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Precore and basal core promoter mutations in Asian American patients with hepatitis B e antigen-positive chronic hepatitis B
Precore and basal core promoter mutations in Asian American patients with hepatitis B e antigen-positive chronic hepatitis B ALIMENTARY PHARMACOLOGY & THERAPEUTICS VuTien, P., Trinh, H. N., Nguyen, K., Garcia, R. T., Nguyen, H. A., Levitt, B. S., Nguyen, L., Ha, N. B., Ahmed, A., Daugherty, T., Garcia, G., Nguyen, M. H. 2013; 37 (4): 464-472Abstract
Prior studies have shown that precore mutations abolish and basal core promoter (BCP) mutations down-regulate hepatitis B e antigen (HBeAg) production. Thus, the presence of precore and BCP mutations in HBeAg-positive patients indicates an infection with a mixed viral population of wild-type and precore and/or BCP mutant hepatitis B virus (HBV). To date, there has been limited study of the prevalence and clinical significance of precore and BCP mutations in patients with HBeAg-positive chronic hepatitis B.To determine the prevalence, predictors and clinical characteristics of mixed wild-type and precore/BCP HBV infection, through a cross-sectional study, in a US cohort of patients with chronic hepatitis B.We conducted a retrospective study of 828 chronic hepatitis B patients with HBV genotype and mutation panel testing seen at three US gastroenterology and liver clinics from June 2005 to September 2009.A majority of our patients (92.3%) were either Vietnamese or Chinese American. In the HBeAg-positive cohort, 17% of patients had precore mutations only, 28% had BCP mutations only and 5% had both BCP and precore mutations. On multivariate analyses, HBV genotype C, increasing age, lower HBV DNA level and an ALT quotient >2 were independent predictors for the presence of precore and/or BCP mutations.The current distinction and management recommendations for HBeAg-positive vs. HBeAg-negative patients with chronic hepatitis B should be reassessed. Additional biomarkers and treatment endpoints should be studied for their usefulness in predicting continued viral suppression after treatment discontinuation.
View details for DOI 10.1111/apt.12193
View details for Web of Science ID 000313891900011
View details for PubMedID 23278246