Calcium Acetate Tablets

Patients with hypercalcemia.

Patients with end stage renal disease may develop hypercalcemia when treated with calcium, including calcium acetate.  Avoid the use of calcium supplements, including calcium-based nonprescription antacids, concurrently with calcium acetate.

An overdose of calcium acetate may lead to progressive hypercalcemia, which may require emergency measures.  Therefore, early in the treatment phase during the dosage adjustment period, monitor serum calcium levels twice weekly.  Should hypercalcemia develop, reduce the calcium acetate dosage or discontinue the treatment, depending on the severity of hypercalcemia.

More severe hypercalcemia (Ca>12 mg/dL) is associated with confusion, delirium, stupor and coma.  Severe hypercalcemia can be treated by acute hemodialysis and discontinuing calcium acetate therapy.

Mild hypercalcemia (10.5 to 11.9 mg/dL) may be asymptomatic or manifest as constipation, anorexia, nausea, and vomiting.  Mild hypercalcemia is usually controlled by reducing the calcium acetate dose or temporarily discontinuing therapy.  Decreasing or discontinuing Vitamin D therapy is recommended as well.

Chronic hypercalcemia may lead to vascular calcification and other soft-tissue calcification.  Radiographic evaluation of suspected anatomical regions may be helpful in early detection of soft tissue calcification.  The long term effect of calcium acetate on the progression of vascular or soft tissue calcification has not been determined.

Hypercalcemia (>11 mg/dL) was reported in 16% of patients in a 3-month study of a solid dose formulation of calcium acetate; all cases resolved upon lowering the dose or discontinuing treatment.

Maintain the serum calcium-phosphorus (Ca x P) product below 55 mg2/dL2.

Hypercalcemia may aggravate digitalis toxicity.

Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to estimate their frequency or to establish a causal relationship to drug exposure.

The following additional adverse reactions have been identified during post-approval of calcium acetate:  dizziness, edema, and weakness.

The drug interaction of calcium acetate is characterized by the potential of calcium to bind to drugs with anionic functions (e.g., carboxyl and hydroxyl groups).  Calcium Acetate Tablet may decrease the bioavailability of tetracyclines or fluoroquinolones via this mechanism.

There are no empirical data on avoiding drug interactions between calcium acetate and most concomitant drugs.  When administering an oral medication with calcium acetate where a reduction in the bioavailability of that medication would have a clinically significant effect on its safety or efficacy, administer the drug one hour before or three hours after calcium acetate.  Monitor blood levels of the concomitant drugs that have a narrow therapeutic range.  Patients taking anti-arrhythmic medications for the control of arrhythmias and anti-seizure medications for the control of seizure disorders were excluded from the clinical trials with all forms of calcium acetate.

In a study of 15 healthy subjects, a co-administered single dose of 4 Calcium Acetate Tablets approximately 2.7 g, decreased the bioavailability of ciprofloxacin by approximately 50%.

Calcium acetate tablet acts as a phosphate binder. Its chemical name is calcium acetate. Its molecular formula is C4H6CaO4, and its molecular weight is 158.17. Its structural formula is:

Each calcium acetate tablet contains 667 mg of calcium acetate, (anhydrous; Ca (CH3COO)2; MW = 158.17 grams) equal to 169 mg (8.45 mEq) calcium. In addition, each tablet contains following inactive ingredients: crospovidone, magnesium stearate and sodium lauryl sulfate. Calcium Acetate Tablets are administered orally for the control of hyperphosphatemia in end stage renal failure.

Calcium acetate, when taken with meals, combines with dietary phosphate to form an insoluble calcium phosphate complex, which is excreted in the feces, resulting in decreased serum phosphorus concentration.

Orally administered calcium acetate from pharmaceutical dosage forms is systemically absorbed up to approximately 40% under fasting conditions and up to approximately 30% under non-fasting conditions. This range represents data from both healthy subjects and renal dialysis patients under various conditions.

Effectiveness of calcium acetate in decreasing serum phosphorus has been demonstrated in two studies of the calcium acetate solid dosage form.

Ninety-one patients with end-stage renal disease who were undergoing hemodialysis and were hyperphosphatemic (serum phosphorus >5.5 mg/dL) following a 1-week phosphate binder washout period contributed efficacy data to an open-label, non-randomized study.

The patients received calcium acetate tablet [667 mg] at each meal for a period of 12 weeks. The initial starting dose was 2 tablets per meal for 3 meals a day, and the dose was adjusted as necessary to control serum phosphorus levels. The average final dose after 12 weeks of treatment was 3.4 tablets per meal. Although there was a decrease in serum phosphorus, in the absence of a control group the true magnitude of effect is uncertain.

The data presented in Table 2 demonstrate the efficacy of calcium acetate in the treatment of hyperphosphatemia in end-stage renal disease patients. The effects on serum calcium levels are also presented.

There was a 30% decrease in serum phosphorus levels during the 12 week study period (p<0.01). Two-thirds of the decline occurred in the first month of the study. Serum calcium increased 9% during the study mostly in the first month of the study.

Treatment with the phosphate binder was discontinued for patients from the open-label study, and those patients whose serum phosphorus exceeded 5.5 mg/dL were eligible for entry into a double-blind, placebo-controlled, cross-over study. Patients were randomized to receive calcium acetate or placebo, and each continued to receive the same number of tablets as had been individually established during the previous study. Following 2 weeks of treatment, patients switched to the alternative therapy for an additional 2 weeks.

The phosphate binding effect of calcium acetate is shown in the Table 3.

Each Calcium Acetate Tablet USP, intended for oral administration, is white, round tablet, Debossed EP 114 on one side and plain on the reverse side. Each calcium acetate tablet contains 667 mg of calcium acetate (anhydrous Ca(CH3COO)2; MW=158.17 grams) equal to 169 mg (8.45 mEq) calcium and are supplied as follow:

Bottles of 200:    NDC 23155-621-02

STORAGE:  Store at 20° to 25°C (68° to 77°F) excursions permitted between 15° to 30°C (59° to 86°F) [See USP Controlled Room Temperature].