• Norio Akuta, Masahiro Kobayashi, Fumitaka Suzuki, Hitomi Sezaki, Shunichiro Fujiyama, Yusuke Kawamura, Tetsuya Hosaka, Mariko Kobayashi, Satoshi Saitoh, Yoshiyuki Suzuki, Yasuji Arase, Kenji Ikeda, and Hiromitsu Kumada.
• Department of Hepatology, Toranomon Hospital, Tokyo, Japan.
• Oncology. 2016 Jan 1; 91 (6): 341-347.

Background And AimsPredictive factors for hepatocarcinogenesis following eradication of hepatitis C virus (HCV) RNA by antiviral therapy with direct-acting antivirals are unknown. Especially the impact of treatment with or without interferon on hepatocarcinogenesis is not clear.MethodsA total of 958 patients with HCV genotype 1-related chronic liver disease and a sustained virological response defined as negative HCV RNA 24 weeks after cessation of antiviral therapy with direct-acting antivirals (triple therapy of NS3/4A protease inhibitor/peginterferon/ribavirin or all-oral combination therapy with NS3/4A protease inhibitor plus NS5A inhibitor) were included in a retrospective study. None of the patients had hepatocellular carcinoma before and during antiviral therapy.ResultsIn all, 14 patients developed hepatocellular carcinoma during follow-up, and the development rate per 1,000 person-years was 7.35. The cumulative hepatocarcinogenesis rates were 4.2 and 4.2% at the end of 5 and 7 years, respectively. Multivariate analysis identified fibrosis 4 (FIB4) index (≥2.7) and body mass index (≥23.0) as determinants of hepatocarcinogenesis, but they did not identify the treatment regimen. In patients with a FIB4 index ≥2.7, the hepatocarcinogenesis rates with the interferon regimen were not different from those for the regimen without interferon, regardless of gender.ConclusionLiver fibrosis and body mass index, but not treatment regimen, are important predictors of hepatocarcinogenesis following eradication of HCV RNA by direct-acting antivirals.© 2016 S. Karger AG, Basel.

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