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

The incidence of side effects from antacids is low, but patients with renal insufficiency are at risk to develop alkalosis with high doses of calcium carbonate or magnesium hydroxides, or to develop hypercalcemia due to insufficient calcium elimination by the kidneys.--A great potential exists for drug interactions with antacids. In most instances, the effectiveness of other drugs is decreased in the presence of antacids, but effectiveness may be increased for L-dopa (less degradation in stomach) or quinidine (renal elimination reduced). Interactions at the absorption level can be avoided by administering the antacid one hour after intake of the other drugs (one hour after meals) which is also the optimum dosing schedule to ensure good antacid effect. Interactions through changes of urine pH are not eliminated by observing special dosing time schedules, but by modifying the dose or by selecting alternative drug treatment.
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PMID:[Metabolic effects of antacids and interactions with other drugs]. 685 4

The milk-alkali syndrome was first identified in 1923, and continues to occur in patients ingesting large amounts of calcium and absorbable alkali, particularly as calcium carbonate. Hypercalcemia, alkalosis, and renal impairment remain hallmarks of the syndrome, which may occur in acute, subacute, and chronic forms. Although the pathophysiology of the milk-alkali syndrome has not been completely studied, it appears to involve complex interactions between ingested calcium and alkali resulting in an impairment in renal calcium and bicarbonate excretion. The diagnosis of the milk-alkali syndrome is based on a history of calcium and alkali ingestion, the presence of characteristic clinical and laboratory features, and the exclusion of other causes of hypercalcemia. Conservative treatment, including discontinuing calcium and alkali ingestion and supportive measures, is usually effective.
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PMID:The milk-alkali syndrome: current concepts. 704 33

The cortisone suppression test and some biochemical tests were evaluated in 13 patients with hypercalcemia due to primary hyperparathyroidism (PHP) and in 10 with hypercalcemia due to a malignant disease. The biochemical tests revealed that serum chloride was significantly raised in patients with PHP compared to patients with malignant diseases, whereas no differences were observed with regard to the serum values of corrected calcium, serum phosphate, chloride/phosphate ratio, HCO3-. Although serum values of parathyroid hormone were higher in patients with PHP, a consider-able overlap was observed between values in the two patient groups. Corrected serum calcium values were significantly suppressed during cortisone administration in patients with malignant disease compared to patients wit PHP, whereas prednisolone had no suppressive effect. The positive predictive value of the test was 80.0% and the negative predictive value 66.7%. We conclude that there is still no entirely reliable method to distinguish between hypercalcemia due to PHP or malignant disease.
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PMID:Hypercalcemia due to primary hyperparathyroidism or malignant disease. Evaluated by means of biochemical tests and the steroid suppression test. 714 7

The effect of phosphate deprivation on urinary acidification was investigated in rats fed a phosphate-deficient diet and in control rats fed the same diet supplemented with phosphate. Phosphate-deprived animals developed hypophosphatemia, hypercalcemia, and hypophosphaturia, but failed to develop hyperchloremic metabolic acidosis following 30 or 60 days of phosphate deprivation. Baseline urine pH was significantly higher in phosphate-deprived rats than in controls, but baseline urine HCO3 excretion was not significantly different between the two groups. The pattern of HCO3 reabsorption in phosphate-deprived rats was identical to that of controls at both low and high plasma HCO3 levels. During chronic NH4Cl administration, both 30- and 60-day phosphate-deprived rats had a sigificantly higher minimal urine pH and lower titratable acid and net acid excretion than seen in controls. NH4 excretion was significantly lower than controls in the 60-day phosphate-deprived rats only. During Na2SO4 administration the minimal urine pH was significantly lower in controls than in phosphate-deprived rats, but there was overlap of urine pH values. At comparable levels of urine pH, NH4 excretion was significantly lower in phosphate-deprived rats than in controls. Phosphate-deprived rats were able to raise urine-blood CO2 pressure to the same levels as controls during both HCO3 loading and Tris buffer administration. Phosphate-deprived rats had greater extrarenal buffering capacity than controls as evidenced by a lower decline in blood pH and HCO3 during HCl infusion in phosphate-deprived rats. These data demonstrate that phosphate deprivation is associated with distal acidification defect, impaired NH3 excretion, and increased extrarenal buffering capacity. The increased availability of buffer in phosphate deprivation may play an important role in acid-base homeostasis in this condition.
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PMID:Distal acidification defect induced by phosphate deprivation. 741 57

Hypercalcemia and low serum parathyroid hormone (PTH) levels are features of the adynamic lesion (AD) of renal osteodystrophy, but there is little information about parathyroid gland function in this disorder. Therefore, the four parameter model was used to evaluate calcium-regulated PTH release in patients with either adynamic bone or secondary hyperparathyroidism (OF) as documented by bone biopsy and in normal volunteers (NL). Patients had undergone CCPD for 20 +/- 4.2 months, and all received calcium carbonate as the sole phosphate-binding agent. During two hours infusions of sodium citrate, the rate of decline in serum ionized calcium levels did not differ among groups; serum PTH levels rose from 136 +/- 38 to 342 +/- 140 pg/ml in AD and from 691 +/- 99 to 869 +/- 121 pg/ml in OF. Maximum PTH levels were 322 +/- 42% of baseline values in AD but only 146 +/- 9.7% of baseline in OF (P < 0.001), and the increase above baseline levels in AD did not differ from that in NL (300 +/- 25%, NS). During calcium infusions, serum PTH levels fell from 164 +/- 75 to 39 +/- 11 pg/ml in AD and from 622 +/- 76 to 171 +/- 29 pg/ml in OF; minimum serum PTH levels, expressed as a percentage of pre-infusion values, were 25 +/- 2% in AD and 26 +/- 5% in OF (NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium-regulated parathyroid hormone secretion in adynamic renal osteodystrophy. 747 73

To determine whether metastatic calcification during neointima formation can result in neointimal calcification that simulates advanced human atherosclerosis, 32 giant Flemish rabbits (weight 5.5 +/- 0.6 kg) underwent overstretch balloon injury of bilateral iliac arteries and received diet therapy for 8 weeks: high cholesterol (2%) and low calcium-vitamin D2 regimen (250 mg of calcium carbonate orally 5 times weekly and 50,000 U of calciferol intramuscularly 3 times weekly; group 1; n = 5); low cholesterol (0.5%) and high calcium-vitamin D2 regimen (500 mg of calcium carbonate orally 5 times weekly and 100,000 U of calciferol intramuscularly three times weekly; group 2; n = 19); or 0% cholesterol and high calcium-vitamin D2 regimen (group 3; n = 8). The incidence of vascular calcification was highest (71.4%) in group 2. Eighty-one percent of calcification was medial. Residual strain measurements of 7 thoracic aortas from group 2 compared to normal thoracic aortas from 8 control rabbits showed that residual strain was significantly increased in the calcified atherosclerotic aortas (12.3% vs 5.2%; p = 0.001). We conclude that diet-induced hypercalcemia predominantly affects the media despite the presence of concomitant neointima formation from balloon artery injury with or without hypercholesterolemia and increases the residual strain more than twofold compared to normal thoracic aortas.
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PMID:Vascular effects of diet-induced hypercalcemia after balloon artery injury in giant Flemish rabbits. 757 83

Twelve dialysis patients received oral pulse therapy with 1-alpha-hydroxyvitamin D3 in a dose of 0.1 microgram/kg body weight twice weekly and daily calcium carbonate (1.5-3.5 g) for a period of 8-12 months. This treatment was very effective in suppressing secondary hyperparathyroidism without causing hypercalcaemia and/or hyperphosphataemia.
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PMID:Oral pulse therapy with vitamin D3 for control of secondary hyperparathyroidism. 769 13

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

Hyperphosphataemia plays a key role in the pathogenesis of renal osteodystrophy, and phosphate-binding agents are required in many chronic dialysis patients. Aluminium hydroxide and calcium carbonate are well-established phosphate binders, but their use is associated with toxicity or poor efficacy. Calcium acetate is known to be a potent phosphate binder, and has recently been used successfully in chronic dialysis patients. In this randomized cross-over trial in 31 chronic haemodialysis patients, equimolar doses of calcium acetate and calcium carbonate were administered for 6 weeks each. Compliance was estimated from tablet counts, and biochemical parameters were measured at the end of each treatment period. Of the 31 patients 23 completed both treatment arms; of the remainder, three withdrew due to adverse symptoms, hypercalcaemia necessitated treatment withdrawal in two, and three died. Non-compliance was significantly higher with acetate (18.3% tablets not taken) than with carbonate (8.7%). Serum phosphate was significantly lower after treatment with acetate (1.51 mmol/l) than with carbonate (1.80), as was the Ca x PO4 product (3.59 vs 4.18 respectively) and PTH (17.8 vs 25.4 pmol/l respectively). Serum calcium was significantly higher after acetate therapy (2.40 vs 2.32 mmol/l). No significant difference was found for sodium, potassium, bicarbonate, urea, creatinine, and haemoglobin. This study confirms that the treatment of hyperphosphataemia is more effective with calcium acetate than with calcium carbonate. For the first time an associated beneficial effect on secondary hyperparathyroidism has also been demonstrated. Patient tolerability of calcium acetate was considerably poorer, probably due in part to tablet formulation and bulkiness, as well as possible direct gastrointestinal effects of the acetate salt.
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PMID:Calcium acetate versus calcium carbonate as phosphate-binding agents in chronic haemodialysis. 780 Feb 11

Phosphate retention plays a major role in the pathogenesis of hyperparathyroidism at all stages of renal insufficiency. Dietary phosphate restriction is mandatory only for adults and is not advised for children because of the recommended diet allowance. Dietary restriction is usually not sufficient, and phosphate binders are almost always necessary when the glomerular filtration rate falls below 40 mL/min. Because long-term administration of aluminum phosphate binders is associated with risk of aluminum intoxication despite the use of so-called "safe doses", alternative phosphate binders should be used. Magnesium hydroxide and carbonate can be used only for dialysis patients because a low dialysate magnesium concentration is necessary to prevent the hazards of hypermagnesemia. Therefore, the major alternative is the use of alkaline salts of calcium. The most recently proposed salt, acetate, has a higher phosphate-binding capacity than carbonate but exposes patients to the same incidence of hypercalcemia despite the use of half the dose of elemental calcium. These salts should be taken with meals in order to complex more dietary phosphate and decrease calcium absorption and therefore the risk of hypercalcemia. Oral calcium alone, without 1 alpha OH-vitamin D3 derivatives, can prevent hyperphosphatemia and hyperparathyroidism in most uremic patients before dialysis and in about half of the patients dialyzed with a dialysate calcium of 1.5 to 1.65 mmol/L. 1 alpha OH-vitamin D3 derivatives, which increase intestinal absorption of phosphate, should be used only when hyperphosphatemia has been prevented by oral calcium and diet and when plasma parathyroid hormone levels increase above three times the upper limit of normal. To decrease hypercalcemic risk, patients should be given 1 alpha OH-vitamin D3 derivatives, preferably at night, as an intermittent bolus (intravenous or oral). In dialysis patients, the dialysate concentration of calcium may have to be further decreased in order to prevent hypercalcemia when high doses of oral calcium are necessary to control hyperphosphatemia.
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PMID:Management of hyperphosphatemia in patients with renal failure. 785 19


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