Vitamin D and Multiple Sclerosis: Are We Still in the Dark? (P6.144)

BACKGROUND Multiple sclerosis (MS) displays a long-recognized latitudinal variation in prevalence rates, increasing with distance from the equator. As latitude correlates both with sunlight intensity and serum 25-hydroxyvitamin (25(OH)D) levels, it is suggested that 25(OH)D could be a key environmental factor in the development of MS. Numerous reports have suggested associations between low 25(OH)D serum levels and a range of clinical or paraclinical features of MS. Despite these, it remains unclear whether the association reflects a central role for 25(OH)D in the pathogenesis of the disease, or whether this is an epiphenomenon. This issue has key implications for our monitoring and treatment of patients with MS. DESIGN/METHODS A prospective cohort-study of 184 patients (gender and age matched) consisting of 63 MS patients (51 relapsing-remitting MS, 12 primary-progressive MS) and 121 controls (105 other neurological diseases, 16 other neurological inflammatory diseases). 25(OH)D was measured in blood sera via liquid chromatography-tandem mass spectrometry. The data was correlated with age, sex, subtype of diagnosis, month of sampling and MRI lesion load in MS patients. A comprehensive literature review on the topic was performed. RESULTS There were no significant differences in the mean of 25(OH)D in the MS group versus controls (p=0.248). Mean 25(OH)D levels in MS patients were 33.7 (95% CI: 28.5-39.9) and 37.8 nmol/l in controls (95% CI: 33.8-42.2). As expected, 25(OH)D levels were found to differ significantly across the months. After controlling for this, the difference remained non-significant (p=0.219). Our literature review revealed 596 references, consisting of 285 reviews and 162 observational studies, of which only 67 provided 25(OH)D measurements. CONCLUSION The analysis was powered to detect a difference of approximately 30% between the groups, equivalent to 14.6 nmol/L. In this cohort of patients recruited at the earliest point in disease, there were no differences in 25(OH)D levels between MS patients and controls. These results raise concerns as to the validity of current models of the role of 25(OH)D in MS. Disclosure: Dr. Douglas has received personal compensation for activities with Biogen Idec. Dr. Durant has nothing to disclose. Dr Hassan-Smith has received personal compensation for activities with Biogen Idec and Novartis. Dr. Hodson has nothing to disclose. Dr. Curnow has nothing to disclose. Dr. Tsentemeidou has nothing to disclose.