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

The "enteque seco" is a disease of calcinosis, i.e., pathological deposition of calcium phosphate in soft tissues, which occurs in grazing cattle in Argentina and is of considerable economic importance. The ingestion of leaves of Solanum malacoxylon has been identified as the cause of the disease. Hypercalcemia and/or hyperphosphatemia and mineralization of the cardiovascular and pulmonary systems are usually seen in bovines or experimental animals exposed to this plant. The symptoms of the disease resemble those of vitamin D intoxication. In agreement with these observations, a glycoside derivative of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the hormonally active form of vitamin D in animals, has been identified as the toxic principle of S. malacoxylon. Glycoside conjugates of its precursors, 25-hydroxyvitamin D3 and vitamin D3, may also be present. Recent studies indicate that the plant factor is modified in the rumen of bovines through cleavage of the glycosidic linkage and further conversion of the released 1,25(OH)2D3 to a more polar metabolite, possibly 1,24,25-trihydroxyvitamin D3. Excess free 1,25(OH)2D3 may alter extracellular and intracellular Ca homeostasis in intoxicated animals through a receptor-mediated mechanism and activation of membrane Ca channels. In addition, 1,24,25(OH)3D3 may potentiate the effects of 1,25(OH)2D3 on intestinal Ca transport.
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PMID:Solanum malacoxylon: a toxic plant which affects animal calcium metabolism. 307 67

The efficacy and safety of calcium carbonate as a phosphate binder was evaluated in 20 patients on chronic hemodialysis who had previously received aluminum hydroxide. During the control period the patients were on aluminum hydroxide and calcitriol therapy and had plasma phosphorus levels less than 6 mg/dL (4.95 +/- 0.8 mg/dL). Aluminum hydroxide was then discontinued and no phosphate binder was prescribed for 1 month. Every patient developed hyperphosphatemia so that calcium carbonate treatment was begun and calcitriol dose was adjusted in relation to plasma calcium changes. After 24 months of calcium carbonate therapy, plasma phosphorus was 4.85 +/- 0.7 mg/dL, using a daily dose of calcium carbonate of 2.57 +/- 1.3 g (range, 1 to 6 g). The daily dose per patient of calcitriol was not different from that prescribed during the control period, but in five patients calcitriol was permanently withdrawn for hypercalcemia. At the end of the study plasma calcium, magnesium, bicarbonate, alkaline phosphatase, and parathyroid hormone values were unchanged in comparison with the control period, whereas a significant reduction in plasma aluminum and plasma aluminum increase induced by deferoxamine infusion was observed. The frequency of hypercalcemic and hyperphosphatemic episodes during the last 12 months of calcium carbonate therapy (6.2% and 16.6%, respectively) was not different from that observed during the 12 months on aluminum hydroxide therapy preceding the control period (4.5% and 14.7%, respectively). It was concluded that calcium carbonate is effective in the control of hyperphosphatemia and secondary hyperparathyroidism in patients on chronic hemodialysis and that the incidence of hypercalcemia is low when the daily dosage is less than 6 g.
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PMID:Efficacy and safety of long-term treatment with calcium carbonate as a phosphate binder. 314 60

We evaluated musculoskeletal complaints related to arthropathy in 28 patients with end stage renal failure receiving maintenance dialysis. Twenty-three of 28 patients had arthritic complaints and 14 had an arthropathy. Six of 14 patients with arthropathy had a pattern resembling calcium pyrophosphate dihydrate deposition (CPPD) disease, 4 patients had moderately severe osteoarthritis, 3 had calcific periarthritis, and 1 patient had acute arthritis with intermittent pain and swelling. Factors which predispose to metabolic arthropathies were observed as follows: 29% elevated ferritin; 39% history of hyperparathyroidism; 68% elevated parathormone; 54% hyperphosphatemia; 36% hypercalcemia, 29% HLA haplotypes A3, B7, or B14; and 60% hyperaluminemia. The arthropathy group had more abnormalities per patient (mean 3.6) than the group without arthropathy (mean 2.7) (p less than 0.05). Our data suggest that (1) arthritic complaints occur frequently in patients receiving dialysis; (2) arthropathy accounted for 61% of the complaints; (3) 43% of patients with arthropathy had CPPD-type; (4) renal osteodystrophy caused 17% of arthritic complaints; and (5) in patients receiving dialysis, there is a high incidence of metabolic abnormalities that are known to be associated with arthropathy.
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PMID:Musculoskeletal symptoms related to arthropathy in patients receiving dialysis. 323 May 70

After 7 days in air on wet filter paper mudskippers had normal body weight and normal levels of plasma sodium, potassium, and phosphate. They were, however, significantly hypercalcemic. The hypercalcemia could be reduced by the daily intraperitoneal injection of synthetic eel calcitonin (1.67 microgram kg-1 day-1) and this effect was dose dependent with a maximal response at a dose of 3.33 micrograms kg-1 day-1. Calcitonin had no effect on plasma calcium levels of fish held in water but did induce significant hyperphosphatemia whether the fish were held in water or in air on wet filter paper with this effect being greater under the latter conditions. The hypocalcemic action of calcitonin was restricted to conditions under which the fish displayed patent hypercalcemia. Under no conditions did calcitonin produce significant hypocalcemia so it appears that the action of synthetic eel calcitonin in the mudskipper, Periophthalmodon schlosseri, is dependent upon the presence of excess plasma calcium and is thus more accurately described as being anti-hypercalcemic rather than hypocalcemic.
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PMID:Effects of calcitonin on plasma calcium and phosphate in the mudskipper, Periophthalmodon schlosseri (Teleostei), in water and during exposure to air. 338 5

The efficacy of calcium carbonate (CaCO3) as a phosphate binder has been limited by its tendency to cause hypercalcemia. Since standard dialysate calcium concentrations (3.0-3.5 mEq/l) increase the risk of developing hypercalcemia with large doses of CaCO3 by inducing positive calcium balance during hemodialysis (HD), we compared control of hyperphosphatemia in 41 HD patients during 4 months each of aluminum hydroxide (Al(OH)3) and CaCO3 when the dialysate calcium concentration was lowered, as required, to maintain the predialysis serum calcium concentration within the normal range. Mean predialysis serum phosphorus and calcium concentrations were 5.0 +/- 0.2 mg/dl and 9.3 +/- 0.1 mg/dl, respectively, during 4 months CaCO3 (9.2 +/- 0.3 g/day) and 4.9 +/- 0.2 g/dl and 9.1 +/- 0.1 mg/dl during the previous 4 months Al(OH)3 therapy (2.9 +/- 0.2 g/day). Reducing the dialysate calcium concentration to below 3.0 mEq/l (mean 2.1 +/- 0.04) in the 11 patients who developed hypercalcemia on CaCO3 decreased serum calcium (-1.1 +/- 0.15 mg/dl) and ionized calcium (-0.3 +/- 0.04 mEq/l) during HD, enabled CaCO3 (8.8 +/- 0.4 g/day) to be continued, and maintained predialysis serum calcium and phosphorus at 10.4 +/- 0.1 mg/dl and 5.2 +/- 0.3 mg/dl, respectively. No improvement in acidosis or biochemical hyperparathyroidism was observed during CaCO3 therapy but serum aluminum was significantly decreased after CaCO3 (p less than 0.005). We conclude that CaCO3 prevents interdialytic hyperphosphatemia as effectively as Al(OH)3 without increasing the predialysis serum calcium x phosphorus product, provided serum calcium is maintained within the normal range by adjusting the dialysate calcium concentration.
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PMID:Calcium carbonate is an effective phosphate binder when dialysate calcium concentration is adjusted to control hypercalcemia. 342 32

Preventive administration of vitamin D3 active metabolites 1.25(OH)2D3 and 24.25(OH)2D3 into growing rats, kept under conditions of long-term hard hypokinesia, normalized Ca metabolism and the state of bone tissue depending on the preparations dose and their combination. 1.25(OH)2D3 at a dose of 0.03 microgram per an animal daily augmented effectively the Ca absorption in small intestine, corrected hypocalcemia, increased slightly the bone tissue density and the Ca and P content in the tissue as well as it elevated the volume of spongiosa, width of the epiphysial growth plate (EGP) and the amount of osteoclasts. After an increase of the metabolite dose up to 0.15 microgram hypercalcemia, hyperphosphatemia, intensive resorption of bone tissue, distinct increase in the osteoclasts content and ectopic calcification were observed. Administration of 1.35(OH)2D3 and 24.25(OH)2D3 combination (0.03 microgram and 0.25 or 1.25 micrograms, respectively) or only 24.25(OH)2D3 at a dose of 1.25 micrograms caused a restoration of Ca absorption in intestine and of its level in blood as well as mineral composition, density of bone tissue, volume of primary and secondary spongiosa were normalized, while the EGP width and amount of osteoclasts remained decreased. Synergic effect of 1.25(OH)2D3 and 24.25(OH)2D3 in rats appears to depend on their various functions in regulation of Ca metabolism, in development and remodelation of bone tissue, thus indicating that these metabolites of vitamin D3 should be used simultaneously under conditions of hypokinesia for prophylactic purposes.
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PMID:[Comparative study of the effect of 1,25 dihydroxyvitamin D3 and 24,25-dihydroxyvitamin D3 on calcium homeostasis and bone tissue state in rats during hypokinesia]. 349 67

Pulmonary calcinosis is a recognized complication of renal failure. The resulting pulmonary compromise may be severe or even fatal. The potential contribution of hypercalcemia, hyperphosphatemia, and increased calcium-phosphorus product to the development of pulmonary calcinosis has been controversial. We describe four patients (ages 2 1/4 to 18 years) who had severe pulmonary calcinosis and respiratory failure within three to five days after renal transplantation. Initial clinical and roentgenographic findings suggested noncardiogenic pulmonary edema. Marked pulmonary hypertension was present in the two patients in whom pulmonary artery pressure data were available. Other clinical features in common included poor allograft function with persistent uremia requiring dialysis and evidence of moderate to severe secondary hyperparathyroidism. In three of the patients, the calcium-phosphorus product increased markedly after transplantation, to peak values of 122 to 147. This increase occurred at the same time as the onset of respiratory failure. Peak serum calcium levels were 10.0 to 11.0 mg/dL and peak serum phosphorus levels were 9.2 to 13.5 mg/dL. All patients died of respiratory failure five to 58 days after transplantation. The posttransplantation period may be a time of increased risk of potentially fatal pulmonary calcinosis in pediatric renal transplant recipients. The diagnosis should be considered in any patient with respiratory failure of unknown cause following renal transplantation.
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PMID:Pulmonary calcinosis after renal transplantation in pediatric patients. 352 Dec 66

The control of hyperphosphatemia in dialysis patients is frequently achieved using aluminium hydroxide (A1(OH)3) and/or calcium carbonate (Ca CO3). However, this effect is counterbalanced by risk of aluminium intoxication and hypercalcemia. An alternative to the use of these phosphate binders is the prescription of magnesium hydroxide (Mg(OH)2) in association with a magnesium free dialysate. 19 patients with subtoxic plasma aluminium concentration received such a therapy. 9 months after starting the essay 4 patients had been excluded for digestive intolerance (3 cases) and neuro-psychic symptoms related to hypermagnesemia (1 case) after therapy with maximal doses of 6 to 12 g/d. Plasma inorganic phosphorus was decreased from 2.47 +/- 0.32 to 1.86 +/- 0.40 mmol/l (P less than 0.05) and plasma aluminium from 3.03 +/- 0.93 to 1.52 +/- 0.15 mumol/l (P less than 0.05). The results have been obtained without any significant increase in plasma and red cell magnesium levels. Metabolic alkalosis has been observed in association with the increase of ion exchange resin (sodium polystyrene sulfonate: Kayexalate) to treat progressive hyperkalemia. With the exception of possible metabolic effects occurring on a long term basis, Mg(OH)2 in association with magnesium-free dialysate seems of value to treat dialysis hyperphosphatemia.
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PMID:[Magnesium hydroxide treatment of hyperphosphatemia in chronic hemodialysis patients with an aluminum overload]. 361 5

In 93 children, end-stage renal disease was treated with the new dialytic methods of continuous ambulatory peritoneal dialysis (CAPD) or continuous cycling peritoneal dialysis (CCPD) over 5 years. Modality survival rates at 36 months with CAPD, CCPD, or both were 20%, 93%, and 87%, respectively. Use of CCPD as the primary dilaytic method increased during the study period. The peritonitis rate was one episode per 11.8 patient treatment months and was similar with both CAPD and CCPD. Gram-positive organisms were cultured in 34% of these episodes of peritonitis. Staphylococcus aureus peritonitis was associated with a recurrence rate of 40% and led to catheter replacement in 45% of the episodes. Peritoneal membrane failure necessitating switching to hemodialysis was related to peritonitis in three patients. Of the 74 peritoneal catheters that required replacement, 70% were infected. Serial serum levels of urea nitrogen, potassium, calcium, phosphorus, albumin, and alkaline phosphatase remained stable, whereas serum creatinine level rose slightly over time. Episodes of hyperkalemia, hypercalcemia, and hyperphosphatemia were observed at a frequency of one episode per 12.2, 4.6, and 2.5 treatment months, respectively. Blood transfusions were required in once per 1.5 and 3.3 treatment months in seven anephric patients and in 35 patients with their own kidneys, respectively (P = 0.05). In prepubertal patients who received CAPD or CCPD for greater than 1 year, little or no improvement in growth occurred in relationship to either chronologic or bone age.
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PMID:Five years' experience with continuous ambulatory or continuous cycling peritoneal dialysis in children. 365 81

Orally administered calcium carbonate was evaluated as a phosphate binding agent in 15 children, ages 0.6 to 17.2 years, receiving maintenance dialysis. Changes in plasma aluminum concentration were assessed after discontinuation of treatment with aluminum-containing gels. The mean daily dose of calcium carbonate was 5.1 +/- 2.5 gm (384 +/- 315 mg/kg/day), and correlated inversely with body weight (r = 0.72, P less than 0.01) and age (r = 0.71, P less than 0.01). Mean serum calcium, phosphorus, and bicarbonate values were unchanged throughout the study. Plasma aluminum concentration fell from 90 +/- 51 to 34 +/- 22 micrograms/L (P less than 0.005). Dietary phosphorus intakes were 44 +/- 21 and 42 +/- 19 mg/kg/day during the control period and at the end of the study, respectively. Transitory hypercalcemia was the only side effect in 92% of the patients. In none of the patients did uncontrolled hyperphosphatemia, metabolic alkalosis, diarrhea, or symptoms or signs of hypercalcemia develop. Our data indicate that calcium carbonate is an effective phosphate binding agent in children receiving dialysis, and should be used in lieu of aluminum-containing gels in young children with renal failure.
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PMID:Effects of oral calcium carbonate on control of serum phosphorus and changes in plasma aluminum levels after discontinuation of aluminum-containing gels in children receiving dialysis. 370 25


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