Giris ve amaç: Yakin dönemlerde sigaranin muhtemel hepatotoksisitesi epidemiyolojik ve deneysel olarak gösterilmistir. Çalismamizda kronik hepatit B ve C’de sigara içimi ile fibrozisin muhtemel iliskisini saptamaya çalistik. Gereç ve yöntem: Çalismaya tanilari biyopsi ile dogrulanan, 55 kronik hepatit B, 51 kronik hepatit C’li vaka dahil edildi. Hastalar yas, cinsiyet, sigara ve alkol kullanimi, biyopsilerinde HAI skoru ve fibrozis açisindan degerlendirildi. Bulgular: Kronik hepatit B’li 32 (%58) vaka, C’li 22 (%43) vaka sigara içmekteydi. Sigara kullanan kronik hepatit C’li hastalar içmeyenlere oranla daha yüksek oranda fibrozis (0.042) ve HAI (0.013) skoruna sahiptiler. Ayni durum kronik hepatit B’de saptanmadi (HAI skoru için p:0.456). Ancak fibrozis açisindan anlamsi zlik sinirda idi (p:0.084). Alkol kullanmayan hastalar ayrica degerlendirildiginde ayni durum her iki grup içinde devam etmekteydi (HAI skoru ve fibrozisde; kronik hepatit B için p>0.05, kronik hepatit C için p:0.053 ve p:0.042 sirasiyla). Sonuç: Sigara içimi kronik hepatit C’de karaciger lezyonlarinin ciddiyetini arttirsa da, ayni durum kronik hepatit B’de saptanmamistir.
Background and aims: The possible hepatotoxicity of cigarette smoke has been recently discussed in epidemiological and experimental studies. This study examined the possible relationship between smoking and degree of liver fibrosis in patients with chronic hepatitis B and chronic hepatitis C. Material and methods: The study was performed on a group of 55 patients with chronic hepatitis B and of 51 patients with chronic hepatitis C in whom the diagnosis had been confirmed by liver biopsy. Patients were evaluated according to age, gender, number of cigarettes smoked, alcohol consumption, scores of HAI and fibrosis on the liver biopsy. Results: Thirty-two (58%) chronic hepatitis B and 22 (43%) chronic hepatitis C patients were smokers. In patients with chronic hepatitis C, smokers had high HAI score (0.013) and fibrosis (0.042) on liver biopsy compared with non-smokers. Such results were not found in patients with chronic hepatitis B (for HAI score p: 0.456 and for fibrosis p: 0.084). If patients with no history of alcohol consumption are taken as a separate group, there were similar results in each group (in patients with chronic hepatitis B, p value for both HAI score and fibrosis was >0.05, and in patients with chronic hepatitis C, p value for HAI score and fibrosis was 0.053 and 0.042, respectively). Conclusions: Smoking increases the severity of hepatic lesions in patients with chronic hepatitis C but in not in those with chronic hepatitis B.