Chronic hepatitis B (CHB) remains a difficult-to-treat disease because no current treatments provide an optimal virological and immunological control, there is a high rate of relapse following any antiviral therapy, and there are no identified clinical useful treatment stopping rules, especially in hepatitis B e antigen (HBeAg)-negative patients treated with nucleoside or nucleotide analogues (NUCs). Taking into account the limited options of antiviral drugs, the response-guided therapy seems to be the best approach for optimization of treatment response. Hepatitis B surface antigen (HBsAg) can be considered a surrogate marker of HBV immune control during antiviral therapy, regardless of virological response reflected by serum HBV DNA. Thus, the decrease of HBV DNA level represents a reduction of viral replication, while serum HBsAg decline signifies a reduction of messenger RNA translation. The most important on-treatment predictors of the antiviral treatment response, especially Peg-IFN α-2a, are the quantitative HBsAg and HBV DNA evolution during therapy. A combination of no HBsAg decline and <2 log10 IU/mL decrease of HBV DNA seems to be a predictor of nonresponse in European HBeAg-negative patients with genotype D. The reduction of HBsAg levels during NUCs treatment in HBeAg-positive patients may identify cases with subsequent HBeAg or HBsAg loss.
Part of the book: Advances in Treatment of Hepatitis C and B