Analysis of the efficacy of treatment with peginterferon alpha-2a and ribavirin in patients coinfected with hepatitis B virus and hepatitis C virus.

OBJECTIVE

To study the virological features of patients coinfected with hepatitis B virus (HBV) and hepatitis C virus (HCV) and the efficacy of combination therapy with peginterferon alpha-2a and ribavirin in these patients.

METHODS

The epidemiological and virological data of 50 patients coinfected with HBV and HCV were analysed. The virological response rates of patients treated with peginterferon alpha-2a and ribavirin between the HBV and HCV coinfection group and the HCV monoinfection group were compared.

RESULTS

HCV-dominant virus strains accounted for 92.0% of the 50 coinfected individuals, and HCV- and HBV-dominant virus strains accounted for the remaining 8.0%. The HBV DNA level of the patients coinfected with HBV and HCV was 4.6+/-0.9 log(10) copies/ml, which was significantly lower than that in the HBV monoinfection group (5.9+/-1.2 log(10) copies/ml) (t=5.964, P<0.01). The HBeAg-positive rate (12.0%, 6/50) of the coinfection group was significantly lower than (45.3%, 19/42) that of the HBV monoinfection group (chi(2)=12.743, P<0.01). The partial early virological response (pEVR) rate and the end-of-treatment virological response (ETVR) rate (50.0%, 15/30; 90.0%, 27/30) of patients with genotype 1 in the coinfection group were significantly higher than those (16.0%, 4/25; 56.0%, 14/25) in the HCV monoinfection group (chi(2)=6.971, P=0.008; chi(2)=8.307, P=0.004). The relapse rate (55.6%, 15/27) of patients with genotype 1 in the coinfection group was significantly higher than that (21.4%, 3/14) in the HCV monoinfection group (chi(2)=4.360, P=0.037). The sustained virological response (SVR) rate (40.0%, 12/30) of patients with genotype 1 in the coinfection group was compared with that of the HCV monoinfection group (44.0%, 11/25) (chi(2)=0.090, P=0.765). There was no significant difference in the on-treatment virological response, ETVR, SVR and relapse rates between two groups for patients with genotype 2. The incidence of side effects (30%, 15/50) of patients in the coinfection group was significantly higher than that (13%, 6/46) in the HCV monoinfection group (chi(2)=4.031, P=0.045). The reactivation rate of HBV DNA (33.3%, 9/27) with HCV SVR was significantly higher than that of patients without SVR (8.7%, 2/23) (chi(2)=4.393, P=0.036).

CONCLUSIONS

The replication of HBV was suppressed, and HCV was the dominant virus strain. Compared with HCV-monoinfected patients, pEVR, ETVR and relapse rates of patients with genotype 1 in the coinfection group were high, while they shared similar SVR rates. HBV and HCV coinfection had no impact on the rate of virological response for genotype 2.