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

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was not different from that prescribed during the control period, but in five patients calcitriol was permanently withdrawn for hypercalcemia.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

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

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

Two patients with extensive tumoral calcinosis were treated with aluminium hydroxide. Initial metabolic studies showed positive calcium and phosphorus balances which became negative with aluminium hydroxide treatment. One subject, who had renal impairment, developed transient hypercalcaemia, parathyroid suppression, low levels of 1,25-dihydroxyvitamin D and calcium malabsorption during treatment with aluminium hydroxide. The second patient developed calcium malabsorption due to vitamin D deficiency. When she was replete with vitamin D there were supranormal levels of 1,25-(OH)2D in the serum and enhanced calcium absorption during treatment with aluminium hydroxide. Both subjects developed hypercalciuria and there was dissolution of many of the calcific tumours. The patient with renal impairment accumulated aluminium in the bone.
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PMID:Tumoral calcinosis: clinical and metabolic response to phosphorus deprivation. 365 64

We evaluated the effectiveness of calcium carbonate as a phosphate binder in 19 children with chronic renal failure; ten children were undergoing dialysis therapy (eight maintained by CAPD and two by hemodialysis). Twelve children had previously received aluminum hydroxide, while calcium carbonate was the primary phosphate binder used in seven children. Among all the children, the serum phosphorus level on no phosphate binder was 7.4 +/- 0.9 mg/dL, which decreased significantly (P less than .001) to 5.9 +/- 0.8 mg/dL during calcium carbonate therapy, while the serum calcium, bicarbonate, and creatinine were unchanged. The reduction in the serum phosphorus level occurred while dietary intake of calcium and phosphorus were unchanged, as demonstrated by three-day dietary records. The dose of calcium carbonate required to maintain the serum phosphorus in the normal range varied from 600 mg to 15 g/d (mean 7.4 g/d). Among the 12 children and four others who had received aluminum hydroxide, serum aluminum levels fell from 108.8 +/- 121.8 ng/mL to 36.1 +/- 29.1 ng/mL after aluminum hydroxide was stopped (P less than .05). Serum alkaline phosphatase and parathyroid hormone (PTH) levels during aluminum hydroxide therapy were similar to levels obtained during calcium carbonate therapy, while PTH levels fell in children treated initially with calcium carbonate. All the children have been observed for a mean of 12.0 months (range 4 months to 3 1/2 years). Hypercalcemia occurred in seven children, usually when vitamin D therapy was initiated or the dose changed. Hypercalcemia resolved with adjustment of the vitamin D or calcium carbonate dose in all but one patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium carbonate is an effective phosphorus binder in children with chronic renal failure. 382 69

After confirming hypercalcemia by 3 successive measurements of the total plasma calcium corrected for a plasma protein concentration of 72 g/l, which excludes spurious hypercalcemia due to dehydration, the physician orientates the aetiological diagnosis bearing in mind that primary hyperparathyroidism PHPT is the cause of 85 p. 100 of all asymptomatic forms of hypercalcaemia whilst overt or occult malignancy is the main cause (60 p. 100) of symptomatic forms of hypercalcaemia with PHPT responsible for 20 p. 100 of cases. Other causes, including drug toxicity with Vit D, calcium, Vit A, lithium, thiazide and aluminium hydroxide, sarcoidosis, hyperthyroidism, Addison's disease, pheochromocytoma and familial endocrine disorders are much rarer. Nevertheless, these rarer causes must be excluded on the clinical history and examination followed by radiological (chest X ray, plain abdomen X ray, bone X rays) and simple biological tests. The latter and/or scans tests should also help in a rapid diagnosis of metastatic carcinoma and multiple myeloma, so that the major diagnostic problem is to distinguish primary HPT from occult malignancy. This problem is greatly facilitated by reliable assays of C terminal or medium PTH rather than renal CAMP which is increased in 80 p. 100 of occult malignancies. When PTH assays is unavailable or unreliable Dent's hydrocortisone suppression test may be useful as a fall in'serum calcium is associated with occult malignancy in 70 p. 100 of cases and non-suppression is associated with PHPT in 91 p. 100 of cases. Discriminant analysis of the usual biochemical parameters may be helpful in this differential diagnosis and is accurate in about 90 p. 100 of cases. However, the association of PHPT and malignancy is also possible and not fortuitous.
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PMID:[Stages of the etiological diagnosis of hypercalcemia]. 389 Jun 61

Thirty-seven osteodystrophic and chronically haemodialyzed patients have been treated for 1-22 months by means of 1,25(OH)2D3. Under treatment a marked improvement of symptomatology and radiographic findings has been observed in the majority of cases; from the haematochemical viewpoint a rise of calcemia and phosphoremia, a fall in alkaline phosphatase and a variable course of PTH have been observed. Several episodes of asymptomatic hypercalcemia ceased with posology reduction; only 3 cases needed stopping the treatment for this reason, one of them definitively; 12/37 cases needed hypophosphoric diets and increase in oral aluminium hydroxide doses to control hyperphosphoremia. The Authors conclude that, to achieve a correct management of a 1,25(OH)2D3 therapy for renal osteodystrophy, is mandatory a strict and accurate biochemical control: in this way is possible to obtain an effective modulation of the posology avoiding the appearance of side-effects as hypercalcemia and ectopic calcifications.
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PMID:[Course and significance of various biochemical parameters in 1,25-dihydroxyvitamin D3 therapy of uremic osteodystrophy]. 668 45

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

In a patient recovering from acute renal failure, hypercalcemia abruptly developed at a time when the serum creatinine level remained high (5 mg/dl) but well after the serum phosphate level had been restored to normal by oral aluminum hydroxide therapy. The renal damage had been severe, with oliguria lasting six weeks. Parathyroid hormone (PTH) immunoreactivity was measured with two different "carboxyterminal" PTH assays, giving high-normal or slightly mild renal failure could have accounted for the increased immunoreactivity. After five months of hypercalcemia, prednisone was administered and produced a prompt and sustained normalization of serum calcium. This prolonged variant of hypercalcemia after renal failure is not well recognized in the literature. The response to glucocorticoids suggests that abnormal metabolism of vitamin D or osteoclast activating factor might be involved in its genesis.
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PMID:Hypercalcemia after acute renal failure. 744 7

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


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