A randomized trial of high-dose vitamin D2 in relapsing-remitting multiple sclerosis

Stein, Mark S.; Liu, Y; Gray, Orla; Baker, Josephine; Kolbe, Scott; Ditchfield, Michael; Egan, Gary F.; Mitchell, Peter; Harrison, Leonard C.; Butzkueven, Helmut; Kilpatrick, Trevor J.

doi:10.1212/wnl.0b013e3182343274

Cited by 175 publications

(126 citation statements)

References 40 publications

Supporting

Mentioning

121

Contrasting

Unclassified

Order By: Relevance

“…There was also a significant association between the vitamin D serum level and the new gadolinium-enhancing lesions in another study on 88 patients during 6 months before the prescription of an IFNβ, this relation being no longer observed under this treatment for 18 months . The absence of a significant effect of vitamin D supplementation on MRI findings in four other controlled studies may be explained, as in the case of clinical variables (see above), by the smallness of the sample size and the shortness of the follow up [Wingerchuk et al 2005;Mosayebi et al 2011;Stein et al 2011], and the unusually benign profile of patients at baseline .…”

Section: Other Variablesmentioning

confidence: 98%

Contribution of vitamin D insufficiency to the pathogenesis of multiple sclerosis

Pierrot‐Deseilligny

Souberbielle

2013

Ther Adv Neurol Disord

View full text Add to dashboard Cite

Abstract:The contribution of vitamin D insufficiency to the pathogenesis of multiple sclerosis (MS) is reviewed. Among the multiple recently discovered actions of vitamin D, an immunomodulatory role has been documented in experimental autoimmune encephalomyelitis and in humans. This action in the peripheral immune system is currently the main known mechanism through which vitamin D might influence MS, but other types of actions could be involved within the central nervous system. Furthermore, vitamin D insufficiency is widespread in temperate countries and in patients with MS at the earliest stages of the disease, suggesting that the deleterious effects related to vitamin D insufficiency may be exerted in these patients. In fact, many genetic and environmental risk factors appear to interact and contribute to MS. In genetics, several human leukocyte antigen (HLA) alleles (more particularly HLA-DRB1*1501) could favour the disease whereas some others could be protective. Some of the genes involved in vitamin D metabolism (e.g. CYP27B1) also play a significant role. Furthermore, three environmental risk factors have been identified: past Epstein-Barr virus infection, vitamin D insufficiency and cigarette smoking. Interactions between genetic and environmental risk or protective factors may occur during the mother's pregnancy and could continue during childhood and adolescence and until the disease is triggered in adulthood, therefore possibly modulating the MS risk throughout the first decades of life. Furthermore, some clinical findings already strongly suggest that vitamin D status influences the relapse rate and radiological lesions in patients with MS, although the results of adequately powered randomized clinical trials using vitamin D supplementation have not yet been reported. While awaiting these incontrovertible results, which might be long in coming, patients with MS who are currently in vitamin D insufficiency should be supplemented, at least for their general health status, using moderate doses of the vitamin.

show abstract