Type: Paper
Authors: Greg Blaney, MD, Paul J. Albert, Amy D. Proal
Publication: Annals of the New York Academy of Sciences
Citation: Vitamin D metabolites as clinical markers in autoimmune and chronic disease. Ann N Y Acad Sci. 2009 Sep;1173:384-90. doi: 10.1111/j.1749-6632.2009.04875.x.
[PMID: 19758177] [DOI: 10.1111/j.1749-6632.2009.04875.x] .
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Recent research has implicated vitamin D deficiency (serum levels of 25-hydroxyvitamin D <50nmol/L) with a number of chronic conditions including autoimmune conditions such as multiple sclerosis, lupus, psoriasis and chronic conditions such as osteoporosis, osteoarthritis, metabolic syndrome, fibromyalgia and chronic fatigue syndrome. It has been assumed that low levels of 25-hydroxyvitamin D (25-DThe vitamin D metabolite widely (and erroneously) considered best indicator of vitamin D "deficiency." Inactivates the Vitamin D Nuclear Receptor. Produced by hydroxylation of vitamin D3 in the liver.) accurately indicate vitamin D storage and vitamin D receptor (VDR) mediated control of calcium metabolism and innate immunityThe body's first line of defense against intracellular and other pathogens. According to the Marshall Pathogenesis the innate immune system becomes disabled as patients develop chronic disease.. To evaluate this assumption, 25-D and 1,25-dihydroxyvitamin D3 (1,25-DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol.) levels were measured in 100 Canadian patients with these conditions. Additionally, other inflammatory markers (CK, CRP) were measured. Results showed a strong positive association between these autoimmune conditions and levels of 1,25-D >110 pmol/L. However, there was little association with vitamin D deficiency or the other inflammatory markers. These findings support the use of 1,25-D as a clinical marker in autoimmune conditions. It also suggests either a disruption of the controlling cytochrome P450 enzymes and/or reduced VDR responsiveness in these conditions. Finally, the results challenge the assumption that measurement of 25-D is an accurate index of vitamin D metabolism.