Occult hepatitis B virus infection as a risk factor for hepatocellular carcinoma in patients with chronic hepatitis C in whom viral eradication fails
Article first published online: 2 JAN 2008
© 2007 The Japan Society of Hepatology
Volume 38, Issue 6, pages 546–556, June 2008
How to Cite
Miura, Y., Shibuya, A., Adachi, S., Takeuchi, A., Tsuchihashi, T., Nakazawa, T. and Saigenji, K. (2008), Occult hepatitis B virus infection as a risk factor for hepatocellular carcinoma in patients with chronic hepatitis C in whom viral eradication fails. Hepatology Research, 38: 546–556. doi: 10.1111/j.1872-034X.2007.00316.x
- Issue published online: 29 APR 2008
- Article first published online: 2 JAN 2008
- Received 19 July 2007; revision 6 November 2007; accepted 12 November 2007.
- chronic hepatitis C;
- hepatocellular carcinoma;
- interferon therapy;
- multivariate analysis;
- occult HBV infection;
- risk factor
Aim: Recent studies have suggested that an occult hepatitis B virus (HBV) infection negative for HBsAg but positive for HBV-DNA contributes to hepatocellular carcinoma (HCC) development in patients with chronic hepatitis C. Some follow-up studies have suggested the clinical importance of occult HBV infections in HCC development even after interferon (IFN) therapy, but a recent study denies the significance of the impact of occult HBV infection. Focusing on HCC development in patients in whom hepatitis C virus (HCV) eradication by interferon (IFN) therapy had failed, we conducted this study in order to assess the impact of occult HBV infections on HCC development in these patients.
Methods: We enrolled 141 patients with chronic hepatitis C (histological stage F2 or F3) who were seropositive for HCV-RNA even after IFN therapy. Serum HBV-DNA was assayed using the real-time polymerase chain reaction. During follow-up, ultrasonography and/or computed tomography (CT) were performed at least every 6 months to monitor HCC development.
Results: The cumulative incidence rates of HCC were 8.9%, 25.7% and 53.7% at 5 years, 10 years and 15 years, respectively, after IFN therapy. Multivariate analysis indicated that low platelet counts (<12 × 104/mm3), occult HBV infection, high ALT levels (≥80 IU/L) after IFN therapy and the staging of liver fibrosis were important independent factors affecting the appearance of HCC.
Conclusions: Occult HBV was a risk factor for HCC development in patients with chronic hepatitis C in whom HCV eradication had failed. Therefore, patients with chronic hepatitis C with occult HBV should be monitored carefully for HCC after IFN therapy.