21st Congress of the European Committee for the Treatment and Research in Multiple Sclerosis
10th Annual Meeting of the Americas Committee for Treatment and Research in Multiple Sclerosis

28.09.2005 - 01.10.2005
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28.09.2005
29.09.2005
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Home - 29.09.2005 - Therapy - immunomodulation - Part I


Therapy - immunomodulation - Part I

Thursday, September 29, 2005, 15:30 - 17:00

The effect of interferon beta-1a (Rebif) on relapse rate, disability, free radicals and neuroimaging in MS patients

M.D. Paramo, M.A. Gamero, L. Dinca, J.L. Ruiz Peņa, J. Garcia-Moreno, M. Lucas, F. Sanchez, A. Ucles, R. Bolaņos, C. Duran, G. Izquierdo (Seville, Badajoz, E)

Background: Oxidative stress is known to be an important pathogenic factor in multiple sclerosis (MS). Several studies have shown increased free radicals both in central nervous system (CNS) and peripheral blood samples of MS patients.
Goals of the study: To determine the effect of interferon beta 1a injected three times a week subcutaneously (Rebif) on relapse rate, disability measures, systemic free radicals and radiologic parameters in MS patients.
Methods: We have studied a cohort of 43 relapsing-remitting MS patients undergoing treatment with Rebif for 2 years. After informed consent, each patient underwent scheduled visits at month 0, 3, 6, 9, 12, 18 and 24 that included neurologic assesment and measurement of sulfhydryls in serum.
Besides, a brain magnetic resonance imaging (MRI) scan was performed at month 0, 12 and 24.
Results: Mean age was 34,6 years and male/female ratio was 2:2,5. Average time from onset of the disease was 1,85 years and mean relapse rate was 1,37/year.
Median EDSS was 2,5. After two years of treatment, 3 patients withdrew the study but where included in the analysis. No serious adverse events were recorded. Mean relapse rate became 0,87/year, median EDSS was 2,0 and seric sulfhydryl oxidation decreased 15%. Semiquantitative analysis of lesion load on MRI showed a decreased number of T2-weighted lesions in most patients.
Conclusions: Interferon beta 1a decreased seric markers of oxidative stress in our patients, suggesting a peripheral effect of this molecule on the reactivity of white blood cells.