Vitamins / Minerals

Neutralizes gastric acidity.
Caution needed for maintenance of nervous, muscular, skeletal, enzyme reactions, normal cardiac contractility, coagulation of blood.
Effects secretory activity of endocrine and exocrine glands.
Vitamin D levels in humans depend on two sources : (1) Explosure to the ultraviolet rays of the sun for conversion of 7-dehydrocholesterol in the skin to vitamin D3 (2) dietary intake of either vitamin D2. Vitamin D2 and Vitamin D3 must be metabolically activated in the liver and the kidney before becoming fully active on target tissues. The initial step in the activation process in the introduction of a hydroxyl group in the side chain at C-25 by the hepatic enzyme, CYP 27. The products of this reaction are 25 -(OH)D2 and 25 -(OH)D3, respectively. Further hydroxylation of these metabolities occurs in the mitochondria of kidney tissue, catalyzed by renal 25-hydroxyvitamin D-1-hydroxylase to produce 1, 25(OH)2D2, the primary biologically active form of vitamin D2 and 1 ,25(OH)2D3, the biologically active form of vitamin D3.

Calcium carbonate is indicated Hyperphosphatemia, Hypertension in pregnancy, Osteoporosis, Prevention and treatment of hypocalcemia, Hyperacidity (antacid), Hypoparathyroidism.

Calciferol is indicated for the reduction of elevated iPTH levels in the management of secondary hyperparathyroidism in patients undergoing chronic renal dialysis.

Hyperphosphatemia : 1-17 g per day in divided doses.
Hypocalcemia : 1.25 g 4-6 tablets per day, chewed with water.
Antacid : 500 mg to 1 g 1-3 hour after meals and at bedtime as needed.
Hypertension in pregnancy : 500 mg tid during third trimester.
Osteoporosis : 1200 mg per day.

The recommended initial dose of calciferol is 10.0 ùg administered 3 times weekly at dialysis. The initial dose should be adjusted, as needed, in order to lower blood iPTH into the range of 150-300 pg/ml. The dose may be increased at 8 week intervals by 2.5 ùg if iPTH is not lowered by 50% and fails to reach the target range. The maximum recommended dose of calciferol is 20 ùg administered 3 times a week at dialysis for a total of 60 ùg/week.

Hypercalcemia, hypercalciuria, hyperparathyroidism, bone tumors, digitalis toxicity, ventricular fibrillation, renal calculi, sarcoidosis. Calciferol should not be given to patients with a tendency towards hypercalcemia or evidence of vitamin D toxicity.

Magnesium-containing antacids and calciferol should not be used concomitantly, because such use may lead to the development of hypermagnesemia.
Calcium channel blockers : Calcium administration may inhibit calcium channel blocker activity.
Digoxin, digitoxin : Elevated calcium concentrations associated with acute digitalis toxicity.
Doxycycline, tetracycline : Co-therapy with tetracycline and calcium carbonate can reduce the serum concentrations and efficacy of tetracyclines.
Iron : Some calcium antacids reduce the GI absorption of iron; inhibition of the hematological response to iron has been reported.
Itraconazole, ketoconazole : Antacids containing calcium may reduce antifungal concentrations.
Quinidine : Calcium antacids capable of increasing urine pH may increase serum quinidine concentrations.
Quinolones : Reduced bioavailability of quinolone antibiotics.

Cardiovascular : Bradycardia, cardiac arrest, dysrhythmias, heart block, hemorrhage, hypotension, rebound hypertension, shortened QT interval.
Gastrointestinal : Anorexia, constipation, diarrhea, eructation, flatulence, nausea, obstruction, rebound hyperacidity, vomiting.
Genitourinary : Renal dysfunction, renal failure, renal stones.
Metabolic : Hypercalcemia, metabolic alkalosis; milk-alkali syndrome.

Potential adverse effects of calciferol are in general similar to those encountered with excessive vitamin D intake. The early and late signs and symptoms of vitamin D intoxication associated with hypercalcemia include :
Early : Weakness, headache, somnolence, nausea, vomiting, dry mouth, constipation, muscle pain, bone pain and metallic taste.
Late : Polyuria, polydipsia, anorexia, weight loss, nocturia, conjunctivitis, pancreatitis, photophobia, rhinorrhea, pruritus, hyperthermia, decreased libido, elevated blood urea nitrogen, cardiac arrhythmias and rarely overt psychosis.

Administration of calciferol to patients in excess doses can cause hypercalcemia, hypercalciuria, hyperphosphatemia and over-suppression of PTH secretion leading in certain cases to adynamic bone disease. High intake of calcium and phosphate concomitant with calciferol may lead to similar abnormalities. High levels of calcium in the daily state bath may contribute to hypercalcemia.

General treatment of hypercalcemia consists of immediate suspension of calciferol therapy, institution of a low calcium diet and withdrawal of calcium supplements. Serum calcium levels should be determined at least weekly until normocalcemia ensues. Hypercalcemia usually resolves in 2-7 days. When serum calcium levels have returned to within normal limits, colecalciferol therapy may be reinstituted at a dose that is at least 2.5 ùg lower for capsules. Serum calcium levels should be obtained weekly after all dosage changes during subsequent dosage titration. Persistent or markedly elevated serum calcium levels may be corrected by dialysis against a reduced calcium or calcium free dialysate.

Keep in cool, dry place and protect from moisture and light. Store at a temperature of 25°C.