It is used to treat and prevent vitamin D deficiency and associated diseases, including rickets. It is also used for familial hypophosphatemia, hypoparathyroidism that is causing low blood calcium, and Fanconi syndrome. It is usually taken by mouth.
The active form of Vitamin D3, Calcitriol, exerts its effect by binding to the Vitamin D receptors (VDRs) which are widely distributed through many body tissues.Vitamin D3 has a half life of about 50 days as it is fat soluble.Vitamin D3 is absorbed in the small intestine and bound to specific a-globulins and transported to the liver where it is metabolised to 25-hydroxy Vitamin D3 (Calcidiol). A second hydroxylation to 1,25-dihydroxy Vitamin D3 (Calcitriol) occurs in the kidney. This metabolite is responsible for the vitamin's ability to increase the absorption of calcium. Non-metabolised Vitamin D3 is stored in tissues such as fat and muscle.Vitamin D3 is eliminated via faeces and urine.
ORAL Nutritional deficiency: Adult: 10 mcg (400 units) daily. May also be given via IM inj. Deficiency due to malabsorption states or liver diseases: Adult: Up to 1 mg (40 000 units) daily. May also be given via IM inj. Hypocalcaemia caused by hypoparathyroidism: Adult: Up to 5 mg (200 000 units) daily. May also be given via IM inj.
Drug interaction with medication: Concomitant treatment with phenytoin or barbiturates can decrease the effect of vitamin D because of metabolic activation. Concomitant use of glucocorticoids can decrease the effect of vitamin D. The effectsof digitalis and other cardiac glycosides may be accentuated with the oral administration of calcium combined with vitamin D. Strict medical supervision is needed and, if necessary monitoring of ECG and calcium. Simultaneous treatment with ion exchange resins such as cholestyramine or laxatives such as paraffin oil may reduce the gastrointestinal absorption of vitamin D. The cytotoxic agent actinomycin and imidazole antifungal agents interfere with vitamin D activity by inhibiting the conversion of 25-hydroxyvitamin D to 1, 25-dihydroxyvitamin D by the kidney enzyme, 25-hydroxyvitamin D-1-hydroxylase.
Hypercalcaemia. Evidence of vit D toxicity. Excessive intake may lead to development of hyperphosphataemia or hypercalcaemia. Infants, renal impairment or calculi, heart disease. Monitor plasma phosphate & Ca level. Pregnancy, lactation.
Hyperphosphataemia or hypercalcaemia (in excessive intake). Associated effects of hypercalcaemia include hypercalciuria, ectopic calcification, & renal & CV damage.
The required dose of vitamin D during lactation has not been adequately studied; doses similar to those for pregnant women have been suggested. Chronic ingestion of large doses of vitamin D by the mother may lead to hypercalcemia in the breastfed infant.
The most serious consequence of acute or chronic overdose is hypercalcaemia due to vitamin D toxicity. Symptoms may include nausea, vomiting, polyuria, anorexia, weakness, apathy, thirst and constipation. Chronic overdoses can lead to vascular and organ calcification as a result of hypercalcaemia. Treatment should consist of stopping all intakes of vitamin D and rehydration.
Store in a cool (below 25°C) and dry place protected from light. Keep away from the reach of children.
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