|Values are valid only on day of printing.|
As a second-order test in the assessment of vitamin D status, especially in patients with renal disease
Investigation of some patients with clinical evidence of vitamin D deficiency (eg, vitamin D-dependent rickets due to hereditary deficiency of renal 1-alpha hydroxylase or end-organ resistance to 1,25-dihydroxy vitamin D)
Differential diagnosis of hypercalcemia
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.
<16 years: 24-86 pg/mL
> or =16 years: 18-64 pg/mL
<16 years: 24-86 pg/mL
> or =16 years: 18-78 pg/mL
1,25-Dihydroxy vitamin D concentrations are low in chronic renal failure and hypoparathyroidism.
1,25-Dihydroxy vitamin D concentrations are high in sarcoidosis and other granulomatous diseases, some malignancies, primary hyperparathyroidism, and physiologic hyperparathyroidism.
1,25-dihydroxy vitamin D concentrations are not a reliable indicator of vitamin D toxicity; normal (or even low) results may be seen in such cases.
No significant cautionary statements.
The new, 1,25-dihydroxy vitamin D liquid chromatography-tandem mass spectrometry (LC-MS/MS) assay correlates well with the current immunoassay:
-LC-MS/MS=0.95 RIA (pg/mL) + 2.5 pg/mL; correlation coefficient=0.822
-Inter-assay precision: 7 to 12% CV (19 to 287 pg/mL)
-Interferences: C-3 epimers (EPI) of 1,25 dihydroxyvitamin D3 3.0%
1. Endres DB, Rude RK: Vitamin D and its metabolites. In Tietz Textbook of Clinical Chemisty. Third edition. Edited by CA Burtis, ER Ashwood. Philadelphia, WB Saunders Company, 1999, pp 1417-1423
2. Bringhurst FR, Demay MB, Kronenberg HM: Vitamin D (calciferols): metabolism of vitamin D. In Williams Textbook of Endocrinology. Ninth edition. Edited by JD Wilson, DW Foster, HM Kronenberg, PR Larsen. Philadelphia, WB Saunders Company, 1998, pp 1166-1169