Giris ve amaç: Multipl skleroz daha çok genç adultlarda, MSS beyaz cevherde inflamasyon, demiyelinizasyon ve glial sklerozla karekterize kronik bir hastaliktir. Genetik yatkinlik, otoimmun mekanizmalar ve viral infeksiyonlar demiyelinizasyonda rol oynayabilirler. Hepatit B virusu ve özellikle Hepatit C virusunun Hasimato tiroiditi, Tip II ve Tip III kriyoglobulinemi, membranoproliferatif glomerülonefrit, Sjögren sendromu, diabetes mellitus, idiyopatik pulmoner fibrozis, poliarteritis nodaza v.b otoimmun hastaliklarla birlikteligi bilinmektedir. Gereç ve yönetm: Biz Agustos 2000 - Eylül 2001 tarihleri arasinda hastanemizde Multipl skleroz tanisi ile takip edilen 84 hastada anti Hepatit C virusu anti HBsAg ve HBsAg seropozitifligine baktik. Ölçümlerde üçüncü jenerasyon ELISA kiti kullanildi. Bulgular: Bizim çalismamizda Multipl skleroz’li hastalarda anti Hepatit C virusu, anti HBsAg ve HBsAg pozitifligi kontrol grubu ve de Türkiyedeki genel popülasyona göre daha düsük saptandi ancak istatistiksel olarak fark yoktu (P>0.05). Sonuç: Bizim sonuçlarimiz Multipl skleroz patogenezinde Hepatit C virusu veya Hepatit B virusu’nin rolünü desteklememektedir.
Background and aims: Multiple sclerosis is a chronic disease that most commonly affects young adults and is characterized pathologically by multiple areas of central nervous system white matter inflammation, demyelination and glial sclerosis. The cause of multiple sclerosis is unknown. Genetic susceptibility, autoimmune mechanisms and viral infections may play a pathogenic role in demyelination. Hepatitis B virus and especially Hepatitis C virus has been associated with immunological disorders such as Hashimoto’s thyroiditis, type II and type III cryoglobulinaemia, membranoproliferative glomerulonephritis, Sjögren’s syndrome, diabetes mellitus, idiopathic pulmonary fibrosis and polyarteritis nodosa. Materials and methods: Sera from 84 consecutive patients with a confirmed diagnosis of multiple sclerosis seen at our hospital between August 2000 and September 2001 was tested for anti Hepatitis C virus, anti HBsAg and HBsAg, using third generation enzyme linked immunosorbent assays. Results: The prevalance of anti hepatitis C virus anti HBsAg and HBsAg was no higher patients with multiple sclerosis than in controls or in the general population in Turkey. Conclusions: The findings of the present study do not support a role for hepatitis C virus or hepatitis B infection in the pathogenesis of multiple sclerosis.