CALCIUM ACETATE- calcium acetate tablet

Land: USA

Sprog: engelsk

Kilde: NLM (National Library of Medicine)

Aktiv bestanddel:

CALCIUM ACETATE (UNII: Y882YXF34X) (CALCIUM CATION - UNII:2M83C4R6ZB)

Tilgængelig fra:

Paddock Laboratories, LLC

INN (International Name):

CALCIUM ACETATE

Sammensætning:

CALCIUM ACETATE 667 mg

Indgivelsesvej:

ORAL

Recept type:

PRESCRIPTION DRUG

Terapeutiske indikationer:

Calcium Acetate Tablets, USP are indicated for the control of hyperphosphatemia in end stage renal failure and does not promote aluminum absorption. Patients with hypercalcemia.

Produkt oversigt:

In tablet form with "P113" debossed on one side and plain on the other, for oral administration. Each white round tablet contains 667 mg calcium acetate (anhydrous; Ca(CH3 COO)2 ; MW = 158.17 grams) equal to 169 mg (8.45 mEq) calcium; polyethylene glycol 8000; and magnesium stearate. Tablets, NDC 0574-0113-02, bottles of 200. Store at 20° to 25°C (68° to 77°F) [see USP Controlled Room Temperature] Rx Only Manufactured By Perrigo® Minneapolis, MN 55427 2202147 (12-12)

Autorisation status:

Abbreviated New Drug Application

Produktets egenskaber

CALCIUM ACETATE- CALCIUM ACETATE TABLET
PADDOCK LABORATORIES, LLC
----------
CALCIUM ACETATE TABLETS, USP
NDC 0574-0113-02
RX ONLY
DES CRIPTION:
Each white to off-white, round, biconvex tablet (debossed with "P113"
on one face) contains 667 mg
calcium acetate, USP (anhydrous; Ca(CH COO) ; MW = 158.17 grams) equal
to 169 mg (8.45 mEq)
calcium; polyethylene glycol 8000; and magnesium stearate. Calcium
Acetate Tablets, USP are
administered orally for the control of hyperphosphatemia in end stage
renal failure.
CLINICAL PHARMACOLOGY:
Patients with advanced renal insufficiency (creatinine clearance less
than 30 mL/min) exhibit phosphate
retention and some degree of hyperphosphatemia. The retention of
phosphate plays a pivotal role in
causing secondary hyperparathyroidism associated with osteodystrophy,
and soft-tissue calcification.
The mechanism by which phosphate retention leads to
hyperparathyroidism is not clearly delineated.
Therapeutic efforts directed toward the control of hyperphosphatemia
include reduction in the dietary
intake of phosphate, inhibition of absorption of phosphate in the
intestine with phosphate binders, and
removal of phosphate from the body by more efficient methods of
dialysis. The rate of removal of
phosphate by dietary manipulation or by dialysis is insufficient.
Dialysis patients absorb 40% to 80% of
dietary phosphorus. Therefore, the fraction of dietary phosphate
absorbed from the diet needs to be
reduced by using phosphate binders in most renal failure patients on
maintenance dialysis. 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
Tablets, USP are 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