BACKGROUND: Interferon (IFN) combined with ribavirin (RBV) is an effective therapy for hepatitis C virus (HCV)-infected patients. Those who are coinfected with hepatitis B virus (HBV), however, might suffer from HBV reactivation. The aim of this study was to assess HBV reactivation in HCV-coinfected inactive HBV carriers following IFN/RBV. METHODS: A total of 32 HBV carriers with <or=4 log(10) copies/ml HBV DNA and with chronic hepatitis C were consecutively evaluated; 22 (16 men, median age 52 years and 11 with cirrhosis) received RBV associated to either standard IFN (n=14) or pegylated (PEG)-IFN-alpha2b (n=8) for 24 or 48 weeks, according to HCV genotype. Serum alanine aminotransferase (ALT), HBV DNA (lower limit of quantification 2,000 copies/ml) and HCV RNA (limit of detection 25 IU/ml) were evaluated every 3-6 months during the study period. RESULTS: Nine (41%) patients had a sustained virological response (SVR). In 3 patients (14%; 1 SVR and 2 non-responders) serum HBV DNA increased to >4 log(10) copies/ml (range 5.2-6.5 log(10) copies/ml); however, these patients had no ALT flare either on treatment (n=2) or off treatment (n=1). During follow-up, 8 (36%) treated patients and 4 controls lost serum hepatitis B surface antigen (HBsAg; annual rate 6.5% versus 6.9%; P-value non-significant), whereas 4 and 2 patients seroconverted to antibodies against HBsAg, respectively. Hepatocellular carcinoma developed in 1 patient with SVR and 1 non-responder under nucleoside therapy for HBV, both with cirrhosis. No patient clinically decompensated. CONCLUSIONS: Inactive HBV carriers coinfected with HCV might achieve an SVR following IFN/RBV. Combination therapy carries a low risk of on- and off-treatment HBV reactivation and does not prevent HBsAg seroclearance.
BACKGROUND: Interferon (IFN) combined with ribavirin (RBV) is an effective therapy for hepatitis C virus (HCV)-infectedpatients. Those who are coinfected with hepatitis B virus (HBV), however, might suffer from HBV reactivation. The aim of this study was to assess HBV reactivation in HCV-coinfected inactive HBV carriers following IFN/RBV. METHODS: A total of 32 HBV carriers with <or=4 log(10) copies/ml HBV DNA and with chronic hepatitis C were consecutively evaluated; 22 (16 men, median age 52 years and 11 with cirrhosis) received RBV associated to either standard IFN (n=14) or pegylated (PEG)-IFN-alpha2b (n=8) for 24 or 48 weeks, according to HCV genotype. Serum alanine aminotransferase (ALT), HBV DNA (lower limit of quantification 2,000 copies/ml) and HCV RNA (limit of detection 25 IU/ml) were evaluated every 3-6 months during the study period. RESULTS: Nine (41%) patients had a sustained virological response (SVR). In 3 patients (14%; 1 SVR and 2 non-responders) serum HBV DNA increased to >4 log(10) copies/ml (range 5.2-6.5 log(10) copies/ml); however, these patients had no ALT flare either on treatment (n=2) or off treatment (n=1). During follow-up, 8 (36%) treated patients and 4 controls lost serum hepatitis B surface antigen (HBsAg; annual rate 6.5% versus 6.9%; P-value non-significant), whereas 4 and 2 patients seroconverted to antibodies against HBsAg, respectively. Hepatocellular carcinoma developed in 1 patient with SVR and 1 non-responder under nucleoside therapy for HBV, both with cirrhosis. No patient clinically decompensated. CONCLUSIONS: Inactive HBV carriers coinfected with HCV might achieve an SVR following IFN/RBV. Combination therapy carries a low risk of on- and off-treatment HBV reactivation and does not prevent HBsAg seroclearance.