Vitamin D is used to describe a group of five fat-soluble secosteroid vitamins required for the homeostasis of serum calcium and phosphorus. Vitamin D is a prohormone that exists in two forms in humans (D2 and D3).
Cholecalciferol (D3) acts by regulating calcium and phosphorus intestinal absorption and controls the mobilisation of the electrolytes from bone stores, the later contributing to the synthesis of parathyroid hormone. One of its precursors (7-Dehydrocholesterol) is converted to cholecalciferol by UV light in the skin, hence vitamin D deficiency is encounted in populations with little or no sunlight exposure.
Vitamin D2 is artificially created by irradiation of ergosterol from yeast or fungi and is used for supplementation and pharmaceutical purposes. Vitamin D3 is the endogenously produced compound resulting from ultraviolet exposure to 7-dehydrocholesterol in the deeper layers of the skin.
Both Vitamin D2 and D3 must undergo two sequential hydroxylations at the carbon 25 position in the liver and kidneys to the active hormonal form 1,25-dihydroxyvitamin D3 (1,25[OH]2D3). The 1α hydroxylating enzyme is found exclusively in renal tissue (25-OH-D-1α hydroxylase).
The active hormonal form acts on the intestine and bone for homeostatic maintenance of serum calcium and phosphorus levels and mineralization of bone.
Pathological manifestations can occur both in excess and deficiency:
- hypervitaminosis D is rare and leads to hypercalcaemia, facilitating calcium deposition in soft tissues, such as the arteries and kidneys.
- hypovitaminosis D
- hypophosphatemic vitamin D-refractory rickets and osteomalacia
- vitamin D-dependent rickets (a.k.a. pseudovitamin D-deficiency rickets)
- vitamin D-resistant rickets
- X-Linked hypophosphatemia
- parathyroid gland abnormalities