Slawomir Michalak, Lukasz Jernas, Ewa Wysocka, Krystyna Osztynowicz, Elzbieta Tokarz-Kupczyk, Halina Wygladalska-Jernas and Wojciech Kozubski
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.
