Vitamin D in Systemic Lupus Erythematosus

Diane Kamen; Cynthia Aranow


Curr Opin Rheumatol. 2008;20(5):532-537. 

In This Article

Sources and Measurement of Vitamin D

Without oral supplementation, the primary source of vitamin D precursors is the skin upon exposure to ultraviolet (UV) light (cholecalciferol, vitamin D3), with a lesser contribution from most diets (ergocalciferol, vitamin D2). These precursors are then hydroxylated at the 25 carbon atom in the liver forming 25-hydroxyvitamin D3 (25D). The subsequent hydroxylation at the 1 carbon atom creating the biologically active form of the hormone, 1,25(OH)2vitamin D3 (1,25D), is now known to occur in many extra-renal sites including cells of the immune system. Because of the very short half-life and tight regulation of 1,25D by parathyroid hormone (PTH), the serum 25D level is the best indicator of true vitamin D status. A 'normal' 25D level at most laboratories was set at more than 20 ng/ml (50 nmol/l) on the basis of studies of distributions in populations we now know to be largely deficient. Using PTH elevation as a biomarker reflecting physiologic low levels of vitamin D, recent reports indicate that vitamin D deficiency would be more accurately defined as a 25D concentration of less than 32 ng/ml (80 nmol/l). Whether 'normal' serum levels of vitamin D are sufficient for immune homeostasis is not known.


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