Adults

For severe vitamin D deficiency: 40,000 IU once weekly for 7-10 weeks, followed by a maintenance dose as directed by a physician. Dosage varies based on individual needs and deficiency severity.

Elderly

Similar to adult dosage, but close monitoring for hypercalcemia is recommended.

Renal_impairment

Use with caution and monitor calcium/phosphate levels. Dosage adjustments may be necessary, and active forms of vitamin D might be preferred due to impaired renal activation of cholecalciferol.

Onset

Effects on serum calcium levels can be observed within days to weeks. Full therapeutic effects on bone mineral density may take several months.

Excretion

Primarily excreted in bile and feces, with a minor amount excreted renally.

Half life

The elimination half-life of 25-hydroxyvitamin D (calcifediol) is approximately 2-3 weeks; the half-life of the active form, 1,25-dihydroxyvitamin D (calcitriol), is 4-6 hours.

Absorption

Well absorbed from the small intestine in the presence of bile salts, primarily via facilitated diffusion and micellar solubilization.

Metabolism

Initially hydroxylated in the liver by CYP2R1 and CYP27A1 to 25-hydroxyvitamin D (calcifediol). Further hydroxylation occurs in the kidneys by CYP27B1 to the active form, 1,25-dihydroxyvitamin D (calcitriol).

Mineral oil

May impair vitamin D absorption.

Corticosteroids

May reduce the effects of vitamin D by inhibiting calcium absorption and increasing urinary calcium excretion.

Thiazide diuretics

May increase the risk of hypercalcemia by reducing urinary calcium excretion.

Cardiac glycosides (e.g., digoxin)

Hypercalcemia caused by vitamin D can potentiate the effects and toxicity of cardiac glycosides, leading to arrhythmias.

Anticonvulsants (e.g., phenytoin, barbiturates)

May increase vitamin D metabolism, reducing its effectiveness.

Bile acid sequestrants (e.g., cholestyramine, colestipol) and Orlistat

May impair vitamin D absorption by interfering with fat absorption.