The Effect of Methylprednisolone, Interferon Beta and Glatiramer Acetate Treatment on the Levels of Leptin, Adiponectin and Resistin in Multiple Sclerosis Patients

Abstract

Objective: Adipocytokines are cytokine-like mediators that link adipose tissue function with inflammatory and autoimmune processes, and have a suggested role in the pathogenesis of multiple sclerosis (MS). The aim of this study was to analyze the effects of methylprednisolone, interferon-1b (INF) and glatiramer acetate (GA) on leptin, resistin, and adiponectin concentrations in relapsing-remitting MS (RRMS) patients. Methods: The study included 154 RRMS patients who were hospitalized in the Department of Neurology, Poznan University of Medical Sciences. The comparison group included 31 patients with myasthenia gravis (MG) and 39 healthy controls. Serum levels of leptin, adiponectin, and resistin were evaluated before treatment initiation. In the RRMS patients treated with methylprednisolone, adipocytokine evaluation was performed one day after the therapy. Patients treated with INF or GA were evaluated at 1 month and 6 months. Routine neurological examination and expanded disability status scale (EDSS) scoring were performed, and MRI scans were analyzed for the localization of demyelinating plaques. Body mass index, glycemia, and insulin levels were evaluated and homeostatic model assessment insulin resistance index (HOMA-IR) was calculated. Results: Adiponectin and resistin levels in RRMS and MG patients were increased compared to controls, but adiponectin levels were lower in RRMS than MG patients. Intravenous methylprednisolone in RRMS with relapse caused an elevation of leptin concentration. INF treatment caused a significant, time-dependent effect on resistin concentration. GA administration influenced only resistin concentration as a long-term effect. No relationship between adipocytokines and metabolic status or insulin resistance was found. Conclusions: We identified resistin as the most important adipocytokine associated with RRMS. Its concentrations are reduced by first line immunomodulatory treatment, which produces a milieu of beneficial inflammatory and metabolic processes. On the other hand, the routine treatment of MS relapses with methylprednisolone induces harmful metabolic and inflammatory effects that may be mediated by elevated leptin levels.