Vit D

Oral
Nutritional deficiency
Adult: 10 mcg (400 units) daily. May also be given via IM inj. 
Oral
Deficiency due to malabsorption states or liver diseases
Adult: Up to 1 mg (40 000 units) daily. May also be given via IM inj. 
Oral
Hypocalcaemia caused by hypoparathyroidism
Adult: Up to 5 mg (200 000 units) daily. May also be given via IM inj.

Hypercalcaemia. Evidence of vitamin D toxicity.

Excessive intake may lead to development of hyperphosphataemia or hypercalcaemia. Infants, renal impairment or calculi, heart disease. Monitor plasma phosphate & calcium level. Pregnancy, lactation.

Hyperphosphataemia or hypercalcaemia (in excessive intake). Associated effects of hypercalcaemia include hypercalciuria, ectopic calcification, & renal & CV damage.

Increased risk of hypercalcaemia if given with thiazide diuretics, calcium or phosphate. Antiepileptics (e.g. carbamazepine, phenobarbitone, phenytoin & primidone) may increase vitamin D requirements. Rifampicin & isoniazid may reduce efficacy of vitamin D. Corticosteroids may counteract the effect of vitamin D. Digoxin or any cardiac glycoside. Reduced absorption when taken with cholestyramine, colestipol, mineral oil, orlistat. Ketoconazole.

Olestra (fat substitute).

Vit D may have anti-osteoporotic, immunomodulatory, anticarcinogenic, antipsoriatic, antioxidant & mood-modulatory activities. Along with parathyroid hormone & calcitonin, regulate serum calcium conc.
Onset: Slow.
Duration: Relatively prolonged duration of action.
Absorption: Well absorbed from the GI tract. Presence of bile is essential for adequate intestinal absorption. Hence absorption may be decreased in patients with decreased fat absorption.
Distribution: Bound to a specific α-globulin. Can be stored in adipose & muscle tissue for long periods of time. Slowly released from storage sites & skin where it is formed in the presence of sunlight or uv light. May distribute into breast milk.
Metabolism: Hydroxylated in the liver by the enzyme vitamin D 25-hydroxylase to form 25-hydroxycholecalciferol (calcifediol). Further hydroxylated in the kidneys by the enzyme vitamin D1-hydroxylase to form the active metabolites 1,25-dihydroxycholecalciferol (calcitriol). Further metabolism also occurs in the kidneys, including the formation of the 1,24,25-trihydroxy derivatives.
Excretion: Mainly in the bile & faeces with only small amounts appearing in urine.

A: Adequate and well-controlled human studies have failed to demonstrate a risk to the fetus in the first trimester of pregnancy (and there is no evidence of risk in later trimesters