title: Chronic Hepatitis B Virus Infection: Disease Revisit and Management Recommendations.
abstract: Chronic hepatitis B virus (HBV) infection evolves from immune-tolerance phase, through immune clearance phase to a quiescent phase or reactivation as hepatitis B e antigen-negative hepatitis. Persistent infection may result in the development of cirrhosis and hepatocellular carcinoma (HCC). Host factors including gender, age, family history, HLA-DP, and viral factors including HBV DNA, genotypes, precore mutations, pre-S deletions, and hepatitis B surface antigen (HBsAg) level are associated with the development of these complications. Risk scores for the development of HCC have been derived. Patients with persistently elevated alanine aminotransferase levels (>30 for males; >19 U/L for females) and HBV DNA levels >2000 IU/mL should be treated. Patients with established cirrhosis with detectable HBV DNA should also be treated. The recommended first-line agents include pegylated interferon and 2 nucleos(t)ide analogs, entecavir and tenofovir. NAs require long-term treatment to maintain suppression of HBV DNA. They have been shown to decrease hepatic fibrosis, or reverse cirrhosis and to reduce the development of HCC. They have very low rates (0% to 1.2%) of resistance. HBsAg seroclearance, although the ideal endpoint, is only achievable in 10% to 12% of patients by multicenter trials usually studying relatively young patients. Patients on long-term treatment should be monitored for viral breakthrough that may be due to noncompliance or the development of resistance. Newer agents are under trials to enhance the rate of HBsAg seroclearance. However, even with the current NAs, long-term treatment of >6 years can markedly reduce the covalently closed circular DNA, the viral component responsible for initiation of viral replication.
authors: *Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road, Hong Kong†Department of Internal Medicine, Yonsei University College of Medicine, Brain Korea 21 Project for Medical Science, Seoul, South Korea‡Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan§Royal Free and University College, School of Medicine, London, UK∥Hepatology Unit and Key Laboratory for Organ Failure Research, Nanfang Hospital, Southern Medical University, Guangzhou, China¶Southwestern Medical Center, University of Texas, Dallas, TX#The Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Ichikawa, Japan**INSERM Unité 1052, Cancer Research Center of Lyon, Lyon University, Lyon, France.
authors: Man-Fung
authors: MF
authors: Yuen
authors: Sang Hoon
authors: SH
authors: Ahn
authors: Ding-Shinn
authors: DS
authors: Chen
authors: Pei-Jer
authors: PJ
authors: Chen
authors: Geoffrey M
authors: GM
authors: Dusheiko
authors: Jin-Lin
authors: JL
authors: Hou
authors: Willis C
authors: WC
authors: Maddrey
authors: Masashi
authors: M
authors: Mizokami
authors: Wai-Kay
authors: WK
authors: Seto
authors: Fabien
authors: F
authors: Zoulim
authors: Ching-Lung
authors: CL
authors: Lai
mesh_terms: D000998:Antiviral Agents / Q000009:adverse effects / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D004279:DNA, Viral / Q000097:blood; D024882:Drug Resistance, Viral; D005838:Genotype; D006514:Hepatitis B Surface Antigens / Q000097:blood; D006515:Hepatitis B virus / Q000187:drug effects* / Q000235:genetics / Q000276:immunology; D019694:Hepatitis B, Chronic / Q000175:diagnosis / Q000188:drug therapy* / Q000453:epidemiology; D054884:Host-Pathogen Interactions; D006801:Humans; D016896:Treatment Outcome; D019562:Viral Load
chemical_list: D000998:Antiviral Agents; D015415:Biomarkers; D004279:DNA, Viral; D006514:Hepatitis B Surface Antigens