Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Due to toxic side effects of aluminum-containing agents for treatment of uremic hypophosphatemia, much interest has been focused upon aluminum-free phosphate binder alternatives. From results of experimental studies with calcium acetate, this salt has been suggested as a possible effective and safe phosphate binder. In the present study, calcium acetate was used during a mean of 11 months for serum phosphate control in 30 uremic patients previously treated with aluminum and/or calcium carbonate. Satisfactory control of serum phosphate was achieved during the study (mean phosphate concentration +/- SE: 2.15 +/- 0.12 mmol/l compared to prestudy 2.23 +/- 0.19 mmol/l). Mean serum concentrations of calcium, alkaline phosphatase and parathyroid hormone did not change significantly during the study. Serum aluminum decreased significantly (p less than 0.01). Moderate hypercalcemia was observed in 6 patients. Calcium acetate treatment was withdrawn in 2 patients due to gastrointestinal discomfort. It is concluded that calcium acetate seems to be an effective phosphate binder alternative with relatively few side effects.
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PMID:Calcium acetate used as phosphate binding treatment in uremic hyperphosphatemia. 168 Apr 30

In this study, we prospectively evaluated the efficacy of calcium acetate in patients with chronic renal insufficiency on hemodialysis programme with secondary hyperparathyroidism and hyperphosphatemia, which are difficult to control by means of the usual finders (calcium carbonate and aluminium hydroxide) and who were treated with pulses of calcitriol. We studied 10 patients. The inclusion criteria were: a serum phosphorus higher than 6.5 mg/dl, a serum PTHi higher than 250 pg/ml and a serum calcium higher than 9.5. The former therapy was stopped at the time of the patient was included in the study. Calcium acetate was initially introduced with doses between 2.5-4 g/day according to previous calcium and phosphate values. Also, all patients were initially treated with intermittent subcutaneous bolus of Calcitriol were modified and adjusted according to serum concentrations of calcium, phosphorus and PTHi. The concentration of calcium in the dialyzed was of 1.25 mmol/l. Fortnightly total calcium, phosphate and alkaline phosphatase serum determinations and monthly aluminium and PTHi serum determinations were carried out. During the 6 months treatment, a decrease was observed in serum concentrations of phosphate (p < 0.01), aluminum (p < 0.02) and PTHi (p < 0.001) with no changes in the values of calcium (p = ns) nor alkaline phosphatase (p = ns). The incidence of hypercalcemia was low during the follow-up period (11% of all biochemical serum determinations) and was easily controlled. We can conclude that calcium acetate is a sure and effective finder of phosphorus with a very good tolerance. Administered together with pulses of calcitriol, and the use of a low calcium concentration in the dialysate, it does not increase the risk of hypercalcemia.
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PMID:[Usefulness of calcium acetate as a chelating of phosphorus in patients in hemodialysis with secondary hyperthyroidism]. 892 27

We compared the effectiveness of calcium acetate as a phosphate binder with that of calcium carbonate by substituting one for the other in patients undergoing continuous ambulatory peritoneal dialysis. Twenty patients who had been receiving calcium carbonate as a phosphate binder were instead given calcium acetate, initially with two thirds of the previous dose of elemental calcium. The calcium acetate dose was adjusted to achieve adequate calcium-phosphate balance; 65.6% of the previous dose of elemental calcium in calcium carbonate was required. Eighteen of the 20 patients completed the 3-month study. There were no significant differences in the pre-study and study levels of serum phosphate (1.81plus minus0.04 [SEM] versus 1.89plus minus0.06 mmol/L), corrected serum calcium (2.54plus minus0.04 versus 2.57plus minus0.03 mmol/L), calcium phosphate product (4.60plus minus0.15 versus 4.87plus minus0.18), serum alkaline phosphatase (64.75plus minus4.17 versus 69.94plus minus3.77 U/L), and serum parathyroid hormone (122plus minus31 versus 124plus minus27 ng/L). Three patients developed a total of five episodes of hypercalcaemia (corrected calcium level greater-than-or-equal2.85 mmol/L) and four other patients developed gastrointestinal upset. Calcium acetate can thus achieve similar phosphate control to calcium carbonate, using 65.6% of the dose of elemental calcium in calcium carbonate; however, its clinical superiority was not demonstrated in this study.
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PMID:Effectiveness of calcium acetate as a phosphate binder in patients undergoing continuous ambulatory peritoneal dialysis. 1183 48