1,25-Dihydroxyvitamin D, Serum
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
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
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.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
<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.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
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%
Clinical Reference Provides recommendations for further in-depth reading of a clinical nature
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