Clinical Information

Vitamin D is a generic designation for a group of fat-soluble, structurally similar sterols including ergocalciferol D2 from plants and cholecalciferol D3 from animals. Vitamin D in the body is derived from 2 sources: exogenous (dietary: D2 and D3) and endogenous (biosynthesis: D3). Endogenous D3 is produced in the skin from 7-dehydrocholesterol, under the influence of ultraviolet light. Both forms of vitamin D are of similar biologic activity.

Vitamin D is rapidly metabolized in the liver to form 25-hydroxy (OH) vitamin D. Additional hydroxylation of 25-OH vitamin D takes place in the kidney by 1-alpha hydroxylase, under the control of parathyroid hormone, to yield 1,25-dihydroxy vitamin D.

1,25-Dihydroxy vitamin D is the most potent vitamin D metabolite. It stimulates calcium absorption in the intestine and its production is tightly regulated through concentrations of serum calcium, phosphorus, and parathyroid hormone.

1,25-Dihydroxy vitamin D levels may be high in primary hyperparathyroidism and in physiologic hyperparathyroidism secondary to low calcium or vitamin D intake. Some patients with granulomatous diseases (eg, sarcoidosis) and malignancies containing nonregulated 1-alpha hydroxylase in the lesion may have elevated 1,25-dihydroxy vitamin D levels and hypercalcemia.

1,25-Dihydroxy vitamin D levels are decreased in hypoparathyroidism and in chronic renal failure.

While 1,25-dihydroxy vitamin D is the most potent vitamin D metabolite, levels of the 25-OH forms of vitamin D more accurately reflect the body's vitamin D stores. Consequently, 25HDN / 25-Hydroxyvitamin D2 and D3, Serum is the preferred initial test for assessing vitamin D status. However, in the presence of renal disease, 1,25-dihydroxy vitamin D levels may be needed to adequately assess vitamin D status.