Are Hepatitis B e Antigen (HBeAg)–Positive Chronic Hepatitis B and HBeAg-Negative Chronic Hepatitis B Distinct Diseases?

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The current algorithm for the treatment of chronic hepatitis B is primarily dependent on 3 factors: (1) hepatitis B virus (HBV) DNA levels, (2) alanine aminotransferase levels, and (3) hepatitis B e antigen (HBeAg) status [1, 2]. The presence of HBeAg is pivotal for deciding whether to start and when to stop antiviral therapy. For HBeAg-positive chronic hepatitis B, current guidelines recommend treatment if the serum HBV DNA level is >20,000 IU/mL and the alanine aminotransferase level is elevated or if there is significant liver disease found by examination of a liver biopsy specimen. Treatment with oral antiviral medication is continued until HBeAg seroconversion has been achieved. This occurs when serum HBeAg becomes undetectable and antibody to HBeAg is detected. After HBeAg seroconversion is achieved, antiviral therapy is most often continued for another 6–12 months (i.e., consolidation therapy) and then stopped. With consolidation therapy after HBeAg seroconversion, most patients have sustained viral suppression while not receiving medication; however, relapse, with reappearance of serum HBV DNA and detection of HBeAg, occurs in a significant proportion of patients (20%–30%) [3–6].