OBJECTIVE: The influence of hepatitis C virus (HCV) subtypes on hepatocellular carcinogenesis was prospectively investigated. METHODS: A total of 593 patients with HCV-related cirrhosis were recruited and their HCV subtype was determined. RESULTS: The carcinogenesis rates in the patients with HCV group 1 (genotype 1a +1b, n = 442) and group 2 (genotype 2a +2b, n = 136) were 32.0 and 26.6% at the end of the 5th year, 57.4 and 48.1% at the end of the 10th year and 71.8 and 71.0% at the end of the 15th year, respectively (p = 0.10). As to those patients without a history of regular drinking (i.e. less than 200 kg on a pure alcohol basis), the carcinogenesis rates in group 1 (n = 277) and group 2 (n = 90) were 30.8 and 16.3% at the end of the 5th year, 52.8 and 34.4% at the end of the 10th year and 70.6 and 67.1% at the end of the 15th year, respectively (p = 0.025). Although HCV subtype did not influence carcinogenesis in patients with a drinking history of 200 kg or more (p = 0.62), it significantly affected the carcinogenesis rate in patients without a history of regular drinking. Multivariate analysis showed that HCV subtype group 1 significantly increased the carcinogenesis in the group without a history of regular drinking after adjustment for age and gender (hazard ratio = 2.57, p = 0.0085). CONCLUSION: The interaction between HCV subtype and drinking history should be considered in the prediction of carcinogenesis using a multiplicative proportional hazard model. Copyright 2002 S. Karger AG, Basel
OBJECTIVE: The influence of hepatitis C virus (HCV) subtypes on hepatocellular carcinogenesis was prospectively investigated. METHODS: A total of 593 patients with HCV-related cirrhosis were recruited and their HCV subtype was determined. RESULTS: The carcinogenesis rates in the patients with HCV group 1 (genotype 1a +1b, n = 442) and group 2 (genotype 2a +2b, n = 136) were 32.0 and 26.6% at the end of the 5th year, 57.4 and 48.1% at the end of the 10th year and 71.8 and 71.0% at the end of the 15th year, respectively (p = 0.10). As to those patients without a history of regular drinking (i.e. less than 200 kg on a pure alcohol basis), the carcinogenesis rates in group 1 (n = 277) and group 2 (n = 90) were 30.8 and 16.3% at the end of the 5th year, 52.8 and 34.4% at the end of the 10th year and 70.6 and 67.1% at the end of the 15th year, respectively (p = 0.025). Although HCV subtype did not influence carcinogenesis in patients with a drinking history of 200 kg or more (p = 0.62), it significantly affected the carcinogenesis rate in patients without a history of regular drinking. Multivariate analysis showed that HCV subtype group 1 significantly increased the carcinogenesis in the group without a history of regular drinking after adjustment for age and gender (hazard ratio = 2.57, p = 0.0085). CONCLUSION: The interaction between HCV subtype and drinking history should be considered in the prediction of carcinogenesis using a multiplicative proportional hazard model. Copyright 2002 S. Karger AG, Basel