Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

25-Hydroxyvitamin D (25-OHD) levels were measured in 39 patients with metabolic bone disease or hypoparathyroidism who had been treated with a constant high dose of vitamin D2 or D3 for at least 12 weeks. Plasma 25-OHD levels rose with increasing dosage, the relationship between dose and plasma level being approximately linear whether or not the dose was expressed on a weight-corrected basis. A therapeutic range of 25-OHD to be expected when patients with these conditions are treated with vitamin D has been established. There may be certain exceptions in which plasma 25-OHD levels within the range are associated with either an inadequate response to treatment or, conversely, the hypercalcaemia of vitamin D toxicity. There was no correlation between plasma calcium level and 25-OHD concentration in the group of patients studied. There was also no difference between the dose/25-OHD relationship of patients treated with vitamin D2 and that of patients receiving vitamin D3. Ten patients were started on treatment with large doses of vitamin D during the period of the study. The rate of rise of plasma 25-OHD was followed during treatment. The incremental rise in 25-OHD was calculated at the end of the first week of treatment in terms of dose per unit body weight. The rate of rise of plasma 25-OHD level was highly correlated with the dose used. Plasma 25-OHD levels after one weeks' treatment were only 15-20% of the expected steady-state level on the same dosage. The importance of a high priming dose when a rapid response is needed is thus emphasised.
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PMID:25-Hydroxyvitamin D levels in patients treated with high-dosage ergo- and cholecalciferol. 19 73

A patient presented with the classic features of anticonvulsant-induced osteomalacia. Following discontinuance of diphenylhydantoin therapy and repletion with physiologic quantities of vitamin D, hypercalcemia and persistent biochemical hyperparathyroidism developed, and a parathyroid adenoma was removed. A history of nephrolithiasis and hypercalcemia preceding the institution of drug therapy allowed this patient's underlying parathyroid disease to be defined as primary hyperparathyroidism, which had been obscured by anticonvulsant therapy.
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PMID:Primary hyperparathyroidism presenting as anticonvulsant-induced osteomalacia. 19 3

The early fine structural changes in the arteries of rats induced by excess vitamin D3 perorally or parenterally were essentially similar, except the latter had a more prominent toxic effect to the vascular wall. The ultrastructural features, incidental to calcification, included the appearance of increased ground substance with a separation of collagenous and elastic fibrils, and degenerative changes in smooth muscle cells. Atherosclerosis was greatly accelerated at the sites of vascular injury when cholesterol, cholic acid and thiouracil were added to the basal diet. Calcification was initially observed in relation to elastic fibrils or degenerated cells in the upper and middle layers of the arteries, although there were few such deposits in the thickened intima of the coronary arteries. Calcium deposition could not be a direct effect of hypercalcemia, but the functional activity of smooth muscle cells did seem to promote the mineralization of calcium and phosphate. Furthermore, vitamin D-induced sclerosis did not prevent intimal thickening of the arteries when vitamin D3 was withdrawn.
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PMID:Vitamin D sclerosis in rats. 22 74

Calcium balance studies and measurement of 25-hydroxyvitamin D3 (25[OH]D3) levels were performed on a vitamin D intoxicated, hypoparathyroid patient before, during, and after successful management of hypercalcemia with oral prednisone therapy. Prednisone effected a dramatic reduction in both mean serum calcium levels and mean 24-hour urinary calcium excretion within four days on two separate occasions. No changes were apparent in fecal calcium excretion. Calcium balance became less negative with prednisone treatment. Levels of 25(OH) D3 during the same period did not change. Decreased calcium mobilization from bone best accounted for the glucocorticoid-mediated amelioration of hypercalcemia.
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PMID:Glucocorticoid effects in vitamin D intoxication. 22 30

The occurence of hypercalcemia appears to be unusual in leukemia. The mechanisms are numerous: secretion of PTH of PTH like substance, prostaglandin E2 or vitamin D like sterols. The reported case is one of lymphoblastic acute leukemia and hypercalcemia associated with osteoclast activating factor secreted by leukemic cells. In this patient the serum levels calcium closely paralleled the course of acute leukemia.
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PMID:[Hypercalcemia and osteoclast activating factor (OAF) associated with acute lymphoblastic leukemia (author's transl)]. 22 85

The myopathy associated with vitamin D deficiency has not been well characterized, and it is not known if weakness is a result of a specific effect of vitamin D deficiency on skeletal muscle. Chicks were raised from hatching on a vitamin D-deficient diet, and by 3 wk of age were hypocalcemic and appeared weak. Tension generated by triceps surae during repetitive stimulation of posterior tibial nerve was significantly less than that developed by chicks given vitamin D(3) supplements (309 g tension/g wet weight of triceps surae, SD 60, for vitamin D-deficient chicks; 470, SD 77, for vitamin D(3)-treated chicks, P < 0.01). Histochemical and electron microscopic examination of skeletal muscles of these chicks showed no abnormalities, and there were no electrophysiologic evidences of motor nerve or neuromuscular junction dysfunction. The concentration of ATP in skeletal muscle of the vitamin D-deficient chicks (5.75 mumol/g wet weight, SD 0.17) was not significantly different from that in vitamin D-treated chicks (5.60, SD 0.50). There was no correlation between strength and serum calcium, serum inorganic phosphate, or skeletal muscle inorganic phosphate. Relaxation of tension after tetanic stimulation was slowed in the vitamin D-deficient chicks (20.6 ms, SD 1.7, vs. 15.4, SD 1.3, in vitamin D-treated chicks and 15.3, SD 1.0, in normal control chicks), and in vitro (45)Ca(++) transport by sarcoplasmic reticulum from the vitamin D-deficient chicks was reduced. Calcium content of mitochondria prepared from leg muscles of vitamin D-deficient chicks (24 nmol/mg mitochondrial protein, SD 6) was considerably lower than that of mitochondria from normal control chicks (45, SD 8) or from chicks treated with vitamin D for 2 wk or more (66-100, depending upon level and duration of therapy). Treatment of the vitamin D-deficient chicks from hatching with sufficient dietary calcium to produce hypercalcemia did not significantly raise skeletal muscle mitochondrial calcium content (31 nmol/mg mitochondrial protein, SD 7) and did not prevent weakness. These studies demonstrate objective weakness as a result of myopathy in vitamin D-deficient chicks, and provide evidence that vitamin D deficiency has effects on skeletal muscle calcium metabolism not secondary to altered plasma concentrations of calcium and phosphate.
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PMID:Skeletal muscle calcium metabolism and contractile force in vitamin D-deficient chicks. 22 25

Acute massive vitamin D overdosage occurred in a family after eating food cooked in a nut oil containing 5 million units of vitamin D3/ml. The plasma vitamin D was 55 and 60 i.u./ml in the father and mother respectively, and 9.6 i.u./ml in their 11-month-old infant (normal range, 0--1.6 i.u/ml). All the family presented with symptoms of hypercalcaemia and the infant responded quickly to prednisone. After steroids had failed to control the hypercalcaemia in the parents, neutral phosphate was successful, although necessary for 9 months. Before phosphate therapy it was shown that both parents were in strongly negative calcium balance, indicating that the vitamin D was mobilizing calcium from bone. Eleven years later all 3 patients are well but a renal biopsy in one of them shows persistent nephrocalcinosis.
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PMID:A family with massive acute vitamin D intoxication. 23 12

Twelve children with chronic renal failure (CRF) and sixteen children receiving regular dialysis therapy (RDT) were treated with between 10,000 and 50,000 IU of vitamin D daily. This was associated with an increase in serum calcium levels and reduction in PTH levels. In the children with CRF, secondary hyperparathyroidism was improved with treatment but its development was not completely prevented nor was healing complete. In the patients receiving RDT, treatment with vitamin D improved the changes associated with secondary hyperparathyroidism in 50% of cases but these features sometimes reappeared despite continuing treatment. Hypercalcaemia or metastatic calcification was not seen. Subsequently, 1,25(OH)2D3 was administered to 14 children receiving RDT. This was associated with the return of serum calcium levels to normal, inhibition of PTH synthesis and an improvement in intestinal calcium absorption. Fibro-osteoclasia was cured and there was improvement in actual bone resorption. There was also improvement in osteoidosis in those children who showed disturbances of mineralisation. Calcification in the limbus area of the eyes may occur and hypercalcaemia was seen commonly. Treatment with 1,25(OH)2D3 should only be offered to children with severe renal bone disease. Neither vitamin D3 nor 1,25(OH)2D3 can guarantee complete recovery of osteodystrophy and of growth arrest in uraemic children.
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PMID:Renal bone disorders in children: therapy with vitamin D3 or 1,25-dihydroxycholecalciferol. 23 17

A synthetic biologically active derivative of vitamin D (350 microgram of 1alpha-hydroxycholecalciferol [1alpha(OH)CC]) was injected into 2 nonlactating 7-year-old Israeli-Friesian cows. Plasma calcium values increased after 24 hours, peaked at 48 hours, and returned to base-line values 120 hours after injection. An injection of 350 microgram of 1alpha(OH)CC was given to 23 parturient-paresis-prone Israeli-Friesian cows from 7 days to 6 hours prepartum; 13 cows were injected once, 6 were injected twice, and 4 were injected 3 times, all at 48-hour intervals. Parturient-paresis-prone cows (n = 23) of the same breed were used as controls. Within 0 to 36 hours postpartum, plasma calcium concentrations were found to be higher in cows injected with 1alpha(OH)CC than in the control cows. The increase was highly significant (P less than 0.01) in cows injected at least twice. None of the cows injected with 1alpha(OH)CC, within 72 to 24 hours prior to calving developed parturient paresis; but 9 of 23 control cows developed parturient paresis. Prior to calving, none of the injected cows developed hypercalcemia and there was no local or systemic clinically detectable signs of toxiosis. When given at the right time prepartum, 1alpha(OH)CC is considered to be an improvement over previous methods of preventing bovine parturient paresis.
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PMID:Use of 1alpha-hydroxycholecalciferol in the prevention of bovine parturient paresis. 24 72

Patients with steroid-induced, juvenile and senile osteoporosis were studied using balance techniques. The changes in calciun and phosphorus balance associated with glucocorticoid therapy were corrected with vitamin D and bendrofluazide given in combination. No hypercalcaemia occurred in osteoporotic patients who continued to receive glucocorticoids. Calcium and phosphorus balance was also improved in the osteoporotic subjects not receiving steroids, but these patients became hypercalcaemic during treatment. It is suggested that vitamin D, bendrofluazide and steroids antagonize the actions of one another on the renal tubule, gut and bone and in this way prevent the increased calciuria which occurs with glucocorticoid therapy. Since the increased calciuria and negative calcium balance induced by glucocorticoids is considered to be the result of excessive bone resorption, an adequate dose of bendrofluazide and vitamin D in combination might prevent the development of, or even reverse, steroid-induced osteoporosis.
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PMID:Possible prevention and treatment of steroid-induced osteoporosis. 30 43


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