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The Effect of Methylprednisolone, Interferon Beta and Glatiramer Acetate Treatment on the Levels of Leptin, Adiponectin and Resistin in Multiple Sclerosis Patients | Abstract
ISSN: 2155-9562

Journal of Neurology & Neurophysiology
Open Access

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Research Article

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

Slawomir Michalak1,2*, Lukasz Jernas3#, Ewa Wysocka4, Krystyna Osztynowicz1, Elzbieta Tokarz-Kupczyk3, Halina Wygladalska-Jernas3 and Wojciech Kozubski3

1Department of Neurochemistry and Neuropathology, Poznan University of Medical Sciences, 60-355 Poznan, Przybyszewskiego str. 49, Poland

2Neuroimmunological Unit, Polish Academy of Sciences, 60-355 Poznan, Przybyszewskiego str. 49, Poland

3Department of Neurology, Poznan University of Medical Sciences, 60-355 Poznan, Przybyszewskiego str. 49, Poland

4Department of Clinical Biochemistry and Laboratory Medicine, Chair of Chemistry and Clinical Biochemistry, Poznan University of Medical Sciences, Poland

#Equally Contributed

Corresponding Author:
Slawomir Michalak
Department of Neurochemistry and Neuropathology
Poznan University of Medical Sciences
60-355 Poznan, Przybyszewskiego str. 49, Poland
Tel: +48 61 8691 443
Fax: +48 61 8691 444
E-mail: [email protected]

Received date: December 21, 2013; Accepted date: February 19, 2014; Published date: February 27, 2014

Citation: Michalak S, Jernas L, Wysocka E, Osztynowicz K, Kupczyk ET, et al. (2014) The Effect of Methylprednisolone, Interferon Beta and Glatiramer Acetate Treatment on the Levels of Leptin, Adiponectin and Resistin in Multiple Sclerosis Patients. J Neurol Neurophysiol S12:005. doi:10.4172/2155-9562.S12-005

Copyright: © 2014 Michalak S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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.

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