G-Hypophos is indicated for the control of hyperphosphatemia in end stage renal disease (ESRD) and does not promote aluminum absorption.
Calcium Acetate when taken with meals, combines with dietary phosphate to form insoluble Calcium Phosphate which is excreted in the feces. Maintenance of serum phosphorus below 6.0 mg/dl is generally considered as a clinically acceptable outcome of treatment with phosphate binders. Calcium Acetate is highly soluble at neutral pH, making the Calcium readily available for binding to phosphate in the proximal small intestine. Orally administered Calcium Acetate from pharmaceutical dosage forms has been demonstrated to be 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.
The recommended initial dose of Calcium Acetate for the adult dialysis patient is 2 tablets with each meal. The dosage may be increased gradually to bring the serum phosphate level below 6 mg/dl, as long as hypercalcemia does not develop. Most patients require 3-4 tablets with each meal. Pediatric Use : The safety and efficacy of Calcium Acetate have not been established. Geriatric Use : In clinical studies, no overall differences in safety or effectiveness were observed between the geriatric and younger subjects, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out.
Always consult a registered doctor before taking any medicine. This information is for general knowledge only.
Patients may occasionally experience nausea during G-Hypophos therapy. Hypercalcemia may occur during treatment with G-Hypophos. Mild hypercalcemia (Ca >10.5 mg/dl) may be asymptomatic or manifest itself as constipation, anorexia, nausea and vomiting. More severe hypercalcemia (Ca >12 mg/dl) is associated with confusion, delirium, stupor and coma. Mild hypercalcemia is easily controlled by reducing the G-Hypophos dose or temporarily discontinuing therapy. Severe hypercalcemia can be treated by acute hemodialysis and discontinuing G-Hypophos therapy. Decreasing dialysate calcium concentration could reduce the incidence and severity of G-Hypophos induced hypercalcemia. The long-term effect of G-Hypophos on the progression of vascular or soft-tissue calcification has not been determined. Isolated cases of pruritus have been reported which may represent allergic reactions.
Calcium Acetate is contraindicated in patients with hypercalcemia.
G-Hypophos may decrease the bioavailability of tetracycline.
Excessive dosage of G-Hypophos induces hypercalcemia; therefore, early in the treatment during dosage adjustment serum calcium should be determined twice weekly. Should hypercalcemia develop, the dosage should be reduced or the treatment discontinued immediately depending on the severity of hypercalcemia. G-Hypophos should not be given to patients on digitalis, because hypercalcemia may precipitate cardiac arrhythmias. G-Hypophos therapy should always be started at low dose and should not be increased without careful monitoring of serum calcium. The patient should be informed about compliance with dosage instructions, adherence to instructions about diet and avoidance of the use of nonprescription antacids. Patients should be informed about the symptoms of hypercalcemia.