MAY 23, 2017 10:00 AM PDT

WEBINAR: Vitamin D Metabolites and Clinical Relevance

C.E. CREDITS: P.A.C.E. CE | Florida CE
  • Director, Endocrine Laboratory, Mayo Clinic
      Ravinder J. Singh, Ph.D., is the director of the Mayo Clinic Endocrine Laboratory. He has a focused area of investigation that has broad applicability to the field. Dr. Singh studies the application of liquid chromatography-tandem mass spectrometry (LC-MS/MS) to clinical laboratory analysis. Many of the methods that Dr. Singh developed are now considered reference methods. They have subsequently been utilized for method standardization efforts as well as to establish clinical disease correlates, which he has published with his collaborators.

      Dr. Singh's work has directly contributed to improving methods for the clinical diagnosis of Cushing's disease, pheochromocytoma and congenital adrenal hyperplasia. He continues to work to discover innovative ways to better understand the uses of LC-MS/MS in providing patients with faster and more accurate diagnoses.


    DATE: May 23, 2017
    TIME: 10:00am PT, 1:00pm ET

    A number of studies have shown that vitamin D deficiency is very common in both the developing and developed world. This has increased the interest of the general public. 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 have similar biologic activities. Exogenous or endogenous Vitamin D3 are rapidly converted to 25(OH)D3 by liver vitamin D3-25 hydroxylase thus Vitamin D3 has very short half-life in circulation. Additional hydroxylation of 25-OH vitamin D takes place in the kidney1-alpha hydroxylase (CYP27B1), producing bioactive hormone 1,25-dihydroxy vitamin D (1,25-(OH)2-D). Production of 1,25-(OH)2-D is therefore tightly regulated through concentrations of serum calcium, phosphorus, and parathyroid hormone. 1,25-(OH)2-D a hormone,  plays a critical role in calcium absorption through interaction with vitamin D receptor (VDR). Excess 25-OH vitamin D is removed from circulation and is converted to inactive 24, 25-dihydroxy vitamin D (24,25-(OH)2-D), catalyzed by 24 hydroxylase (CYP24A1). CYP24A1 gene, encoding the vitamin D-24-hydroxylase, is of major clinical and physiologic importance, serving to regulate the catabolism of 1,25-(OH)2D, the physiologically active vitamin D metabolite. In addition to facilitating catabolism of 1,25-(OH)2D, CYP24A1 also enhances the turnover and elimination of 25-OHD, the abundant precursor metabolite and storage form of the vitamin D. 

    Learning Objectives:

    • Pathophysiology of Vitamin D
    • Applications in the Clinical Laboratories

    Show Resources
    Loading Comments...