Metabolic Syndrome and Disability in Multiple Sclerosis: A Retrospective Study (P6.168)

OBJECTIVE: Study the association between metabolic syndrome (MetS) and disease severity in multiple sclerosis (MS). BACKGROUND: MS is an autoimmune inflammatory disease characterized by demyelination and axonal loss. MetS is believed to be a chronic low-grade inflammatory state. We hypothesized that MS patients with MetS will have increased disability and enhanced inflammation on MRI. DESIGN/METHODS: Data including age, sex, disability scores, MRI, and laboratory data on MS patients were retrospectively collected. MetS was defined as: obesity(BMI蠅25kg/m2) and any of the following: fasting blood glucose >100mg/dL, BP>130/85, serum triglyceride >150mg/dL, HDL cholesterol <40mg/dL in men, <50mg/dL in women. EDSS, time to 25-foot walk [T25-FW] and modified 9-hole peg test [mNHPT] were used as disability measures. MRI activity was defined as presence of new T2 and/or gadolinium enhancing lesion on brain MRI at last follow-up. EDSS was dichotomized into two groups: <4 and >4 for statistical analysis, while T25-FW and mNHPT were analyzed as continuous variables. Univariate regression analyses with EDSS, NHPT, and T25-FW as outcome variables were initially performed. Multivariate linear regression analyses were performed to determine if presence of MetS predicted disability measures after adjusting for age, severity and gender. RESULTS:Total 399 (75% relapsing, 25% progressive) MS patients (mean age ±SD, 48±13.2 years; 74% women) were included. Total 38 (10%) patients were identified with MetS. Mean T25-FW and mNHPT were higher in patients with MetS compared to the group without MetS (P for both <0.05); no difference in EDSS between the groups was seen. In multivariate linear regression analysis, presence of MetS was an independent predictor of slower T25-FW (P=0.025) and NHPT (P=0.005) after adjusting for age, gender and disease severity. No difference in active MRI lesions was seen between groups. CONCLUSIONS: Presence of MetS is associated with higher disability but no increase in MRI lesions in MS patients. Disclosure: Dr. Berrios Morales has nothing to disclose. Dr. Saipetch has nothing to disclose. Dr. Turetsky has nothing to disclose. Dr. Kane has nothing to disclose. Dr. Garg has received personal compensation for activities with Biogen Idec, Bayer Pharmaceuticals Corp., Teva Neuroscience, and EMD Serono. Dr. Garg has received research support from Novartis. Dr. Riskind has received personal compensation for activities with EMD Serono, Questcor Pharmaceuticals, and Biogen Idec as a consultant, and with Teva Neuroscience as a speaker. Dr. Riskind has received research support from Biogen Idec, Teva Neuroscience, Hoffman-LaRoche, Genentech Inc., and Novartis.