HBsAg loss with HBsAg/anti-HBs seroconversion and non-detectable HCV-RNA in a patient with chronic HBV e-minus/HCV hepatitis treated with two cycles of antiviral therapy

Introduction: Loss of HBsAg is observed in only 3-4% of patients who receive interferon for chronic HBV+HCV hepatitis, and there are few reports of HBsAg loss induced by treatments other than interferon. We report a case of chronic HBV+HCV hepatitis, in which a positive outcome was achieved with a new therapeutic strategy.
Case report: The patient was a 49-year-old Caucasian woman found to be HBsAg+ in 1978 and HCVAb+ in 1997. During 2000-2003, the patient had markedly increased AST/ALT, histology grade 5, stage 1 (Ishak) disease with HBsAg positivity, HBV-DNA 1,450 cp/mL, HCV-RNA 7.57x105 IU/mL (genotype 1b). In May 2003 she began a 48-week course of PEG-IFNa2b (80 mg/week) without ribavirin. The latter drug was not used because it had recently been observed that in some HBV/HCV-coinfected patients treated with the two drugs, the hepatic flares preceding the seroconversion to HBsAb caused fulminant liver failure. Neither the HBV and HCV infections responded to this treatment, but during follow-up the HBV-DNA dropped to 40 cp/mL and the patient presented persistently normal transaminase values (6th month) followed by loss of HBsAg (24th month) and the appearance of anti-HBs (36th month). By December 2008, the HBV negativity and HBsAg/anti-HBs seroconversion were well-established, but HCV replication persisted. The decision was therefore made to administer PEG-IFNa2a (180 mg/week) and ribavirin (1,000 mg/day). There was no evidence of an RVR or EVR, so therapy was continued for 48 weeks. At the scheduled 12-month treatment, the patientwas found to be HCV-RNA negative by TaqMan PCR.
Conclusions: In our opinion this case is of great interest because: 1) it is the first report of a virological response in a HBV/HCV-coinfected CH patient treated with PEG-IFN; 2) control of the two viral infections was achieved with a new therapeutic strategy that included two phases: a) HBV-DNA loss at 6 months and HBsAg/anti-HBs seroconversion between months 24 and 36, after PEG-IFNa2b mono-therapy, which was administered when the HCV replication seemed to prevail over that of HBV; b) ETR for HCV after 72 weeks of PEG-IFNa2a+ribavirin, which was continued in spite of the lack of an EVR, as this does not preclude the possibility of a SVR.