Cases reported "Calcinosis"

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1/89. Osseous metaplasia in a growth hormone-secreting pituitary adenoma.

    A case of growth hormone-secreting adenoma of the pituitary gland showing osseous metaplasia is described in a 56-year-old acromegalic female. The tumor was composed of nests of densely granulated cells separated by and intermixed with calcifications, trabeculae of mature bone and fat. Calcifications are seldom found in pituitary adenomas. In rare instances, calcium deposits can be prominent enough to lead to the formation of pituitary stones and bone which replace the entire tumor mass. Analogously with metaplastic meningiomas, we propose using the term metaplastic adenoma to define cases with osseous metaplasia in order to distinguish between lesions containing bone from the more frequently seen calcified adenomas.
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2/89. The amyloid deposit in calcifying epithelial odontogenic tumor is immunoreactive for cytokeratins.

    Calcifying epithelial odontogenic tumor, also known as Pindborg tumor, is a rare benign tumor with locally aggressive behavior. It is characterized by squamous epithelial cells, calcifications, and eosinophilic deposits that have been identified as amyloid. We report a case of calcifying epithelial odontogenic tumor and investigate the nature of the amyloid, using histologic, immunohistochemical, and ultrastructural studies. The amyloid was immunohistochemically negative for basement membrane components and positive for all cytokeratin stains performed (cocktail of cytokeratins 1, 5, 6, 8, 13, and 16, and cytokeratins AE1 and AE3). The amyloid stained focally in a glandular-like pattern, reminiscent of the epithelial glandlike structures of the tumor. We conclude that the amyloid is derived from filamentous degeneration of keratin filaments that originate from the tumor squamous epithelium. The keratin degeneration is part of a developmental or aging process that the tumor undergoes.
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3/89. Dramatic worsening of vascular calcifications after kidney transplantation in spite of early parathyroidectomy.

    vascular calcification is a common feature in chronic dialysis patients, but their clinical significance is debated and the role of kidney transplantation (TP) in the natural history of their development has received scanty attention. We will describe a case of dramatic worsening of vascular calcifications during TP in a young patient in spite of early and successful parathyroidectomy (PTX), and will discuss other causes which might be putatively linked to vascular damage during the time of TP. A 37-year-old man on regular dialytic treatment (RDT) for 11 years, received his first cadaveric transplantation in January 1993. He underwent PTX 6 months after TP because of the lack of decreasing in parathyroid hormone values despite normal graft function. Although PTX was effective, a dramatic worsening was evident in large as well as in medium and small-sized arteries during the following three years of TP. In February 1997, few months after starting dialysis again because of the recurrence of his primary membranoproliferative glomerulonephritis (MPGN), the patient experienced myocardial infarction followed by aorto-coronary bypass (right coronary artery and anterior descending coronary artery) and leg "claudicatio". Though a role for parathyroid hormone in vascular disease has been commonly accepted, the case here reported clearly shows that blunting parathyroid gland activity may be unable to avoid the worsening of a process of vascular disease during the time of TP. Many other factors--linked to the time of TP--may be involved in vascular diseases, such as nephrotic syndrome, dyslipidemia, hypertension and drugs. In the case of our patient, a clear cut risk factor for his progressive atherosclerosis can be designated hyperlipidema and other disturbancies secondary to a nephrotic syndrome due to relapse of MPGN, together with persistent hypertension. This is the first case report in the English literature which clearly demonstrates that TP may add fuel to the fire of vascular disease also in young people and even in the absence of parathyroid hyperactivity, perhaps on the basis of a favorable genetic background. Furthermore, the history of our patient demonstrates that vascular calcifcation heralds major cardiovascular diseases.
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4/89. Idiopathic hypoparathyroidism with intracranial calcifications and dominant skin manifestations.

    Presented here is an unusual case of a 41-year-old man with idiopathic hypoparathyroidism strongly connected with dermatological, ophthalmological and neurological disorders. Since the age of 4 he had been treated ineffectively for mycosis resulting in complete baldness and atrophic nail plate changes. At the age of 35 he was diagnosed with idiopathic hypoparathyroidism. He underwent surgery twice due to bilateral cataract. CT scans of the head demonstrated numerous symmetrically located calcifications in both frontal lobes, subcortical nuclei, the paraventricular region, brain fornix, and both cerebellar hemispheres. The neuropsychological examination demonstrated the occurrence of psychosensory disorders under the form of hallucinations accompanied by a sense of fear and anxiety. It seems essential to investigate the parathyroid gland for any sign of pathology, especially amongst patients with severe dermatological and/or neuropsychological symptoms. early diagnosis and treatment of patients with hypoparathyroidism may prevent the development of many serious complications or at least result in marked improvement of neurological manifestations.
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5/89. Case report: Calcifying fibrous pseudotumour of the adrenal gland.

    Calcifying fibrous pseudotumour is a distinct pathological entity usually occurring in the soft tissue of the extremities, trunk, axilla, pleura, mediastinum and peritoneum. This report describes the hitherto unreported occurrence of this tumour of the adrenal gland in a 10-year-old girl whose imaging findings closely resembled a neuroblastoma. This entity is a potential pitfall in diagnosing adrenal neuroblastoma.
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6/89. Case report: plasma adrenalin in a child with ketotic hypoglycemia and calcifications of the suprarenal glands.

    Urinary excretion of adrenalin has been reported to be reduced during insulin-induced hypoglycemia in a significant proportion of children having ketotic hypoglycemia. By employing a sensitive double-isotope derivative technique, plasma adrenalin and plasma noradrenalin were determined in a boy 6 years 9 months old who had had ketotic hypoglycemia with intermittent hypoglycemic symptoms from the age of 10 months. Bilateral calcifications of the suprarenal glands were present. The adrenocortical function was normal. The plasma adrenalin response to hypoglycemia were practically absent, being only 4% of the value obtained in healthy children. The results were related to previous findings of a low plasma adrenalin response in patients with ketotic hypoglycemia without adrenal calcifications and support the assumption that ketotic hypoglycemia is associated with hypoadrenalinemia.
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7/89. Ewing's sarcoma family of tumor arising in the adrenal gland--possible diagnostic pitfall in pediatric pathology: histologic, immunohistochemical, ultrastructural, and molecular study.

    We present an adrenal Ewing's sarcoma family of tumor (ESFT) arising in an 11-year-old Japanese boy. Although intensive chemoradiotherapy and radical surgery were performed, the patient died of obstinate disease 1 year and 3 months after the initial presentation. The primary site (adrenal gland) with radiologic findings (with foci of calcification), high titer of serum neuron specific enolase, and sheets of monotonous primitive rounded cells on histology mostly favored neuroblastoma. However, a diagnosis of ESFT was confirmed by immunohistochemical profile, including MIC2-positivity and molecular study disclosing EWS-FLI1 chimera gene verified by direct sequencing. Recognition of adrenal ESFT and use of newly developed diagnostic techniques are required for differential diagnosis of undifferentiated small round cell tumor of the adrenal gland.
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8/89. Primary hyperparathyroidism in an infant with three parathyroid glands and pulmonary calcinosis.

    A 2 month-old male infant presented with severe hypercalcemia due to parathyroid hyperplasia. A total parathyroidectomy and partial heterotopic autotransplantation were carried out. hypercalcemia recurred two months later. Normocalcemia was re-established after removing one half of the implanted tissue. Despite two separate surgical explorations and several imaging studies, including 99mTc-sestamibi scintigraphy, ultrasonography, and MRI, only three parathyroid glands were found. Severe pulmonary calcinosis has not previously been reported in children with PHPT. In conclusion, developmental variations of the parathyroid glands may be difficult to identify with present imaging techniques. This may pose difficulties in management of PHPT. The present report describes pulmonary calcinosis as a sequela which can cause additional morbidity in these infants.
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9/89. Calcification of all four parathyroid glands in a hemodialysis patient with secondary hyperparathyroidism revealed by computerized tomography.

    This report describes the parathyroid scan, computerized tomography and histologic findings in a young female hemodialysis patient with severe secondary hyperparathyroidism. These findings included hyperplasia and calcification of all four parathyroid glands.
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10/89. Gastric carcinoma with psammomatous calcification after Billroth II reconstruction: case report and literature review.

    A case of gastric carcinoma with psammomatous calcification arising in the remnant stomach after Billroth II reconstruction is reported. Borrmann type 1 gastric carcinoma was detected in the remnant stomach of an 82-year-old woman, who had a past history of distal partial gastrectomy for a perforated gastric ulcer, with Billroth II reconstruction at 40 years of age. Histologically, the tumor was a tubular adenocarcinoma that invaded the muscularis propria. Numerous psammoma bodies were found in the lumens of the tumor glands. Dystrophic calcification of gastric cancer is rare and psammomatous calcification of gastric cancer has only been reported in five cases previously. To our knowledge, this is the first case of gastric carcinoma with psammomatous calcification arising in the remnant stomach. We also review previously published reports regarding gastric carcinoma with psammomatous calcification.
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