Antiviral therapy leads to histological improvement in HBeAg-negative chronic hepatitis B patients.

We read with great interest the study by Papachrysos et al showing that antiviral therapy leads to histological improvement in HBeAg-negative chronic hepatitis B patients [1]. We agree with the authors that long-term antiviral treatment with nucleos(t)ide analogs suppresses hepatitis B virus (HBV) replication, delays disease progression and contributes to resolution of fibrosis [2,3].

In patients with chronic hepatitis B, persistent viral replication is associated with progression of liver disease and treatment is aimed at maximal viral suppression. A number of potential baseline predictors have been suggested to have an impact on the antiviral treatment outcome: demographic (patient age, gender, body weight, duration of infection, alcohol, and/or drug abuse); histological (grading of necroinflammatory activity, staging of liver fibrosis, presence of liver steatosis); virologic (baseline HBV DNA levels, HBeAg status, HBV genotype, genetic polymorphisms); and biochemical parameters (baseline aminotransferase levels) [4]. The authors showed that hepatic activity index and fibrosis score have significantly declined during the course of treatment. However, information is not clearly available concerning the effect of age, gender, HBV DNA level, genetic subtype, and duration of infection on the histological response to antiviral therapy. Future studies are warranted to determine the predictors associated with the efficacy of antiviral treatment on the histological improvement.