Efficacy of Adding Vitamin D Supplementation to Interferon β-1 in Multiple Sclerosis

Document Type : Original Article (s)

Authors

1 Professor, Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

2 Student of Medicine, School of Medicine AND Student Research Committee, Isfahan University of Medical Sciences, Isfahan, Iran

Abstract

Background: Vitamin D metabolites are involved in immunological signaling that leads to suppression and regulation of autoimmune and inflammatory pathways. Therefore, vitamin D supplementation may be a viable method for treating autoimmune or inflammatory diseases. This study aimed to investigate how treating with interferon beta-1 with vitamin D differs from treating with interferon beta-1 alone in patients with multiple sclerosis (MS).Methods: In this phase II double-blind randomized clinical trial, 59 patients with multiple sclerosis receiving interferon β-1 were split into two groups, one supplemented with vitamin D, to study the clinical effects resulted after 6, 12, and 24 months. We used analysis of magnetic resonance imaging (MRI), evidence of clinical relapses, and expanded disability status scale (EDSS) scores at baseline, 12 and 24 months to perform statistical analysis. Type of statistical analysis varied based on the measured outcomes.Findings: After 2 years of treatment, patients treated with vitamin D experienced decreased EDSS score (P = 0.014), decreased rate of relapse (P = 0.240), and decreased average number of gradient-echo (GE) lesions (P < 0.001).Conclusion: Vitamin D is a viable way to supplement the treatment of multiple sclerosis and its role in autoimmune diseases needs to be further clinically investigated. Our results suggest that in a population of patients with multiple sclerosis, vitamin D levels are a good predictor of the severity of the disease. In conclusion, vitamin D may not be a significant factor to consider in the etiology of multiple sclerosis, but rather a possible environmental exacerbating factor in the progression of the disease.

Keywords


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