Background And Relevant Pharmacokinetics

The name 'vitamin D' actually refers to several related fat-soluble vitamin variants, all of which are sterol (cholesterol-like) substances. Cholecalciferol (D3) is the form found in animal products and fish oils, whereas ergocalciferol (D2) is the major synthetic form of provitamin D and usually found in supplements; however, other forms also exist. These ingested forms of vitamin D have 50-80% bioavailability and are emulsified by the bile salts, then enter through the small intestine into the lymphatic circulation. In the liver and kidneys, these forms are converted to 25-hydroxycholecalciferol and 1,25-dihydroxylcholecalciferol, the major circulating active form of vitamin D.

Vitamin D (as D3) is also produced in the body as a result of the conversion of a cholesterol-based precursor, 7-dehydrocholesterol, which is produced in the sebaceous glands of the skin. Exposure to sunlight (UVB) converts this precursor into cholecalciferol over a 2-3 day period. Prolonged exposure to UVB can inactivate some of the newly-formed vitamin D and its precursors so that eventually a state of equilibrium is reached between vitamin D synthesis and catabolism. Therefore, short periods of sun exposure are considered more efficacious than long periods (Working Group of the Australian and New Zealand Bone and Mineral Society, Endocrine Society of Australia and Osteoporosis Australia 2005). Some vitamin D is stored in adipose tissue and can be mobilised during periods when exposure to sunlight is reduced or shortages develop (Nowson & Margerison 2002). Vitamin D and its metabolites are primarily excreted through bile and the degraded active form is removed via the kidney. Losses are believed to be minor, due to both reabsorption of vitamin D derivatives via the enterohepatic recirculation and limited filtration at the kidneys (Kohlmeier 2003). Parathyroid hormone (PTH), calcium and phosphorus are involved in the regulation of vitamin D metabolism.

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