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)

Injection of about 1 ng/g body wt per day of either vitamin D3 or 1,25-(OH)2-vitamin D3 for 7 days induces hypercalcemia and hyperphosphatemia in fed American eels, Anguilla rostrata, but only hyperphosphatemia in unfed eels. These same analogs also stimulated the uptake of 45Ca from intestinal sacs in situ. The vitamin D3 appeared to be relatively more effective than the 1,25-(OH)2D3 metabolite and chlorpromazine inhibited the effect of vitamin D3 on intestinal calcium uptake. 7-Dehydrocholesterol, vitamin D2, and 24,25-(OH)2D3 did not stimulate hypercalcemia, hyperphosphatemia, or intestinal calcium uptake.
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PMID:Effect of various vitamin D analogs on plasma calcium and phosphorus and intestinal calcium absorption in fed and unfed American eels, Anguilla rostrata. 608 57

Radioactive imaging agents are chemically designed for selective distribution. Another approach to selectivity is to find stable compounds that favorably influence this distribution. Using a rat model of myocardial necrosis, we studied effects of various stable compounds (as a single, large dose or fractionated into short series) on the ratio, uptake of Tc-99m pyrophosphate (PPi) by the target lesion/uptake by the principal nontarget, bone (L/B). Vitamin D3s ability to increase L/B was mediated by the hypercalcemia and hyperphosphatemia that it caused. The hypercalcemia was accompanied by increased [Ca] in the lesion. In contrast, pulse doses of desoxycorticosterone acetate (DOCA) at 7 and 6 hr before killing increased uptake by lesion, increasing L/B from 0.19 +/- 0.03 to 0.45 +/- 0.08 (p less than 0.01), with no change in serum [Ca] and minimal changes in serum [P], [Na], and [K]. DOCA also increased the lesion-to-blood ratio from 6.5 +/- 0.07 to 15.4 +/- 3.9 (p less than 0.05). These results encourage further study of DOCA's effect and investigation of other stable drugs that may influence distribution of other imaging agents.
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PMID:Effect of vitamin D3, other drugs altering serum calcium or phosphorus concentrations, and desoxycorticosterone on the distribution of Tc-99m pyrophosphate between target and nontarget tissues. 626 65

The objectives of this study were to evaluate the effects of vitamin D(3) (D(3)) and 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) on uremic bone disease independent of their action on the intestine. The histomorphology of tibial metaphyses in uremic (5/6 nephrectomized [5/6 Nx]) rats fed a low-calcium-low-phosphorus (LCLP) diet was compared with sham-operated (SO) rats fed an LCLP diet and 5/6 Nx rats fed an LCLP diet and given 15,000 IU D(3) or 5 units (135 ng) 1,25-(OH)(2)D(3) daily for 7 days. A marked osteomalacia characterized by an increased percentage of active and inactive trabecular osteoid surface and thickened growth plates developed in proximal tibial metaphyses in 5/6 Nx rats given the placebo, compared with SO rats. These bone changes were associated with relative hypophosphatemia, hypophosphaturia, and hypercalciuria in 5/6 Nx rats. In 5/6 Nx rats treated with D(3) or 1,25-(OH)(2)D(3) the growth plates had undergone mineralization and vascular invasion and were markedly reduced in thickness. Other parameters of osteomalacia in trabecular bone were not different from 5/6 Nx rats given the placebo. There was a significant decrease in osteoclasts per millimeter of trabecular surface perimeter in D(3)- and 1,25-(OH)(2)D(3)-treated rats. These bone changes were associated with hypercalcemia, hyperphosphatemia, and hyperphosphaturia, compared with 5/6 Nx rats given the placebo. It was concluded that in uremic rats fed the LCLP diet, shortterm treatment with either pharmacologic levels of D(3) or 1,25-(OH)(2)D(3) corrected only lesions in the growth plate. Osteoid seams were not reduced in treated rats, although the serum calcium-phosphorus product was elevated. The 5/6 Nx rat fed the LCLP diet appears to be a useful model for the rapid induction of uremic osteomalacia in adult animals.
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PMID:Short-term effects of vitamin D3 and 1,25-dihydroxyvitamin D3 on osteomalacia in uremic rats fed a low calcium-low-phosphorus diet. 626 57

Experimental hypervitaminosis D was produced in rabbits by feeding 25,000 I.U. vitamin D3 or the corresponding amount of vitamin D3 palmitate per kg of diet. Hypercalcemia and hyperphosphatemia was accompanied by increased CaBP activity and reduced weight gain in the vitamin D3 group as well as in the vitamin D3 ester group. The degree of calcification in the aorta and in the kidney also was similar in both groups. Increasing the vitamin intake by giving 10,000 I.U. vitamin D3 or vitamin D3 palmitate per day resulted in earlier and more widespread calcific deposits. In rats, receiving 50,000 I.U. vitamins D3 or vitamin D3 palmitate per kg of diet, calcification in soft tissue was much less extensive than in rabbits. But again, no difference was seen between vitamin D3 and vitamin D3 palmitate. These results indicate, that vitamin D3 esters are not suitable as a less calcinogenic form of vitamin D3.
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PMID:Calcinogenic activity of vitamin D3 and vitamin D3 palmitate in rat and rabbit. 627 15

Large parenteral doses of vitamin D3 (15 to 17.5 x 10(6) IU vitamin D3) were associated with prolonged hypercalcemia, hyperphosphatemia, and large increases of vitamin D3 and its metabolites in the blood plasma of nonlactating nonpregnant and pregnant Jersey cows. Calcium concentrations 1 day postpartum were higher in cows treated with vitamin D3 about 32 days prepartum (8.8 mg/100 ml) than in control cows (5.5 mg/100 ml). None of the cows treated with vitamin D3 showed signs of milk fever during the peripartal period; however, 22% of the control cows developed clinical signs of milk fever during this period. Signs of vitamin D3 toxicity were not observed in nonlactating nonpregnant cows; however, pregnant cows commonly developed severe signs of vitamin D3 toxicity and 10 of 17 cows died. There was widespread metastatic calcification in the cows that died. Because of the extreme toxicity of vitamin D3 in pregnant Jersey cows and the low margin of safety between doses of vitamin D3 that prevent milk fever and doses that induce milk fever, we concluded that vitamin D3 cannot be used practically to prevent milk fever when injected several weeks prepartum.
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PMID:Vitamin D3 toxicity in dairy cows. 628 38

To clarify the role of vitamin D in renal phosphate transport, weanling rats were fed a vitamin D-deficient diet containing 1.8% calcium and 1.2% phosphorus. After 5-6 wk, the rats were normocalcemic, normophosphatemic, and had normal levels of PTH. Assays of vitamin D metabolites revealed undetectable plasma levels of 25(OH)D, and 1,25(OH)2D levels of 92 +/- 16 pg/ml in partially vitamin D-depleted (PVDD) rats and 169 +/- 58 pg/ml in normal rats. PVDD rats had increased phosphate excretion, both absolute and fractional, and a decrease in Na+ gradient-dependent Pi transport in proximal tubular brush border membrane vesicles (BBMV) prepared from their kidneys. Vitamin D repletion of PVDD rats with 1,25(OH)2D3, 15 pmol/100 g body wt, decreased fractional excretion of Pi from 22.6 +/- 1.9 to 13.5 +/- 1.3%; the latter values were similar to normal rats. Repletion with 1,25(OH)2D3 also increased Na+-dependent phosphate transport in BBMV from 322 +/- 24 pmol X mg protein-1 X 15 s-1 in BBMV from PVDD rats to 698 +/- 70 pmol X mg protein-1 X 15 s-1. Repletion with larger doses of 1,25(OH)2D3 produced hypercalcemia and hyperphosphatemia from intestinal absorption, an increase in phosphate excretion, and a blunted response of Pi transport to 1,25(OH)2D3. Prevention of hyperphosphatemia by dietary adjustments allowed full expression of the stimulatory effects of 1,25(OH)2D3 on Pi transport. These later data may partially explain the inhibitory effects reported in prior studies in which plasma Pi was not controlled and the larger doses of 1,25(OH)2D3 administered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of 1,25-dihydroxycholecalciferol on phosphate transport in vitamin D-deprived rats. 633 Dec 1

Experimental chronic renal failure (CRF) in rats gave rise to azotemia, hyperphosphatemia, reduction in the proportion of the diaphyses, decrease in them of calcium, phosphorus and hydroxyproline, and to the lowering of the calcium content in the epiphyses. Administration to the animals of 0.025 microgram of 1,25-dioxycholecalciferol (1,25(OH)2D3) a day did not make the indicators under consideration return to normal. At the same time 1,25(OH)2D3 enhanced the degree of hyperphosphatemia and demineralization of the epiphyses, provoked moderate hypercalcemia and dramatically enhanced calcinosis in the aorta and in the remainder of the kidney. Administration of 24,25-dioxycholecalciferol (24,25(OH)2D3) in a dose of 0.25 microgram made the majority of the indicators return to normal, increasing the proportion of the diaphyses and the content in them of calcium and phosphorus, reducing the blood phosphorus content and the degree of azotemia. Furthermore, 24,25(OH)2D3 raised the collagen content in the diaphyses and epiphyses. A higher dose of 24,25(OH)2D3 (1.25 microgram) did not appear more effective. In none the doses applied, 24,25(OH)2D3 produced hypercalcemia or calcinosis. Combination of 1,25(OH)2D3 in a dose of 0,025 microgram and 24,25(OH)2D3 in a dose of 1,25 microgram slightly reduced the hypercalcemic, hyperphosphatemic and calcinosis-inducing effects of 1,25(OH)2D3, completely prevented osteoporotic alterations in the diaphyses, but enhanced the demineralization in the epiphyses, which may point to the advisability of reducing the doses of these metabolites on combined use. The data obtained indicate that 24,25(OH)2D3 is a more effective and safer agent for correcting the disturbances of the phosphorus-calcium metabolism and osseous lesions in CRF than 1,25(OH)2D3.
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PMID:[Effect of 24,25-dioxycholecalciferol on calcium-phosphorus metabolism and bone tissue in rats with experimental renal failure]. 633 22

Although hypervitaminosis A is not uncommon, fatal cases are rare. We describe a neonate who died after having ingested more than 60 times the suggested dose of vitamin A per day, for 11 days. His hospital course was marked by hypercalcemia, hyperphosphatemia, a bleeding disorder, and pulmonary insufficiency. An autopsy showed extensive calcifications of the alveolar septa and bronchioles. Metastatic calcifications were also present in the kidneys, stomach, soft tissue, and skin. The skeleton showed prominent alteration of the endochondral bone formation. There was also evidence of accelerated resorption of bone, which is presumably responsible for the development of hypercalcemia and metastatic calcification.
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PMID:Fatal hypervitaminosis A in a neonate. 654 25

Individuals with cancer are subject to fluid and electrolyte imbalances because of the original disease process, therapy, and complications resulting from both the disease process and from therapy. These imbalances are life threatening either when they become extreme or when they occur very rapidly. Although almost any fluid and electrolyte disorder or combination of disorders can occur in people with cancer, this article will focus on the following more common, potentially critical imbalances: water excess, decreased vascular volume, hypercalcemia, hypokalemia, and tumor lysis syndrome, which includes hypocalcemia, hyperphosphatemia, hyperuricemia, and hyperkalemia. These imbalances will each be reviewed with a focus on their causes, signs and symptoms, and treatment. Additional readings on fluid and electrolyte imbalances in patients with cancer can be found in several recent articles.
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PMID:Fluid and electrolyte disturbances associated with cancer and its treatment. 675 72

Symptomatic osteopenia accompanied by subclinical hyperthyroidism developed in three women who were receiving excess thyroid hormone medication. Excessive thyroid replacement therapy resulted in mild hypercalcemia, hyperphosphatemia, and hyperphosphatasemia associated with diffuse skeletal demineralization and multiple fractures. Nondecalcified sections of double tetracycline-labeled iliac crest bone showed an accelerated rate of bone turnover with marked osteoclastosis and resorption of the cortical as well as the trabecular bone, typical of endogenous hyperthyroidism. Since thyroid hormones are among the most frequently prescribed medications, bone loss caused by exogenous hyperthyroidism may be more common than previously recognized.
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PMID:Exogenous hyperthyroidism with osteoporosis. 683 Mar 80


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