D deficiency results in inadequate mineralization of the skeleton causing rickets, which is characterized by widening at the end of the long bones, rachitic rosary, deformations in the skeleton including frontal bossing, and outward or inward deformities of the lower limbs causing bowed legs and knocked knees, respectively (Goldring et al., 1995). In adults, vitamin D deficiency leads to a mineralization defect in the skeleton causing osteomalacia. In addition, the secondary hyperparathyroidism associated with vitamin D deficiency enhances mobilization of calcium from the skeleton, resulting in porotic bone (Favus and Christakos, 1996).

Any alteration in the cutaneous production of vitamin D3, the absorption of vitamin D in the intestine, or the metabolism of vitamin D to its active form, 1,25(OH)2D, can lead to a vitamin D-deficient state (Demay, 1995; Holick, 1995). In addition, an alteration in the recognition of 1,25(OH) 2D by its receptor can also cause vitamin D deficiency, metabolic bone disease, and accompanying biochemical abnormalities (Demay, 1995).

Vitamin D deficiency causes a decrease in ionized calcium in blood, which in turn leads to an increase in the production and secretion of PTH (Fraser, 1980; Holick, 1995). PTH stimulates the mobilization of calcium from the skeleton, conserves renal loss of calcium, and causes increased renal excretion of phosphorus leading to a normal fasting serum calcium with a low or low-normal serum phosphorus (Holick, 1995). Thus, vitamin D deficiency is characterized biochemically by either a normal or low-normal serum calcium with a low-normal or low-fasting serum phosphorus and an elevated serum PTH. Serum alkaline phosphatase is usually elevated in vitamin D deficiency states (Goldring et al., 1995). The elevated PTH leads to an increase in the destruction of the skeletal tissue in order to release calcium into the blood. The bone collagen by-products, including hydroxyproline, pyridinoline, deoxypyridinoline, and N-telopeptide, are excreted into the urine and are usually elevated (Kamel et al., 1994).

It is well recognized that vitamin D deficiency causes abnormalities in calcium and bone metabolism. The possibility that vitamin D deficiency is associated with an increased risk of colon, breast, and prostate cancer was suggested in epidemiologic surveys of people living at higher latitudes (Garland et al., 1985, 1990; Schwartz and Hulka, 1990). At this time, it is premature to categorically suggest that vitamin D deficiency increases cancer risk. Prospective studies need to be carried out to test the hypothesis.



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