Giris ve Amaç: Sitokeratin-18, hepatik ve pankreatit asiner apopitozi-si sirasinda ortaya çikan kaspazlarin bilinen substuratidir. Son zaman-larda yapilan çalismalarda; serum sitokeratin-18 (M30 antijen) düzeyi ile non-alkolik steatohepatit ve kronik hepatit C’nin siddeti ve hepatik fibrozis ile korelasyonu belirtilmistir. Kronik viral hepatit C hastalarin-da, basarili antiviral tedavi ile hepatosellüler apopitozisin anlamli olarak azaldigi, hepatosit apopitozisini göstermede sitokeratin-18’in güvenilir bir markir oldugu gösterilmistir. Bizim amacimiz kronik viral hepatit C’li hastalarda sitokeratin-18 düzeyi ve tedavi yaniti arasindaki korelasyonu belirlemektir. Gereç ve Yöntem: Kronik viral hepatit C tanisi alan 60 hasta çalismaya alindi. Tedavi için uygun hastalara 48 hafta peginterfe-ron-ribavirin tedavisi verildi. Tedavinin 0-12-24. haftalarinda, tedavinin sonunda ve 72. haftada hepatitis C virusu RNA miktari ölçüldü. Ayrica tedavinin 0-24 ve 72. haftasinda sitokeratin-18 düzeyleri ölçüldü. Bul-gular: Altmis hastanin ortalama yasi 52±10.9 yil idi. Hastalarin 31’i (%51,6) kalici viral yanit grubunda iken, 29’u (%48,4) kalici viral yanit elde edilemeyen grupta idi. Kalici viral yanit grubunda 0. haftada sito-keratin-18 düzeyi 243±21 U/L iken, 24. haftada sitokeratin-18 düzeyi 115±12 U/L saptanmis olup 0. hafta ile 24. hafta arasindaki degisim 127±209 U/L bulunmustur (p: 0.014). Kalici viral yanit elde edilemeyen grupta 0. haftada sitokeratin-18 düzeyi 270±14 U/L iken, 24. haftada sitokeratin-18 düzeyi 133±19 U/L saptanmis olup 0. hafta ile 24. hafta arasindaki degisim 136±156 U/L bulunmustur (p>0,5). Kalici viral yanit grubunda, 72. haftada sitokeratin-18 düzeyi 109±38 saptanmis olup 0. hafta ile 72. hafta arasindaki degisim 134±215 bulunmustur (p<0.002).Sonuç: Apopitozisin göstergesi olan sitokeratin-18 ile kronik viral he-patit C hastalarinda kalici viral yanit arasinda korelasyon tespit edildi ve tedavi seyrinde sitokeratin-18 düzeyinde azalma ile kalici viral yanit arasinda iliski bulundugu gösterildi. Bu da sitokeratin-18 düzeylerinde azalmanin kalici viral yaniti ön görmede bir parametre olarak kullanila-bilecegini göstermektedir
Background and Aims: Cytokeratin-18 is the known substrate for caspases, which are encountered during hepatic and pancreatic aci-nar apoptosis. Studies performed in recent years have indicated that the cleavage level of serum cytokeratin-18 (M30 antigen) is correlated with hepatic fibrosis and disease severity in both chronic hepatitis C and non-alcoholic steatohepatitis. It was shown that antiviral therapy in chronic viral hepatitis C patients significantly reduced hepatocellular apoptosis and cytokeratin-18 is accepted as a reliable marker of hepato-cyte apoptosis. Our aim was to determine the correlation between the cytokeratin-18 level and treatment response in patients with chronic viral hepatitis C. Materials and Methods: Sixty patients with chronic viral hepatitis C were included in the study. A 48-week course of pegin-terferon-ribavirin therapy was given to appropriate patients. Hepatitis C virus RNA was measured at 0, 12, and 24 weeks at the end of therapy and 72 weeks. In addition, cytokeratin-18 levels were measured at 0, 24, and 72 weeks. Results: The mean age of 60 patients was 52±10.9 years. While 31 (51.6%) of patients were in the sustained viral response group, 29 (8.4%) of patients were in the non-sustained viral response group. It was determined that while the cytokeratin-18 level at week 0 in the sustained viral response group was 243±21, the cytokeratin-18 level at week 24 was 115±12 U/L and the difference between the level of cytokeratin-18 at weeks 0 and 24 were 127±209 U/L (p: .014). While the cytokeratin-18 level at week 0 in the non- sustained viral response group was 270±14; at week 24, the cytokeratin-18 level was 136±19 U/L and the difference between cytokeratin-18 levels at weeks 0 and 24 was 136±156 U/L (p > .5). At week 72, the cytokeratin-18 level in the sustained viral response group was 109±38 and the difference be-tween weeks 0 and 72 was 134±215 (p < .002). Conclusion: In chronic viral hepatitis C patients, there was a correlation between sustained viral response and cytokeratin-18, which is a marker of apoptosis. During treatment, it was found that there was a relationship between sustained viral response and the decrease in cytokeratin-18 levels. This finding indicates that cytokeratin-18 level monitoring may be used as a predictive marker of sustained viral response.