Published: 4 December 2020
Author(s): Hye Won Lee, Young Eun Chon, Beom Kyung Kim, Terry Cheuk-Fung Yip, Yee-Kit Tse, Grace Lai-Hung Wong, Vincent Wai-Sun Wong, Henry Lik-Yuen Chan, Sang Hoon Ahn
Section: Original article

Among patients with chronic hepatitis B (CHB), a persistently high serum hepatitis B virus (HBV)-DNA level, a surrogate marker of active HBV replication in hepatocytes, is associated with an increased risk of liver disease progression [1,2]. Accordingly, antiviral therapy using oral nucleos(t)ide analogues (NUCs) has become the mainstay of treatment in CHB patients. However, antiviral therapy is not generally recommended in the so-called immune-tolerant (IT) phase of infection.[3,4] According to the European Association for the Study of Liver Diseases (EASL) guidelines, this phase, referred to as “HBeAg-positive chronic HBV infection”, [5] is characterized by a high serum HBV-DNA level and normal alanine aminotransferase (ALT) level, and positivity for hepatitis B e antigen (HBeAg), with dormant histological activity; therefore, the risk of disease progression is minimal [5,6].


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