Treatment Response and Long-Term Outcome of Peginterferon α and Ribavirin Therapy in Korean Patients with Chronic Hepatitis C

Abstract

Background/aims: Peginterferon plus ribavirin remains a standard therapy for patients with chronic hepatitis C (CHC) in Korea. We investigated the efficacy and long-term outcome of peginterferon and ribavirin therapy in Korean patients with CHC, particularly in relation to the stage of liver fibrosis.

Methods: The incidence of sustained virological response (SVR), hepatic decompensation, hepatocellular carcinoma, and liver-related death was analyzed in 304 patients with CHC; the patients were followed up for a median of 54 months.

Results: Among patients with HCV genotype 1, the SVR rate was 36.7% (18/49) and 67% (69/103) for patients with and without cirrhosis, respectively (p<0.001). For patients with non-1 HCV genotypes, the SVR rates were 86.0% (37/43) in cirrhotic patients and 86.2% (94/109) in noncirrhotic patients. SVR significantly reduced the risk of liverrelated death, hepatic decompensation, and hepatocellular carcinoma, which had hazard ratios of 0.27, 0.16, and 0.22, respectively (all p<0.05). However, despite the SVR rate, patients with advanced fibrosis were still at risk of developing liver-related complications.

Conclusions: A relatively high SVR rate was achieved by peginterferon plus ribavirin therapy in Korean patients with CHC, which improved their long-term outcomes. However, all CHC patients with advanced hepatic fibrosis should receive close follow-up observations, even after successful antiviral treatment.

Keywords: Hepatitis C; Hepatitis C virus clinical trials; Hepatitis C virus treatment; Viral hepatitis; clinical.

Fig. 1

Sustained virological response (SVR) rates according to the genotype of hepatitis C virus (HCV), stage of hepatic fibrosis, presence of portal hypertension, genotype of IL-28B, and type of peginterferon. (A) For patients with HCV genotype 1, the SVR rate was significantly lower in patients with cirrhosis than in patients with bridging or less advanced fibrosis. (B) The presence of clinically relevant portal hypertension (CRPH) was not significantly associated with the SVR rate in patients with cirrhosis. (C) For patients with HCV genotype 1, the SVR rate was significantly higher in patients with the CC genotype of interleukin-28B (IL-28B) rs12979860 than in those with the TC/TT genotype. (D) In noncirrhotic patients with the HCV genotype 1, peginterferon α-2a resulted in a significantly higher SVR rate than peginterferon α-2b. However, the SVR rates in patients with non-HCV genotype 1 did not differ according to the stage of hepatic fibrosis, presence of portal hypertension, genotype of IL-28B, or type of peginterferon.

Fig. 2

Kaplan-Meier curves showing the occurrence of clinical events according to the hepatic fibrosis stage and sustained virological response (SVR). (A) The cumulative incidence rates of liver-related deaths tended to differ between the F3 group and F4 group with SVR (p=0.069) but did not differ significantly between the F4 groups with and without SVR. (B) The cumulative incidence rates of liver-related deaths did not differ between the F3 group and the well-compensated F4 group with SVR but did differ significantly between the well-compensated F4 groups with and without SVR. (C) Among patients without hepatic decompensation at baseline, the cumulative incidence rates of hepatic decompensation consistently increased with progression of fibrosis and lack of SVR (p=0.027 between the F0–2 and F3 groups, p=0.020 between the F3 group and the F4 group with SVR, p=0.008 between the F4 groups with and without SVR). (D) The cumulative incidence rates of hepatocellular carcinoma significantly increased with fibrosis progression and lack of SVR (p<0.001 between the F0–2 and F3 groups, p=0.048 between the F4 groups with and without SVR by log-rank test).