Brands, Medical Use, Clinical Data
- Antihypocalcemic Agents
- Antihypoparathyroid Agents
- Essential Vitamin
- Vitamins (Vitamin D)
Brands / Synonyms
Buco-D; Calciferol; Calciferon 2; Condacaps; Condocaps; Condol; Crtron; Crystallina; D-Arthin; D-Tracetten; Daral; Davitamon D; Davitin; De-Rat Concentrate; Decaps; Dee-Osterol; Dee-Ron; Dee-Ronal; Dee-Roual; Deltalin; Deratol; Detalup; Diactol; Divit Urto; Doral; Drisdol; Ercalciol; Ergorone; Ergosterol Activated; Ergosterol, Irradiated; Ertron; Fortodyl; Geltabs; Hi-Deratol; Infron; Metadee; Mulsiferol; Mykostin; Novovitamin-D; Oleovitamin D; Oleovitamin D, Synthetic; Oleovitamin D2; Ostelin; Radiostol; Radstein; Radsterin; Rodine C; Shock-Ferol; Shock-Ferol Sterogyl; Sterogyl; Synthetic Vitamin D; Uvesterol-D; Vigantol; Vio-D; Viostdrol; Viosterol; Viosterol in Oil; Vitamin D; Vitavel-D
For the treament of vitamin D deficiency or insufficiency, refractory rickets (vitamin D resistant rickets), familial hypophosphatemia and hypoparathyroidism, and in the management of hypocalcemia and renal osteodystrophy in patients with chronic renal failure undergoing dialysis. Also used in conjunction with calcium in the management and prevention of primary or corticosteroid-induced osteoporosis.
Used in the treatment of hypcalcemia and in dialysis-dependent renal failure. Ergoalcifediol (Vitamin D2) is a fat soluble steroid hormone precursor of vitamin D that contributes to the maintenance of normal levels of calcium and phosphorus in the bloodstream.
Mechanism of Action
Vitamin D2 is the form of vitamin D most commonly added to foods and nutritional supplements. Vitamin D2 must be transformed (hydroxylated) into one of two active forms via the liver or kidney. Once transformed, it binds to the vitamin D receptor that then leads to a variety of regulatory roles. Vitamin D plays an important role in maintaining calcium balance and in the regulation of parathyroid hormone (PTH). It promotes renal reabsorption of calcium, increases intestinal absorption of calcium and phosphorus, and increases calcium and phosphorus mobilization from bone to plasma. Vitamin D2 and its analogs appear to promote intestinal absorption of calcium through binding to a specific receptor in the mucosal cytoplasm of the intestine. Subsequently, calcium is absorbed through formation of a calcium-binding protein.
Readily absorbed from small intestine (proximal or distal), requires presence of bile salts.
LD50 = 23.7 mg/kg (Orally in mice); LD50 = 10 mg/kg (Orally in rats ); Nausea, vomiting and diarrhea, weight loss, irritability, weakness, fatigue, lassitude, and headache.
Biotrnasformation / Drug Metabolism
Within the liver, ergocalciferol is hydroxylated to ercalcidiol (25-hydroxyergocalciferol) by the enzyme 25-hydroxylase. Within the kidney, ercalcidiol serves as a substrate for 1-alpha-hydroxylase, yielding ercalcitriol (1,25-dihydroxyergocalciferol), the biologically active form of vitamin D2.
Contraindications for vitamin D analogues (Vitamin D2, Vitamin D3, Calcitriol, and Calcidiol):
Vitamin D should not be given to patients with hypercalcemia or evidence of vitamin D toxicity. Use of vitamin D in patients with known hypersensitivity to vitamin D (or drugs of the same class) or any of the inactive ingredients is contraindicated.
Interactions for vitamin D analogues (Vitamin D2, Vitamin D3, Calcitriol, and Calcidiol):
Cholestyramine has been reported to reduce intestinal absorption of fat soluble vitamins; as such it may impair intestinal absorption of any of vitamin D.
The coadministration of phenytoin or phenobarbital will not affect plasma concentrations of vitamin D, but may reduce endogenous plasma levels of calcitriol/ergocalcitriol by accelerating metabolism. Since blood level of calcitriol/ergocalcitriol will be reduced, higher doses of Rocaltrol may be necessary if these drugs are administered simultaneously.
Thiazides are known to induce hypercalcemia by the reduction of calcium excretion in urine. Some reports have shown that the concomitant administration of thiazides with vitamin D causes hypercalcemia. Therefore, precaution should be taken when coadministration is necessary.
Vitamin D dosage must be determined with care in patients undergoing treatment with digitalis, as hypercalcemia in such patients may precipitate cardiac arrhythmias.
Ketoconazole may inhibit both synthetic and catabolic enzymes of vitamin D. Reductions in serum endogenous vitamin D concentrations have been observed following the administration of 300 mg/day to 1200 mg/day ketoconazole for a week to healthy men. However, in vivo drug interaction studies of ketoconazole with vitamin D have not been investigated.
A relationship of functional antagonism exists between vitamin D analogues, which promote calcium absorption, and corticosteroids, which inhibit calcium absorption.
Since vitamin D also has an effect on phosphate transport in the intestine, kidneys and bones, the dosage of phosphate-binding agents must be adjusted in accordance with the serum phosphate concentration.
The coadministration of any of the vitamin D analogues should be avoided as this could create possible additive effects and hypercalcemia.
Uncontrolled intake of additional calcium-containing preparations should be avoided.
Magnesium-containing preparations (eg, antacids) may cause hypermagnesemia and should therefore not be taken during therapy with vitamin D by patients on chronic renal dialysis.