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)

A patient with sarcoidosis and chronic renal failure was treated for hyperphosphatemia with aluminum hydroxide. The subsequent fall in serum phosphorus was followed by the development of hypercalcemia and nephrolithiasis. Corticosteroid therapy normalized the serum calcium and halted the progression of the nephrolithiasis, but did not improve renal function. Hyperphosphatemia may have blocked the expression of sarcoid hypercalcemia in the patient. The mechanism is unclear but inhibition of the synthesis or action of 1,25-dihydroxyvitamin D may have been involved. Reduction of serum phosphorus may lead to severe hypercalcemia in some patients with sarcoidosis.
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PMID:Hypercalcemia and nephrolithiasis provoked by serum phosphorus reduction in a patient with chronic renal failure and sarcoidosis. 684 58

We studied six oliguric patients with rhabdomyolysis-induced acute renal failure. On admission, all had marked hyperphosphatemia and hypocalcemia associated with low levels of 1,25-dihydroxycholecalciferol [1,25(OH)2D]. During the early polyuric phase, moderate hypercalcemia was accompanied by marked elevations in plasma 1,25(OH)2D and persistent elevations in parathyroid hormone (both amino and carboxy terminals). During the late polyuric phase, the levels of serum calcium and 1,25(OH)2D reverted to normal. Thus, in rhabdomyolysis-induced acute renal failure, the hypocalcemia of the oliguric phase may be secondary to decreased synthesis of 1,25(OH)2D; severe hyperphosphatemia may also have a major role. The hypercalcemia of the polyuric phase may be partly due to increased synthesis of 1,25(OH)2D, resulting from the high parathyroid hormone levels and recovery of renal function.
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PMID:The pathophysiology of altered calcium metabolism in rhabdomyolysis-induced acute renal failure. Interactions of parathyroid hormone, 25-hydroxycholecalciferol, and 1,25-dihydroxycholecalciferol. 689 30

A model of the maternal-fetal metabolism of vitamin D3 is depicted in Fig. 2. 25-OHD3 of maternal origin is metabolized by the maternal kidneys to the potent metabolite, 1,25-(OH)2D3, which acts on the maternal intestine, kidneys, and skeleton. The maternal kidneys and other organs can produce 24,25-(OH)2D3, although this pathway may be suppressed near the end of gestation. The placenta has selective permeability to the vitamin D3 metabolites, with 25-OHD3 crossing from the mother to the fetus more readily than the dihydroxylated metabolites. The onset of the placental synthesis of 1,25-(OH)2D3 during gestation is unknown. Likewise the regulation of the placental 25-OHD3-1 alpha-hydroxylase is unknown. 1,25-(OH)2D3 of placental origin may enter the maternal or the fetal circulation or act locally on the placenta by inducing the synthesis of proteins involved in the cellular transport of Ca. Perhaps one placenta cell type synthesizes 1,25-(OH)2D3 and another cell type possessing a cytoplasmic receptor for 1,25-(OH)2D3 responds to this metabolite. The function of the 24,25-(OH)2D3 produced by the placenta is unknown. The concentration of free 25-OHD3 and free 1,25-(OH)2D3 in the fetal circulation exceeds the maternal levels due to the differences in the DBP concentrations of the two bloodstreams. The 1,25-(OH)2D3 in the fetal bloodstream may originate from either the placenta or the fetal kidneys. The latter site may not be active in utero due to the hypercalcemia and hyperphosphatemia relative to the maternal levels of these ions. 1,25-(OH)2D3 in the fetal bloodstream acts on those fetal tissues containing cytoplasmic receptors for this metabolite. The intestinal mucosa apparently lacks these receptors until sometime during neonatal life. In contrast, fetal bone cells possess receptors for the 1,25-(OH)2D3. The 24,25-(OH)2D3 in the fetal bloodstream may also be involved in the growth and differentiation of the fetal skeleton. However, the precise role of both metabolites in the fetus remains conjectural.
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PMID:Vitamin D and pregnancy: the maternal-fetal metabolism of vitamin D. 702 22

Calcification and ossification of soft tissues occurs as a response to a variety of injuries such as atherosclerosis, myositis ossificans, and caseous necrosis. These injuries and others have as a unifying characteristic persistent necrotic tissue elements. Normal tissues may calcify under conditions of hypercalcemia or hyperphosphatemia. The initial mobilization of Ca and P following injury is rapid, as observed in calcergy. The mitochondria of cells, normally a storehouse of Ca, become preferential sites of precipitated Ca when cells are irreversibly injured, and act as foci of progressive calcification. Collagen fibers undergo calcification directly, principally when they are located within devitalized sites such as prosthetic heart valves, and direct calcification of collagen may predominate generally in dystrophic calcification. VArious porous sponges act as foci for calcification and ossification, and the utilization of porous implants may provide for the development of therapeutically useful calcifying and ossifying biomaterials.
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PMID:Mineralization of connective tissue surrounding implanted devices. 733 Nov 58

Rhabdomyolysis occurred in 25 of 1,000 patients (2.5%) with phencyclidine (PCP) intoxication. 10 of these 25 patients (40%) developed acute renal failure and another 7 had mild impairment in renal function. Marked hyperuricemia was present in all 17 patients, and marked hyperphosphatemia and hypocalcemia were noted in the 10 patients with acute renal failure; 3 of the latter developed hypercalcemia during the diuretic phase of the illness. Fever, tachycardia and hypertension were frequent findings among the 25 patients with rhabdomyolysis and all had leukocytosis. The data show that rhabdomyolysis with and without acute renal failure is not infrequent among abusers of PCP.
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PMID:Rhabdomyolysis with and without acute renal failure in patients with phencyclidine intoxication. 734 47

Persistent hypercalcemia is most often due to tumor. Other causes are best eliminated by clinical methods combined with simple tests. Hypocalcemia is most often a result of hypoalbuminemia. Hyperphosphatemia induced by phosphate infusion or enema may cause profound hypocalcemia. Biochemical profiling may uncover severe hypophosphatemia necessitating phosphate administration. Markedly elevated serum alkaline phosphatase in the absence of hepatic disease is most likely to reflect either Paget's disease of bone or metastatic prostate cancer.
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PMID:Calcium and phosphorus studies: interpretation of results and strategies for further testing. 739 85

Secondary hyperparathyroidism is found in a large proportion, but not all patients on dialysis. Calcitriol controls moderate hyperparathyroidism in most patients but only in a proportion of those with advanced hyperparathyroidism. Patients with nodular parathyroid hyperplasia respond less frequently, presumably because of monoclonal growth and diminished calcitriol-receptor expression by parathyroid cells. In patients with nodular parathyroid hyperplasia, parathyroidectomy is an important alternative to calcitriol treatment. A priori reasoning indicates that prophylactic administration of calcitriol (to prevent parathyroid hyperplasia) is a reasonable option, but currently no controlled evidence for long-term efficacy of this approach without side effects is available. Intermittent administration of calcitriol by intravenous or oral routes is effective and, at least in experimental studies, superior to continuous calcitriol. However, in clinical comparisons, no superiority of intravenous versus oral or daily versus intermittent calcitriol has been documented. Calcitriol treatment must be closely supervised to prevent hypercalcemia, hyperphosphatemia, and excessive suppression of parathyroid hormone. Because of an altered dose response relationship, parathyroid hormone levels should not be completely normalized so as to prevent low bone turnover (adynamic bone lesion).
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PMID:Vitamin D therapy in patients receiving dialysis. 761 32

We prospectively studied the long-term effects of intravenous calcitriol in 17 hemodialysis patients with severe secondary hyperparathyroidism (HPT) for 25.7 +/- 3.4 (+/- SE) months. Calcitriol was given thrice weekly after dialysis. Subsequently, changes were made every 3-4 weeks based upon serum chemistries. Total calcium and inorganic phosphorus were measured weekly; alkaline phosphatase (AP) and IRMA-PTH were measured monthly. Inorganic phosphate was controlled with calcium supplements. With calcitriol therapy both IRMA-PTH and AP decreased from 876 +/- 113 to 65 +/- 13 pg/ml (p < or = 0.001) and 432 +/- 106 to 103 +/- 15 U/ml (p < or = 0.001), respectively. Each patient had a reduction in IRMA-PTH and AP. Nadir IRMA-PTH occurred at 55.4 +/- 7.3 weeks. The maximum and mean maximum doses of calcitriol were 8.0 and 4.1 +/- 0.4 micrograms thrice weekly, respectively. Hypercalcemia tended to occur in those patients who were hypercalcemic prior to the initiation of intravenous calcitriol therapy. All hypercalcemic episodes were asymptomatic and reversed either by temporary withdrawal or lowering of the calcitriol dose. Hyperphosphatemia developed in those patients with a history of elevated serum phosphates and was mostly related to dietary and medication noncompliance. We conclude that intravenous calcitriol was uniformly effective and safe for the long-term therapy of severe HPT in ESRD. Careful attention to serum phosphate control is required.
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PMID:Long-term high dose intravenous calcitriol therapy in end-stage renal disease patients with severe secondary hyperparathyroidism. 763 48

Effect of vitamin D3 administration (12,000 IU/100 g body wt.) on levels of serum calcium and inorganic phosphorus levels in the smooth water snake, Enhydris enhydris was investigated. Hypercalcemia and hyperphosphatemia was observed from day one till the end of the experiment (day 14). Maximum values were recorded on the 4th day followed by a steady decline.
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PMID:Effects of vitamin D3 administration on the levels of serum calcium and inorganic phosphorus in the smooth water snake, Enhydris enhydris (Schneider). 766 Aug 31

We evaluated the effect of pulse oral calcitriol (4 micrograms three times weekly for 6 months) on parathyroid function in nine CAPD patients with hyperparathyroidism refractory to conventional low-dose oral calcitriol. Zero calcium peritoneal solutions were used to prevent the development of hypercalcaemia. The peritoneal loss of calcium increased from 168 +/- 40 to 417 +/- 48 mg/day using zero calcium solutions. Pulse oral calcitriol resulted in a significant decrease in PTH (from 617 +/- 272 to 382 +/- 299 pg/ml) by the 15th day of therapy, while serum iCa did not change from baseline. During the first month of therapy the mean PTH levels remained significantly reduced compared to baseline, thereafter PTH increased in four of nine patients. Hyperphosphataemia was not satisfactorily controlled in four patients, despite large amounts of binders used; seven of nine patients developed hypercalcaemia and required either the substitution of calcium acetate for calcium carbonate or reduction of calcitriol dose. Three patients showed a progressive increase in PTH. In conclusion our data suggest that in most CAPD patients with severe hyperparathyroidism oral calcitriol pulse therapy is not effective in maintaining a permanent suppression in PTH levels.
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PMID:High-dose oral calcitriol and zero calcium peritoneal solutions in CAPD patients with refractory secondary hyperparathyroidism. 770 73


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