vdre bone matrix. This causes a disruption in the orderly sequence of events in the differentiation of hypertro-phied chondrocytes in the epiphyseal plates resulting in their disorganization causing a widening of the epiphyseal plates (end of long bones), demineraliza-tion of the skeleton, and bony deformities (Figure 1).

Once the epiphyseal plates are closed later in adolescence, vitamin D deficiency can no longer cause bone deformities. Instead, there is an inability to mineralize newly deposited bone matrix leading to wide osteoid seams within the trabecular and cortical bone causing the bone disease commonly known as osteomalacia. In addition, the secondary hyperparathyroidism that results from vitamin D deficiency results in the mobilization of precious calcium stores from the bone thereby exacerbating bone loss and causing osteoporosis. This can increase a person's risk for fracture.

The hallmark for determining the vitamin D status is the measurement of the circulating concentration of 25(OH)D. The 25(OH)D is low or undetectable in vitamin D deficiency and markedly elevated in vitamin D intoxication. Measurement of 1,25(OH)2D is of little value for determining the vitamin D nutritional status because its synthesis is tightly regulated. Indeed, as a person becomes vitamin D deficient, there is an increase in the secretion of PTH which, in turn, increases the production of 1,25(OH)2D. Thus, early in vitamin D deficiency one can see a normal fasting serum calcium, low-normal to low phosphorus, low 25(OH)D, and elevated PTH, 1,25(OH)2D and alkaline phosphatase. In chronic vitamin D deficiency, all the above are seen with the exception that 1,25(OH)2D is low-normal or low.

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