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)

The treatment of myelodysplastic disorders with vitamins A and D or derivatives and nutrients has been less than satisfactory. Combinations of vitamin D3 and 13-CRA with or without cytosine arabinoside appear to offer no advantage over any of the single agents alone. Until other vitamin D derivatives are developed that are effective but do not cause hypercalcemia, vitamin D3 cannot be recommended for the treatment of MDS. 13-CRA has been shown to be effective in some patients with MDS; however, it cannot be recommended as standard therapy because of the conflicting data cited above. Further clinical trials with 13-CRA perhaps in combination with vitamin E or colony-stimulating factors are clearly indicated for this disease for which we have no effective therapy.
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PMID:New uses for old vitamins. The treatment of myelodysplastic disorders. 832 Oct 79

Fat soluble vitamins (except vitamin K) are protein bounded with subsequent storage in the body. It is generally accepted that plasma level of vitamin A is increased in majority of patients with chronic renal insufficiency (CRI) including those on continuous ambulatory peritoneal dialysis (CAPD). Thus, there is no need to supplement this vitamin in CRI patients (pts). Plasma level of vitamin E in CRI pts may be elevated, normal or decreased. It seems to be justified to supplement this vitamin, in spite of its normal plasma level, in case platelet aggregation is increased. Both in dialyzed and nondialyzed CRI pts a normal serum level of vitamin K has been observed. Decreased or extremely low serum level of vitamin D following the gradual loss of renal tissue is to be observed in CRI pts. This deficit is regarded as the main factor leading to the decrease in serum level of calcium, the secondary hyperparathyroidism and bone changes. Treatment with 1.25(OH)2D3 (calcitriol) proved to be most successful in alleviation of symptoms resulting from the deficit of vitamin D3 in the body. Intravenous "pulsating" administration of calcitriol results in rapid normalization of serum PTH level. Treatment with 25(OH)D3 (calcidiol) given orally 3 times a week ("pulsating" method) revealed also fairly good results in this respect. During treatment with vitamin D3 hypercalcemia tends to develop, serum alkaline phosphatase normalizes, elevated PTH serum level decreases. Vitamin D metabolites are less active than 1.25(OH)2D3 being less hypercalcemic.
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PMID:[Vitamin disturbances in chronic renal insufficiency. II. Fat soluble vitamins]. 871 Nov 72

It is shown, that hepatocytes contain two (microsomal and mitochondrial) vitamin D3 25-hydroxylase enzymes, which differ as to their activity and function with maximal activity at different concentrations to substrate, namely at 15 microM and 100 microM of vitamin D3, accordingly. Activity of vitamin D3 25-hydroxylase enzymes of hepatocytes is regulated by cholecalciferol and alpha-tocopherol. The general and microsomal vitamin D3 25-hydroxylase enzymes activity of hepatocytes is lowered, but mitochondrial isoform is increased under D-hypervitaminosis conditions. Vitamin E increases microsomal vitamin D3 25-hydroxylase activity and decreases mitochondrial isoform activity of rats hepatocytes under D-hypervitaminosis conditions. It is established that D-hypervitaminosis is accompanied by expressed hypercalcemia and hyperphosphatemia, by decreased contents of mineral components in the bone tissue and high activity of alkaline phosphatase in the blood serum. The physiological doses of vitamin E under these conditions normalized the mineral metabolism, contents of calcium, phosphates and activity of alkaline phosphatase isoform in the blood serum.
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PMID:[Features of cholecalciferol hydroxylation in the liver of rats in conditions of D-hypervitaminosis and activity of alpha-tocopherol]. 2068 47

A previously healthy 19 year-old male presented to the hospital with anorexia, nausea, and vomiting. Laboratory studies were significant for hypercalcemia (peak calcium value of 14.8 mg/dL) and acute kidney injury (peak serum creatinine of 2.88 mg/dL). He admitted to using a parenteral formulation of vitamins A, D and E restricted for veterinary use containing 20,000,000 IU of vitamin A; 5,000,000 IU of vitamin D3; and 6,800 IU of vitamin E per 100 mL vial. The patient stated to have used close to 300 mL of the product over the preceding year. Interestingly, the young man was not interested in the massive amounts of vitamins that the product contained; he was only after the local effects of the oily vehicle. The swelling produced by the injection resulted in a silicone-like effect, which gave the impression of bigger muscles. Nevertheless, the product was absorbed and caused hypervitaminosis. The serum level of 25(OH) vitamin D was clearly elevated at 150 ng/mL (reference range from 30 to 60 ng/mL), but in most published cases of vitamin D toxicity, serum levels have been well above 200 ng/mL. His PTH level was undetectable and other potential causes of hypercalcemia were excluded. Therefore, we posit that the severity of the hypercalcemia observed in this case was the result of a synergistic effect of vitamins A and D. The patient was treated with normal saline, furosemide and zolendronic acid, with rapid normalization of calcium levels and renal function.
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PMID:Hypercalcemia and acute kidney injury caused by abuse of a parenteral veterinary compound containing vitamins A, D, and E. 2218 12