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hyperparathyroidism/hypoxie
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12 Ergebnisse
Familial hypocalciuric hypercalcemia involving four members of a kindred including a girl with severe neonatal primary hyperparathyroidism.
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A family with hypercalcemia in four members is reported. The proband, a newborn girl presenting with inadequate sucking due to muscle hypotonia, marked thoracic deformity due to decalcification, hypercalcemia, and hypophosphatemia, suffers from cerebral damage due to hypoxia despite successful total
Myocardial calcification in an extremely low birth weight infant with chronic renal failure and secondary hyperparathyroidism.
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Myocardial calcification has been rarely described in premature infants after myocardial infarction and myocarditis with coxsackievirus B1. In adults and older children, metastatic myocardial calcification has been reported in chronic renal failure. We report a case of myocardial calcification in a
[Hyperparathyroidism in patients with respiratory decompensation].
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Eighteen patients aged between 55 and 65 and affected by respiratory insufficient were included in the study. Serum levels of PTH, total calcium, Ca++ and phosphorus were measured. Special attention was focused on PTH concentrations with in some case provedo to be above normal. Two hypotheses of
Prevalence and risk factors for low bone density in adults with a Fontan circulation.
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Immunohistochemical investigation of angiogenic factors in parathyroid proliferative lesions.
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OBJECTIVE
The pathological distinction between parathyroid neoplasms and hyperplasias remains difficult in several cases. Endoglin (CD105) is a proliferation-associated and hypoxia-inducible protein abundantly expressed in angiogenic endothelial cells. Vascular endothelial growth factor (VEGF)
Uraemic myocardial disease. An experimental study, with special reference to the effect of parathyroidectomy.
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A histopathological study of the myocardium was performed in rats made uraemic by a 5/6 kidney resection. The examinations were performed after intervals up to 36 weeks. Uraemia caused focal myocardial necroses, the incidence and severity of which were related to the length and severity of the
[Etiological factors of acute pancreatitis].
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Acute pancreatitis develops immediately after the causative impulse, while chronic pancreatitis develops after the long-term action of the noxious agent. A typical representative of acute pancreatitis is biliary pancreatitis, chronic pancreatitis develops in alcoholism and has a long latency. As
AN AGGRESSIVE TEMPORAL BONE SDHC PARAGANGLIOMA ASSOCIATED WITH INCREASED HIF-2α SIGNALING.
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OBJECTIVE
To describe a patient with a germline succinate dehydrogenase (SDHC) gene mutation presenting with primary hyperparathyroidism and a large catecholamine-producing temporal bone paraganglioma (PGL).
METHODS
Evaluation of a SDHC mutation-positive PGL tumor biology using staining for tyrosine
Inflammatory diseases of the parathyroid gland.
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OBJECTIVE
Inflammatory disorders of the parathyroid gland are very rare as compared with those of other endocrine organs. The aim of this study was to provide the first systematic review of this condition.
RESULTS
A 42-year-old patient underwent surgery for recurrent secondary hyperparathyroidism.
Serum erythropoietin levels in children with chronic renal failure.
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Serum erythropoietin (EPO) was measured in 64 children with chronic renal failure (CRF) by means of the fetal mouse liver cell assay. The results were compared with two control groups consisting of 20 healthy children and 10 with nonrenal anemia. EPO was analyzed according to the mode of treatment
Erythrocytosis in a patient on hemodialysis for thirteen years.
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Most hemodialysis patients exhibit renal anemia mainly due to erythropoietin deficiency as a result of impaired erythropoetin production in the kidney. However, erythrocytosis in patients with renal failure requiring hemodialysis is extremely rare. We report the development of erythrocytosis in a
Role of Hepcidin-25 in Chronic Kidney Disease: Anemia and Beyond.
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Iron is an essential element for all living organisms, but produces toxic oxidants. Thus, iron homeostasis is tightly regulated in mammals. Hepcidin-25 (hepcidin) has emerged as a molecule that regulates iron metabolism. Binding of hepcidin to its receptor, ferroportin, inhibits intestinal iron
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