Treatment of Exacerbations of Multiple Sclerosis without the Use of Corticosteroids: The Role of Metabolic and Antioxidant Therapy
- 54 Downloads
A multicenter randomized post-registration case-control study was performed with 94 patients with relapsing-remitting and secondary progressive multiple sclerosis (MS) in exacerbation. The patients were divided into two groups: group 1 (n = 53) received Cytoflavin and basal therapy (Trental and group B vitamins), while group 2 (n = 41) received only basal therapy. After five days, treatment results were used to further divide each group into two subgroups: patients of subgroup 1A (n = 22), with clear positive treatment effects, continued to receive Cytoflavin and basal therapy; group 1B (n = 31) additionally received corticosteroid (methipred) pulse therapy; subgroup 2A (n = 14), with significant positive effects, continued to receive basal therapy; group 2B (n = 27) additionally received corticosteroid pulse therapy. The complex treatment, with Cytoflavin, Trental, group B vitamins, and corticosteroids, was found to be safe and well tolerated. The positive effects of including Cytoflavin in complex treatment consisted of a reduction in the need for corticosteroids: 41.5% of patients receiving Cytoflavin no longer needed them, compared with 34% of patients receiving only basal therapy. Patients given Cytoflavin showed more significant regression of neurological symptomatology on the EDSS than the group not given Cytoflavin; there were no patients with no treatment response; lipid peroxidation and anti-myelin basic protein antibody levels decreased; cognitive functions improved.
Keywordsmultiple sclerosis exacerbation Cytoflavin metabolic treatment antioxidant treatment
Unable to display preview. Download preview PDF.
- 1.V. V. Afanasiev and I. Yu. Lukyanova, Features of the Use of Cytoflavin in Current Clinical Practice [in Russian], St. Petersburg (2010).Google Scholar
- 3.E. E. Dubinina, S. O. Burmistrov, D. A. Khodov, and I. S. Porotov, “Oxidative modification of human serum proteins. Assay methods,” Vopr. Med. Khim., 41, No. 1, 24–26 (1995).Google Scholar
- 4.A. L. Kovalenko, M. N. Bizenkova, V. V. Bul’on, et al., “Pathogenetic basis and pharmacotherapeutic efficacy of the use of Cytoflavin in acute cerebral ischemia,” SPbMGA, 3, 79–83 (2006).Google Scholar
- 5.M. M. Odinak, G. N. Gisaga, and I. V. Zarubina, “New approaches to antioxidant therapy in multiple sclerosis,” Zh. Nevrol. Psikhiat., Special issue on Multiple Sclerosis, 72–75 (2002).Google Scholar
- 6.I. D. Stalnaya and T. G. Gorishvili, “A method for estimating malondialdehye with thiobarbituric acid,” in: Current Methods in Biochemistry [in Russian], V. N. Orekhovich (ed.), Meditsina, Moscow (1977), pp. 66–68.Google Scholar
- 9.K. M. Myhr and S. I. Mellgren, “Corticosteroids in the treatment of multiple sclerosis,” Acta Neurol. Scand., Suppl., 73–80 (2009).Google Scholar
- 10.M. Namaka, R. Vandenbosch, R. Gill, et al., “Corticosteroids and multiple sclerosis: to treat or not to treat,” Can. Pharm. J., 138, No. 6, 1–13 (2005).Google Scholar
- 13.A. Scalfari, A. Neuhaus, A. Degenhardt, et al., “The natural history of multiple sclerosis: a geographically based study. 10: relapses and long-term disability,” Brain, 133, No. 7, 1914–1929 (2010).Google Scholar
- 14.C. A. Tyson, K. D. Lunan, and R. I. Stephens, “Age-related differences in G-SH-shuttle enzymes in NO2 or O3 exposed rat lungs,” Arch. Env. Health, 37, No. 3, 167–176 (1982).Google Scholar