|Title:||Chronic Hepatitis B virus infection||Authors:||Yuen M.-F.
|Issue Date:||2016||Publisher:||Lippincott Williams and Wilkins||Journal Volume:||50||Journal Issue:||4||Start page/Pages:||286-294||Source:||Journal of Clinical Gastroenterology||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. ? 2016 Wolters Kluwer Health, Inc.
|ISSN:||0192-0790||DOI:||10.1097/MCG.0000000000000478||SDG/Keyword:||alanine aminotransferase; circular DNA; entecavir; hepatitis B surface antigen; hepatitis B(e) antigen; HLA DP antigen; host factor; lamivudine; peginterferon alpha; tenofovir disoproxil; virus DNA; antivirus agent; biological marker; hepatitis B surface antigen; alanine aminotransferase blood level; alcohol consumption; antiviral resistance; cancer diagnosis; cancer screening; chronic hepatitis B; cross resistance; family history; groups by age; Hepatitis B virus; human; immunological tolerance; liver cell carcinoma; liver cirrhosis; liver histology; long term care; monotherapy; multicenter study (topic); multidrug resistance; nonhuman; patient monitoring; persistent infection; phase 3 clinical trial (topic); priority journal; Review; risk factor; seroconversion; sex difference; treatment duration; virus load; virus reactivation; virus replication; blood; drug effects; genetics; genotype; Hepatitis B, Chronic; host pathogen interaction; immunology; treatment outcome; Antiviral Agents; Biomarkers; DNA, Viral; Drug Resistance, Viral; Genotype; Hepatitis B Surface Antigens; Hepatitis B virus; Hepatitis B, Chronic; Host-Pathogen Interactions; Humans; Treatment Outcome; Viral Load
|Appears in Collections:||臨床醫學研究所|
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