Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A one-year-old boy presented with hypercalciuria and nephrolithiasis following a course of ACTH therapy for infantile spasms. After a successful cystolithotripsy, therapy with chlorothiazide was followed by regression of the hypercalciuria within 42 months. Neither nephrolithiasis nor nephrocalcinosis recurred. Therapy with thiazides to prevent hypercalciuria caused by ACTH is proposed.
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PMID:Thiazide therapy for ACTH-induced hypercalciuria and nephrolithiasis. 132 51

The effects of glucocorticoids on calcium and bone metabolism were investigated in 11 children (aged 6 months to 13 years) who were treated with dexamethasone, prednisolone and depot-ACTH because of different disorders. Alkaline phosphatase activity and osteocalcin in serum, representing indices of osteoblastic bone synthesis, and urinary hydroxyproline in relation to creatinine in morning fasting urine specimens, an index of osteoclastic bone degradation, decreased by 53-61% from baseline (P less than 0.01), with a highly significant relationship of all 3 indices to each other. Additional influences of glucocorticoids were hyperphosphaturia due to decreased renal phosphate reabsorption not mediated by secondary hyperparathyroidism, as well as marked hypercalciuria. As the consequence of the present study the following prophylactic or therapeutic recommendations are given during steroid-treatment: 1. Approvement of the negative balance of calcium and phosphate by correcting the hypercalciuria with hydrochlorothiazide, and the hypophosphatemia with oral phosphate and 2. in elder children with osteoporosis, stimulation of the decreased osteoblastic bone formation by sodium fluoride.
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PMID:[Disorders of calcium and bone metabolism in glucocorticoid treatment]. 284 91

We evaluated the effects of chronic massive elevations of serum GH and PRL on calcium metabolism in rats bearing the MStT/W15 and 7315a transplantable pituitary tumors. MStT/W15 tumor rats manifest elevated serum GH and PRL levels, hypercalcemia, hypercalciuria, and elevated serum levels of PTH and 1,25-dihydroxyvitamin D. The hypercalcemia was not reversed by dexamethasone or propranolol treatment, but was ameliorated by starvation. Parathyroidectomy produced hypocalcemia in the MStT/W15 tumor rats, confirming the parathyroid dependence of the hypercalcemia. The 7315a tumor produced a milder degree of hypercalcemia, along with elevated serum levels of PRL, ACTH, and corticosterone; serum GH was normal. In high concentrations, PRL and/or GH may stimulate the secretion of PTH as well as enhance dietary calcium absorption, in part through the mediation of 1,25-dihydroxyvitamin D.
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PMID:Hypercalcemia in rats bearing growth hormone- and prolactin-secreting transplantable pituitary tumors. 402 91

Cushing's syndrome, which is characterized by excessive circulating glucocorticoid concentrations, may be due to ACTH-dependent or -independent causes that include anterior pituitary and adrenal cortical tumors, respectively. ACTH secretion is stimulated by CRH, and we report a mouse model for Cushing's syndrome due to an N-ethyl-N-nitrosourea (ENU) induced Crh mutation at -120 bp of the promoter region, which significantly increased luciferase reporter activity and was thus a gain-of-function mutation. Crh(-120/+) mice, when compared with wild-type littermates, had obesity, muscle wasting, thin skin, hair loss, and elevated plasma and urinary concentrations of corticosterone. In addition, Crh(-120/+) mice had hyperglycemia, hyperfructosaminemia, hyperinsulinemia, hypercholesterolemia, hypertriglyceridemia, and hyperleptinemia but normal adiponectin. Crh(-120/+) mice also had low bone mineral density, hypercalcemia, hypercalciuria, and decreased concentrations of plasma PTH and osteocalcin. Bone histomorphometry revealed Crh(-120/+) mice to have significant reductions in mineralizing surface area, mineral apposition, bone formation rates, osteoblast number, and the percentage of corticoendosteal bone covered by osteoblasts, which was accompanied by an increase in adipocytes in the bone marrow. Thus, a mouse model for Cushing's syndrome has been established, and this will help in further elucidating the pathophysiological effects of glucocorticoid excess and in evaluating treatments for corticosteroid-induced osteoporosis.
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PMID:An N-ethyl-N-nitrosourea induced corticotropin-releasing hormone promoter mutation provides a mouse model for endogenous glucocorticoid excess. 2430 25