Vitamin D Deficiency

High prevalence of deficiency (much more than previously recognized).

At risk: Dietary insufficiency, breastfed infants, inadequate sun exposure, elderly, nursing home residents, institutionalized, dark skinned individuals, obese, post gastric bypass, IBD.

Genetically predisposed: Rickets, osteomalacia.

Hypocalcemia; vitamin D promotes calcium absorption in the gut and aids in maintenance of calcium and phosphorus levels. Without vitamin D, only 10–15% of dietary calcium and approx 60% of phosphorous is absorbed. Low total body magnesium is also likely.

Calcitriol influences muscle function, CV homeostasis, and immune response.

Deficiency associated with Htn, MI, CHF, and calcific aortic stenosis.

Ample evidence to connect adequacy to risk and/or severity of certain cancers (colorectal, prostate, breast, leukemia) and autoimmune diseases (RA, MS, type 1 DM).

Chronic vitamin D deficiency may lead to impaired mineralization of cervical spine (increased incidence of abn neck mobility). Pediatric pts with deformed chest wall may experience lowered FRC and increased incidence of respiratory infections.

Fat soluble vitamin and biologically inert. Amount obtained through food sources is minimal compared to that from sun exposure.

There are two main forms. Vitamin D ₃ (cholecalciferol) is synthesized in the skin by exposure to ultraviolet (UVB) radiation. Vitamin D ₂ (ergocalciferol) is obtained through irradiation of ergosterol in plants and subsequent dietary intake.

Intake involves two hydroxylations. Vitamins D ₂ and D ₃ are hydroxylated in the liver to 25 vitamin D (calcidiol), the major circulating form. Further hydroxylation in the kidney produces the active metabolite 1,25 vitamin D (calcitriol). Calcitriol is the physiologically active form.

Involved in functioning of hemopoietic cells, skin cells, cancer cells of various origins, islet cells of the pancreas, immune response, as well as CV function (via serum Ca ²⁺ ).

Inadequate sun exposure, dietary insufficiency.

There are two types of vitamin D-dependent rickets: Type I: Inherited autosomal recessive trait (defect in the 25OH-D ₃ conversion into calciferol [true vitamin D]); type II: Autosomal dominant disorder, where single amino acid change in vitamin D receptor results in nonfunctional state.

Osteomalacia is a metabolic disease with inadequate and/or delayed mineralization of osteoids in mature bone.