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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma concentrations of vitamin D3 (cholecalciferol) metabolites have been studied in rainbow trout (Salmo gairdneri) adapted to varying environmental calcium concentrations in both fresh water and artificial seawater, and in natural seawater. In vivo, intraarterial injection of tritiated 25-hydroxycholecalciferol was followed by its transformation to a number of metabolites including compounds that cochromatographed on high performance liquid chromatography (HPLC) with 1,25-dihydroxycholecalciferol and 25,26-dihydroxycholecalciferol. Hypercalcaemia and increased environmental calcium were associated with a greater transformation to the compound cochromatographing with 25,26-dihydroxycholecalciferol, while hypocalcaemia and reduced environmental calcium concentrations induced more conversion to the 1,25-dihydroxycholecalciferol-like compound. In vitro, both metabolites were produced by liver but not by kidney preparations, and the difference in conversion ratios observed in vivo associated with changes in plasma calcium were also seen in vitro. It is concluded that the metabolism of 25-hydroxycholecalciferol in the trout can be influenced by calcium status, but at present the physiological importance of this metabolism and the mechanisms and site(s) of action of the metabolites are unknown.
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PMID:Metabolism of 25-hydroxycholecalciferol in a teleost fish, the rainbow trout (Salmo gairdneri). 355 76

Administration of 1,25-dihydroxycholecalciferol (0.5 microgram/d/100 g body weight) to vitamin D repleted rats produced a significant decrease in the number of femoral marrow cells, specially in the erythroid line. Analysis of blood revealed slight anemia with reticulocytopenia. The survival time of 51-Cr-labelled red cells was unaffected by treatment, suggesting that bone marrow became unable to replace cells at a normal rate. The adverse effect on erythropoiesis appeared related to the degree of the concurrent hypercalcemia, which in turn depends upon the calcium content of the diet.
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PMID:Adverse effect of 1,25-dihydroxycholecalciferol on erythrocyte precursors in the rat. 360 4

The relative potencies of 1,25-dihydroxycholecalciferol, 24-F-1,25-dihydroxycholecalciferol, and 24,24-F2-1,25-dihydroxycholecalciferol at three doses (25, 100 or 400 micrograms) were assessed in nonlactating Jersey cows. The 24,24-F2-1,25-dihydroxycholecalciferol induced a significantly greater hypercalcemia and hyperphosphatemia than did 1,25-dihydroxycholecalciferol. The 24-F-1,25-dihydroxycholecalciferol was intermediate in its hypercalcemic and hyperphosphatemic potency. Urinary hydroxyproline excretion rate and plasma hydroxyproline concentration were not significantly increased by treatment with any of the compounds. This indicates that these compounds did not stimulate bone resorption in nonlactating, nongravid cows. Renal function was significantly impaired in cows that received a 400-micrograms dose of any compound. There was a severe reduction in glomerular filtration rate (up to 42%) and urine specific gravity. Renal function was most severely affected in cows treated with 24,24-F2-dihydroxycholecalciferol and was evident even at the 100-micrograms dosage level.
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PMID:Bone resorption, renal function and mineral status in cows treated with 1,25-dihydroxycholecalciferol and its 24-fluoro analogues. 376 Oct 6

A patient on maintenance hemodialysis had widely disseminated tuberculosis, hypercalcemia, and elevated levels of calcitriol (1,25-dihydroxycholecalciferol). Hypercalcemia was not observed until the eighth month of hemodialysis, when persistent fevers began. At the end of a calcium-free dialysis, the plasma calcium concentration decreased to 6.6 mg/dL (1.65 mmol/L). The baseline calcitriol level was 56 pg/mL (normal, 19 to 50 pg/mL) and increased to 147 pg/mL at the end of hemodialysis. Parathyroid hormone levels by three separate assays did not appreciably increase during the hypocalcemia induced by the calcium-free hemodialysis. The serum phosphate concentration decreased from 7.3 to 4.5 mg/dL (2.36 to 1.45 mmol/L). Extrarenal production of calcitriol may occur in disseminated tuberculosis and may be stimulated by hypocalcemia and reduced serum phosphate. The expected parathyroid hormone response to hypocalcemia may have been inhibited by persistently elevated calcitriol levels or preexisting hypercalcemia.
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PMID:Hypercalcemia and elevated calcitriol in a maintenance dialysis patient with tuberculosis. 376 40

A 58-year-old man was initially seen with fatigue and weight loss. Laboratory examination detected hypercalcemia, elevated 1,25-dihydroxycholecalciferol levels, low parathyroid hormone (PTH) concentrations, and subperiosteal bone resorption. The patient underwent subtotal parathyroidectomy for presumed hyperparathyroidism, but serum calcium and 1,25-dihydroxycholecalciferol levels remained elevated following surgery. Search for another cause of the hypercalcemia disclosed enlarged para-aortic lymph nodes, biopsy specimens of which demonstrated Hodgkin's disease. After treatment of the patient with two cycles of chemotherapy with mechlorethamine hydrochloride, vincristine sulfate, procarbazine hydrochloride, and prednisone, serum calcium, 1,25-dihydroxycholecalciferol, and PTH levels normalized. We speculate that the humoral hypercalcemia in this patient resulted from tumor production of 1,25-dihydroxycholecalciferol.
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PMID:Humoral hypercalcemia in Hodgkin's disease. Association with elevated 1,25-dihydroxycholecalciferol levels and subperiosteal bone resorption. 383 28

A 42-year-old woman, with a previously resected jejunal leiomyoblastoma, was first seen with liver metastases 31/2 years after the tumor resection. Intractable malignant hypercalcemia appeared eight months later, together with renal insufficiency. No osteolytic lesions were detected. Levels of parathyroid hormone, cyclic adenosine monophosphate, and 1,25-dihydroxycholecalciferol (1,25[OH]2D) were not useful in distinguishing between the hypercalcemia of malignancy and concurrent hyperparathyroidism. Despite renal insufficiency, hypercalcemia, and subtotal parathyroidectomy, the 1,25(OH)2D levels remained elevated, consistent with the speculation that a tumor product stimulated 1-alpha-hydroxylation of 25-hydroxycholecalciferol. Phenytoin and phenobarbital (enzyme induction therapy), in combination with phosphorus and glucocorticoids, appeared to be useful in controlling the hypercalcemia.
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PMID:Leiomyoblastoma associated with intractable hypercalcemia and elevated 1,25-dihydroxycholecalciferol levels. Treatment by hepatic enzyme induction. 383 34

1 alpha,25-Dihydroxyvitamin D3 [1 alpha,25(OH)2D3], a hormonally active form of vitamin D3, was found to inhibit the promotional phase of 7,12-dimethylbenz[a]anthracene-induced skin carcinogenesis in female Sencar mice. Topical application of 1 alpha,25-(OH)2D3 once a week at a dose of 1 micrograms or less, a tolerable dose from hypercalcemia, dose dependently inhibited tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). When 1 micrograms of 1 alpha,25(OH)2D3 was applied 30 min before 5 micrograms of TPA, the times required for 50 and 100% tumor incidence were delayed about 2.5 and 7 weeks, respectively, and the number of tumors per mouse was decreased by 25-30%. This inhibitory effect was more pronounced when examined by a two-stage promotion protocol, in which a single application of 5 micrograms of TPA (Stage I) was followed by repeated applications of 5 micrograms of mezerein once a week for 19 weeks (Stage II). When 1 alpha,25(OH)2D3 at 1 micrograms was applied at Stage I + II or Stage II, tumor formation was markedly suppressed, resulting in decrease of about 70-80% in the incidence and 87-90% in the number of tumors per mouse. Application of 1 alpha,25(OH)2D3 at Stage I only did not inhibit tumor formation, indicating that 1 alpha,25(OH)2D3 specifically inhibited Stage II promotion. These results are in good agreement with the previous and present findings that 1 alpha,25(OH)2D3 inhibited induction of epidermal ornithine decarboxylase by TPA and mezerein. The possibility that 1 alpha,25(OH)2D3 suppressed tumor promotion by killing initiated cells rather than inhibiting promotion was ruled out by an experiment in which TPA was applied to the 1 alpha,25(OH)2D3 alone-treated animals.
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PMID:Inhibition of tumor promotion in mouse skin by 1 alpha,25-dihydroxyvitamin D3. 384 Apr 12

In a 26-year-old patient admitted to the emergency ward with acute abdomen, all the symptoms--nausea, vomiting, indeterminate abdominal pain, constipation, renal failure, polyuria and polydipsia--could be explained by calcium intoxication syndrome. Investigation revealed generalized sarcoidosis. Under medical treatment with prednisone all the pathologic findings rapidly regressed. The pathogenesis of hypercalcemia in sarcoidosis, and particularly the disorder of vitamin D metabolism with raised levels of 1,25-dihydroxycholecalciferol, are discussed.
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PMID:[Acute hypercalcemia syndrome in sarcoidosis]. 384 Sep 13

The possible contribution of catecholamines and vitamin D3 metabolites to the high plasma calcitonin (CT) levels in suckling baby rats is unknown. So, in vivo and in vitro (using a perifusion system) effects of beta-adrenergic agents and vitamin D3 metabolites on CT release were studied in the rat during the postnatal development. In 13-day-old rats, the increase in plasma CT levels induced by isoproterenol injection (0.1 micrograms/kg b.w.) was inhibited by a previous administration of propranolol. A significant decrease in plasma CT levels was observed after propranolol injection in baby rats (0.68 +/- 0.05 ng/ml vs. 0.93 +/- 0.01 ng/ml). A daily injection of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3; 25 pmoles/rat/day during 4 days) induced a marked rise in plasma calcium (16.1 +/- 0.2 mg/dl), and a great decrease in thyroidal CT contents (approximately 70% of control values) in 13-day-old rats while no change was noted with 24,25-dihydroxycholecalciferol (24,25-(OH)2D3). A negative correlation between plasma calcium and thyroidal CT stores was found in suckling and in weaning rats treated with different doses of 1,25-(OH)2D3, suggesting an indirect effect of 1,25-(OH)2D3 on CT secretion. The mobilization of the thyroidal CT content was greater in weaning than in suckling rats in response to a given hypercalcemia. In vitro, 5 X 10(-5) M isoproterenol induced a rapid increase in CT secretion rate while 1,25-(OH)2D3 inhibited the rise in CT release induced by 3.0 mM calcium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcitonin secretion during postnatal development in the rat: beta-adrenergic agents and vitamin D3 metabolites. 614 Dec 91

High daily oral doses of 10 micrograms 1 alpha-hydroxycholecalciferol (1 alpha-OHD3) administered to adult rats produced toxic effects such as loss of body weight, hypercalcemia and bone resorption. However, small (0.09 microgram) and moderate (0.9 microgram) daily doses of 1 alpha-OHD3 did not produce toxic effects during six weeks of observation. Serum calcium level was only slightly raised, but bone mass, bone mineral and organic matter contents, including collagen and nucleic acids of the cortical bone matrix, significantly increased, while the amount of glycosaminoglycans was reduced. Treatment with small daily doses of 1 alpha-OHD3 (0.09 microgram/day for six weeks) produced a more pronounced effect on the variables studied than did the moderate dosage (0.9 microgram). 1 alpha-OHD3 promotes new bone formation in the mature rat skeleton after conversion to 1,25 dihydroxycholecalciferol [1,25(OH)2D3] in the liver, probably by exerting a direct effect on bone tissue rather than through indirect hormonal events.
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PMID:Effect of 1 alpha-hydroxycholecalciferol on bone mass and composition of cortical bone in adult male rats. 616 32


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