Chronic Hepatitis B Virus Infection: Disease Revisit and Management Recommendations
Résumé
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 (\\textgreater30 for males; \\textgreater19 U/L for females) and HBV DNA levels \\textgreater2000 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 \\textgreater6 years can markedly reduce the covalently closed circular DNA, the viral component responsible for initiation of viral replication
Mots clés
adverse effects
Antigens
Antiviral Agents
Biomarkers
blood
Brain
Carcinoma
China
Chronic
complications
diagnosis
Dna
drug effects
Drug Resistance
drug therapy
epidemiology
Family
Female
France
genetics
Genotype
Global Health
Hepatitis
Hepatitis B
Hepatitis B Surface Antigens
Hepatitis B virus
history
Host-Pathogen Interactions
Humans
Immune Tolerance
immunology
Infection
Laboratories
London
Male
Medicine
Mutation
Patients
Risk
Tenofovir
therapeutic use
Treatment Outcome
Viral
Viral Load