Abstract
Chronic hepatitis B (CHB) treatment is limited by the availability of antiviral agents and the variable response to those agents. Currently, the only approved antiviral agents are Pegylated interferon and nucleos(t)ide analogues. The response to these therapies varies widely between CHB patients. Thus, the patients with non favorable response are ultimately exposed to unnecessary side effects and costs. All current guidelines provide information regarding the time to initiate therapy. However, a clear consensus regarding the predictors of non response and consequently terminating the treatment is still lacking. Many studies that determine the adequacy of the use of predictive markers early in the course of the disease will be reviewed here. During Pegylated interferon therapy, combination of decline in serum HBV DNA and HbsAg levels from baseline at week 12 could generate a solid stopping rule. Using nucleos(t)ide analogues in chronic HbeAg positive patients, the on-treatment HbsAg quantitation at 6 months appears to have a useful role in determining the duration of therapy in patients who achieve HbeAg loss (or seroconversion) during treatment. In chronic HbeAg negative patients, the Asia pacific association for the study of liver (APASL) stopping rules are adequate with proper off-therapy monitoring. Furthermore, the durability of off-therapy response for both classes based on long term follow up studies will be discussed here. Through this review we will present a clear generation of stopping rules to guide the antiviral therapy early enough to predict non-response and shift to other agents. Therefore, adopting a cost effective approach in the treatment of chronic hepatitis B.
Highlights
Hepatitis B virus (HBV) infection is a major and global health problem
This study revealed that the amount of HBV surface antigen (HBsAg) decline from pretreatment to week 48 was approximately 30 times higher with peg interferon alfa-2a versus lamivudine alone
In peg interferon alfa-2a ± lamivudine-treated patients, Marcellin et al compared the decline in HBsAg level in virological responders (HBV DNA ≤2, 000 IU/ml at the end of treatment and 5 years post-treatment) with that in relapsers and in non-responders (HBV DNA >2,000 IU/ml at the end of treatment and 5 years post treatment) using 10% log10 decline from baseline as a cut-off at weeks 12 and 24
Summary
Hepatitis B virus (HBV) infection is a major and global health problem. Approximately one third of the world’s population has serological evidence of past or present infection with HBV and 350-400 million people are chronic HBV surface antigen (HBsAg) carriers [1, 2]. In peg interferon alfa-2a ± lamivudine-treated patients, Marcellin et al compared the decline in HBsAg level in virological responders (HBV DNA ≤2, 000 IU/ml at the end of treatment and 5 years post-treatment) with that in relapsers (response at end treatment that was not sustained until year 5) and in non-responders (HBV DNA >2,000 IU/ml at the end of treatment and 5 years post treatment) using 10% log10 decline from baseline as a cut-off at weeks 12 and 24.
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