Diabetes enhances hepatocarcinogenesis in noncirrhotic, interferon-treated hepatitis C patients |
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Authors: | Kawamura Yusuke Arase Yasuji Ikeda Kenji Hirakawa Miharu Hosaka Tetsuya Kobayashi Masahiro Saitoh Satoshi Yatsuji Hiromi Sezaki Hitomi Akuta Norio Suzuki Fumitaka Suzuki Yoshiyuki Kumada Hiromitsu |
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Affiliation: | Department of Hepatology, Toranomon Hospital, Tokyo, Japan |
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Abstract: | BackgroundThis retrospective cohort study assessed the impact of diabetes mellitus on hepatocarcinogenesis and determined the predictors of hepatocarcinogenesis in noncirrhotic, interferon-treated patients with hepatitis C virus infection.MethodsA total of 2058 hepatitis C virus-positive, noncirrhotic patients treated with interferon were enrolled. The median follow-up period was 6.7 years. The primary end point was the onset of hepatocellular carcinoma. The cumulative rate of new hepatocellular carcinoma cases was computed by the Kaplan-Meier method and Cox proportional hazard analysis according to diabetic state and response to interferon therapy.ResultsThe cumulative rates of hepatocellular carcinoma in diabetic patients (3.2% at 4 years, 8.5% at 8 years, and 24.4% at 12 years) were significantly higher than those of nondiabetic patients (1.3% at 4 years, 2.2% at 8 years, and 5.6% at 12 years, P <.001). In patients with a sustained virologic response, diabetes had no significant effect on the rate of hepatocarcinogenesis. In contrast, the rate in patients with a nonsustained virologic response was significantly higher in diabetic than in nondiabetic patients. Multivariate analysis identified lack of sustained virologic response (hazard ratio [HR] 7.28; 95% confidence interval [CI], 3.28-16.15; P <.001) and diabetes as independent risk factors for hepatocarcinogenesis (HR 2.00; 95% CI, 1.05-3.84; P = .036).ConclusionsOur results highlight the enhancing effect of diabetes mellitus on hepatocarcinogenesis in noncirrhotic, interferon-treated patients with hepatitis C virus. The sustained virologic response induced by interferon therapy eliminates the influence of diabetes and markedly reduces the rate of hepatocarcinogenesis in such patients. |
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Keywords: | Diabetes Hepatocellular carcinoma Interferon Sustained virologic response |
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