaction for Mycobacterium tuberculosis. Diagnostic thoracentesis revealed a pleural effusion appearing as an exudate with an elevated eosinophil count (34%). Serological tests for parasites (Clonorchis sinesis, Paragonimus westermani, Cysticercus cellulosae, Sparganum) yielded negative results. Serological test for rheumatologic diseases and vasculitides yielded positive results for the antinuclear antibody (>1:1,280, speckled pattern) and the anti-SS-A/Ro (179.09 EU) and anti-SS-B/La antibodies (208.98 EU). Serological tests for rheumatoid factor (RF) (<20 IU/mL), anti-ds DNA, and complement (C3, C4) yielded negative results. Of the medications the patient was receiving, although warfarin was associated with EPE, he had been taking the drug without any side effects since the mitral valve replacement surgery. Therefore, we considered that the possibility of warfarin-associated EPE was low. The patient complained of xerostomia but not of xerophthalmia, Raynaud's phenomenon, skin lesion, or arthralgia. The patient's heart failure was well controlled; he showed no pitting edema, and his NT-pro BNP level had reduced from 2,419 pg/mL to 1,324 pg/mL in a 1-month period. EPE associated with UCTD was considered, and the patient was discharged after 1 L of excess fluid was removed by therapeutic thoracentesis. About 2 weeks later, his dyspnea worsened and the left pleural effusion increased again. Repeated therapeutic thoracentesis temporarily relieved the symptoms, but they aggravated again within 2 weeks. The administration of systemic corticosteroid was considered but was contraindicated by chronic anticoagulation therapy, uncontrolled blood sugar levels, and the patient's age.\nBecause we were reluctant to administer systemic corticosteroid therapy, a single dose of 125 mg methylprednisolone was injected directly into the pleural space. A chest X-ray image obtained 2 weeks later showed a marked decrease in the pleural effusion (). No recurrence was observed during a 1-year follow-up, and serological tests for autoantibodies yielded similar results to those obtained in the previous year (). | [[67.0, 'year']] | M | {'22424194': 1, '11491495': 1, '8869446': 1, '12720042': 1, '11243986': 1, '21831499': 1, '19386682': 1, '12806236': 1, '11372801': 1, '15846590': 1, '21576924': 1, '8915232': 1, '24265645': 2} | {} |
164,295 | 3833938-1 | 24,265,646 | noncomm/PMC003xxxxxx/PMC3833938.xml | A Case of Recurrent Pulmonary Inflammatory Myofibroblastic Tumor with Aggressive Metastasis after Complete Resection | A 47-year-old male patient was referred to our hospital. The patient had discovered a shadow in the upper lung field from a chest X-ray during a medical check-up at an outside hospital on April 2009. A 30-mm sized well-defined low attenuation lesion was observed in the left upper lung on a chest radiography and a computed tomography (CT) (). Positron emission tomography/computed tomography (PET/CT) showed maximum standardized uptake values (SUV) of 10 in the masses in the left upper lung. Bronchoscopy revealed a whitish tumor obstructing the anterior segmental bronchus of left upper lung upper division covered with necrotic material, and biopsy specimens of the tumor was taken during the bronchoscopic examination, and was reported to be spindle cell proliferation according to pathological findings. A radical left upper lobectomy was performed on July 2009 for the purpose of diagnosis and treatment, and an IMT was confirmed by histopathology. On gross examination, the tumor was a single mass with a regular border and adjacent to the bronchus, localized in the lung parenchyma and measured 4.3×3.5 cm (). Microscopic examination revealed spindle cells proliferation without atypia and inflammatory cells (). According to immunohistochemical examination, the myofibroblasts were negative for all cytokeratin, smooth muscle actin, desmin, and Bcl-2. In addition, the myofibroblasts were focally positive for anaplastic lymphoma kinase-1 (ALK1) (). Fluorescence in situ hybridization of ALK rearrangements was not done because of the patient's disagreement. There was no evidence of metastasis with examination of 32 lymph nodes. On postoperative outpatient follow-up, the patient complained of back pain on August 2011, approximately 2 years afterwards. While there was no evidence of recurrence in the lungs from the chest CT performed then, the PET/CT showed multiple bone metastasis (right third rib [SUV, 7.8], thoracic 12th spine [SUV, 10.2], and left sacroiliac bone [SUV, 12.9]) (). According to the biopsy performed on the thoracic spine, a recurrence of the IMT was confirmed. The patient received a total of 36 Gy focal irradiation on the thoracic spine to control the back pain, and was discharged after the pain was alleviated. Afterwards, the back pain aggravated in just 6 months and therefore, the patient made a visit.\nThe patient had no specific past medical history and family history. He has a history of a pack of cigarette smoking for 15 years and quit smoking in 2005. There was no other remark-ability.\nAccording to chest and abdominal check-up, no abnormality was observed, and the patient complained of pain in the left pelvis and pain in the left calf. There were no other specific findings, and there was no clearly palpable tumor.\nAccording to the blood test, the white blood cell count increased to 17,400/mm3, the hemoglobin count was 13.6 g/dL, and platelet was 274,000/mm3, which is within normal range. The blood urea nitrogen, creatinine, liver function test, and electrolyte result were within normal range, and there was a slight increase in C-reactive protein with 1.36 mg/dL. Alkaline phosphatase increased to 130 U/L.\nMultiple pulmonary nodules were observed on the chest CT. PET/CT taken due to the re-aggravated back pain and an aggravation of existing bone metastasis and new bone lesions were observed in the skull base, spine, sternum, both scapulas, pelvis, and both femurs ().\nAfter the patient was hospitalized, an intravenous injection of high dose corticosteroid (methylprednisolone, 2 mg/kg/day) was tried and stereotactic radiation therapy with CyberKnife was administered to 5th lumbar spine metastasis. In addition, prophylactic radiotherapy was administered for weight bearing sight (both hip area) and skull base metastasis.\nOne month after high dose corticosteroid therapy, the patient continued to complain of back pain. Bone scan and CT scan revealed aggravation of pulmonary and bone metastasis. We concluded that corticosteroid was not effective and discontinued administration. For pain control, an additional stereotactic radiation therapy to second lumbar spine and sacrum was performed, and transforaminal 5th lumbar spine root block was undertaken. Afterwards, the patient newly complained of left arm tingling sensation, and T1 and T2 level cord compression was observed, and therefore, additional radiotherapy was administered for the cervical and thoracic spine. During this process, because radiation induced thrombocytopenia was observed, intermittent platelet transfusion was performed.\nOn June 2012, under circumstances where specific treatment plan could not be considered, celecoxib (1,000 mg/day), a selective cyclooxygenase-2 (COX-2) inihibitor, began to be tried. However, the patient newly began to complain of numbness in both legs, and deterioration of their motor grade, and voiding difficulty due to neurogenic bladder. Cervical and thoracic spine CT revealed severe cord compression at T8 and T11 level due to bone metastasis. Although surgery was considered, it was difficult to perform due to thrombocytopenia, and hence, stereotactic radiation therapy was administered. Nonetheless, the patient soon progressed to a state of paraplegia, and urinary catheter was inserted. CT scan showed pleural effusion, and liver, adrenal, and spleen metastasis. Approximately after 3 months of hospitalization, the patient was deceased on July 2012 due to disease progression despite conservative treatment. | [[47.0, 'year']] | M | {'26557237': 1, '11406658': 1, '20058697': 1, '12823044': 1, '32500024': 2, '21572361': 1, '22975556': 1, '26622552': 1, '10320231': 1, '28658093': 1, '15991185': 1, '24265646': 2} | {'7243805-1': 1} |
164,296 | 3833939-1 | 24,265,647 | noncomm/PMC003xxxxxx/PMC3833939.xml | A Case of Primary Pulmonary Lymphoepithelioma-like Carcinoma Misdiagnosed as Adenocarcinoma | A 60-year-old woman visited our outpatient clinic for evaluation of a lung mass incidentally detected on chest computed tomography (CT) during regular medical check-up. Physical and laboratory examination did not reveal any relevant abnormalities. She had no medical illness and was never-smoked. Initial chest radiograph revealed a nodular opacity in the right middle lung field (). On chest CT, there was an approximately 3.1 cm mass in diameter with spiculated margin and heterogeneous enhancement in the right lower lobe of the lung, which invaded right major fissure. In addition, there were adjacent ground-grass opacities posterior to the mass (). Next, we performed PTNB for the histological diagnosis for the mass. Microscopic examination showed that tumor cells were arranged in diffuse pattern and reveal round nuclei without prominent nucleoli and moderate amount of cytoplasm. The tumor cells were diffusely stained with p53, thyroid transcription factor-1, and Ki-67 on immunohistochemical analysis, suggesting that it was a malignant mass such as poorly differentiated adenocarcinoma. As for the staging work-up, positron emission tomography-CT and brain magnetic resonance revealed that the mass was hypermetabolic (standardized uptake value, 9.32) with high uptake of fluorodeoxyglucose () and that there was no metastatic foci or lymphadenopathies, altogether, it was diagnosed as adenocarcinoma of cT2aN0M0 (stage IB) by TNM staging system. For her treatment, she underwent the right lower lobectomy. On histological examination, the tumor was grossly 1.8×1.5 cm-sized and ashen gray-colored mass with ill-defined margin. The mass was firm to palpation without pleural, vascular, and lymphatic invasion. It was composed of large epithelioid malignant cells with undifferentiated appearance, syncytial growth, and adjacent reactive lymphoplasmacytic cells influx (). Moreover, some of the malignant cells were positive for in situ hybridization with EBV-coded small RNA (EBER) (). Any glandular and squamous cell differentiation was not detected. Based on these histologic findings, the mass was finally diagnosed as primary pulmonary LELC of pT1aN0M0 (stage IA). After the surgical resection, there had been no recurrence or complication of disease at follow-up of 3 years. | [[60.0, 'year']] | F | {'22410385': 1, '21433005': 1, '16916325': 1, '32337200': 1, '15950718': 1, '22359203': 1, '2826922': 1, '29387253': 1, '25789039': 2, '24265647': 2} | {'4356418-1': 1} |
164,297 | 3834024-1 | 24,266,016 | noncomm/PMC003xxxxxx/PMC3834024.xml | Abdominal wall defect with large duodenal disruption treated by a free tissue flap with a help of temporary expandable metallic stent | A 64-year-old man underwent emergency surgery after penetrating abdominal trauma. He had intra-abdominal exsanguinating bleeding, duodenal disruption, and multiple small bowel perforation. Duodenojejunostomy, the resection of about 150 cm of small bowel followed by anastomosis, and bleeding control were performed. Despite of repeated reanastomosis due to anastomosis failure, he developed sepsis and multiorgan failure. Therefore, he was referred to our institution 22 days after the first surgery. A surgical reexploration was performed and it revealed duodenojejunal disruption and multiple enteroenteric anastomosis failure; there was a large amount of bilestained fluid in the abdomen. Since less than 1 m of the small bowel remained, pyloric exclusion or pancreaticoduodenectomy could no longer be considered. Therefore, we performed enteroenterostomy and duodenal primary repair, and placed a feeding tube distal to the perforated duodenum. After massive irrigation, the multiple drain tube was placed.\nFortunately, after intensive care, the patient could be transferred to the general ward after ventilator weaning. Enteral feeding through the jejunal feeding tube worked well. However, due to severe retraction of the duodenum, a duodenal disruption gap that was approximately 5 cm long developed. This was associated with an abdominal wall defect (). It was impossible to close either the duodenum or the wall defect primarily. We decided to use a free flap to repair the abdominal wall defect. However, because of persistent leakage of gastric, bile, and pancreatic juice through the duodenal defect, the abdominal wall defect could not be repaired directly with a free flap.\nTherefore, the bile and pancreatic juices were diverted first by placing separate pancreatic duct and bile duct drainage tubes by endoscopic retrograde cholangiopancreaticography. Thereafter, the interventional radiologist placed a 16-mm diameter, 90-mm long covered expandable metallic stent (S&G Biotech, Seongnam, Korea) from the duodenal bulb to the jejunum. This successfully reestablished duodenal continuity. Bile and pancreatic juices were diverted through endoscopic nasobiliary drainage and endoscopic nasopancreatic drainage completely. The stent migrated downward 5 days after placement. It was removed through the abdominal defect without difficulty. A second stent was placed from the gastric antrum to the jejunum. It was 16 mm in diameter and 130 mm long (), and thus was much longer than the first stent. The stent was tightly sutured to the duodenum to prevent stent migration.\nSeven days after stent placement, the patient underwent debridement and closure of the abdominal wall defect with a free flap. Duodenostomy was performed by placing a drainage tube that decompressed the duodenum and prevented infection. Endoscopic images obtained 3 months after stent placement revealed a widely patent stent, although granulation tissue had formed above the stent. The stent was electively removed 112 days after placement by using a stent removal set. Stent placement and stent removal techniques have been described in detail previously []. The pancreatic duct and bile duct drainage tubes were removed 13 days after stent removal.\nThe patient was able to take food orally after stent removal. The abdominal wall defect had healed completely. A small enterocutaneous fistula was observed. On the 234 th postoperative day, an upper gastrointestinal water-soluble contrast study was performed and showed good passage of contrast with a small enterocutaneous fistula and no significant obstruction (). | [[64.0, 'year']] | M | {'20072081': 1, '12407361': 1, '19639436': 1, '17727887': 1, '8782474': 1, '11438264': 1, '10192570': 1, '11058659': 1, '8222749': 1, '21276371': 1, '24266016': 2} | {} |
164,298 | 3834025-1 | 24,266,017 | noncomm/PMC003xxxxxx/PMC3834025.xml | Use of video-assisted thoracoscopic surgery to retrieve a broken guidewire | A 79-year-old female patient diagnosed with ascending colon cancer was admitted to the Division of Colon and Rectal Surgery of our institution for a scheduled operation on July 23, 2012. At admission, the patient's calculated Acute Physiology and Chronic Health Evaluation II score was 10 with a predicted death rate of 11.3%. Central venous catheterization was performed for preoperative, intraoperative, and postoperative volume resuscitation and nutritional therapy. A senior surgical resident used the landmark method to perform catheterization of the right subclavian vein. The Spectrum Central Venous Catheter Set (length, 20 cm; size, 7.0 F; William A. Cook Australia Pty. Ltd., Brisbane, Australia) was used (). The included guidewire had a J-tip ().\nThe right subclavian vein was successfully punctured using the Seldinger technique, and the guidewire was then inserted. The patient was not obese, and her anatomic landmarks were clear. Slight resistance was detected during the guidewire insertion process, but the resident proceeded with it. When guidewire advancement was not possible, its removal was attempted. However, by this point, it could be neither advanced nor removed because of resistance. Forced removal was attempted but resulted in guidewire breakage and entrapment. Its location could not be determined by palpation. Chest radiography was immediately performed to determine the position of the guidewire, and the results indicated guidewire looping and entrapment within the upper right clavicle (). Chest computed tomography scans revealed that the broken guidewire was outside the vein and had not induced hemothorax, pneumothorax, or hematoma of the soft tissues (). After we had explained this to the patient, under local anesthesia, we tried to remove the broken guidewire through infraclavicular skin incision but we could not find the guidewire.\nThe patient was transferred to the operating room for the scheduled operation and underwent VATS of the right thorax. The operation took 120 minutes. The surgical manifestation was metallic foreign body impaction in the upper chest wall that was successfully removed (). The patient was discharged 14 days after the scheduled right colectomy without significant complications. Volume resuscitation was conducted through the internal jugular vein during the operation, while nutritional support was delivered via peripheral venous access. | [[79.0, 'year']] | F | {'9310813': 1, '10431965': 1, '21494105': 1, '8024478': 1, '20175063': 1, '7984193': 1, '2297151': 1, '24266017': 2} | {} |
164,299 | 3834173-1 | 24,294,319 | noncomm/PMC003xxxxxx/PMC3834173.xml | A chronic flexion-distraction injury with a “fistulous wither” on the split spinous process of the L1 vertebra—a case report of a modified transpedicle wedge osteotomy | A 59-year-old man, a retired worker, presented chronic pain in his lower back. There was no history of definitive trauma, but he mentioned that he had experienced a mild motor vehicle crash while wearing a three-point seat belt 6 months earlier and the swelling in his back had been deteriorating for 3 months. The pain was dull in character, and confined to the thoracolumbar spine. He also described that standing, walking, and especially lying in a supine position aggravated the pain.\nPhysical examination revealed that he was poorly nourished. His body mass index was 19.7 (body height, 173 cm; body weight, 59 kg). A visible thoracolumbar gibbus was present. A subcutaneous fluctuation, which seemed to be the size of a large egg, was palpable at the tip of the deformity (Fig. ). Tenderness was also present at the affected spinous process. Five milliliter of bloody serum was aspirated from the fluctuation (Fig. ). Bacterial culture of the fluid was negative. A lateral plain X-ray demonstrated a kyphosis of 35° at T12/L1 (Fig. ). No instability of the fracture site was found in flexion and extension X-rays. MRI was not performed because he had a stainless steel clip in his cranium. Reconstructed CATs in the sagittal plane demonstrated a fracture line through the spinous process, the pedicle, and the upper vertebral body in L1. A lesion containing gas was also seen at the T12/L1 intervertebral disc and the upper vertebral body of the L1 vertebra, whereas no bony protrusion was present in the spinal canal at the affected level (Fig. ). These investigations suggested a diagnosis of a chronic FDI with a bursitis or hematoma on the split spinous process in L1. In spite of a thoracolumbar brace, NSAIDs, and repeated aspiration, no recovery from the symptoms were observed. Corrective surgery for the gibbus and resection of the bursa or hematoma was indicated 6 weeks after his initial visit.\nAt operation, a posterior approach was chosen. The patient was positioned prone on a Hall-Relton spine frame. Thereafter, a midline incision was made, a subcutaneous fibrous cystic lesion, which was connected with the split L1 spinous process, was demarcated and radically excised. It was elliptical in shape and approximately 40 × 50 mm in size. Pathological diagnosis was a bursitis (Fig. ). The supraspinous process on the spinous ligament in L1 was completely torn. Secondarily, the T11 to L2 laminae was exposed subperiosteally. A fracture line of the L1 spinous process was identified. No instability or bleeding was identified. The cephalad portion of the split spinous process and the lamina was resected. Then, the facet joints of T12/L1 were bilaterally removed. Discectomy of T12/L1 and osteotomy of the posterior wall of L1 was then performed. The bilateral L1 pedicles were also subtracted from their base. Anterior soft tissue was released as much as possible with a great care. Resected local bone and two titanium spacers (8° angled, 7 mm in height, 25 mm in length) were placed at the T12/L1 space. Pedicle screws were bilaterally inserted in T11, T12, and L2. Correction was done via compression of the pedicle screws and rods assembly using two titanium spacers as a fulcrum. Postoperatively, the patient was placed in a soft thoracolumbar brace for 3 months. At 1.5-year follow-up, he reported no backache. Recurrence of the bursitis at the spinous process in L1 was not observed. Plain radiograms and reconstructed CAT demonstrated a solid boney fusion with a minimal kyphosis of 5° at T12/L1 (Fig. ). | [[59.0, 'year']] | M | {'6670016': 1, '20072030': 1, '18379391': 1, '14297334': 1, '28331905': 2, '6453878': 1, '2718040': 1, '2325176': 1, '3192481': 1, '15770174': 1, '8852319': 1, '19834769': 1, '12472502': 1, '11927823': 1, '24294319': 2} | {'5351051-1': 1} |
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