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Publication Information
Affiliation
UT Southwestern Medical Center, Dallas, TX, USA.; Graduate School of Public, Health University of Pittsburgh, Pittsburgh, PA, USA.; Toronto Centre for Liver Disease, University of Toronto, Toronto, ON, Canada.; Liver Diseases Branch, NIDDK, NIH, Bethesda, MD, USA.; University of Michigan, Ann Arbor, MI, USA.; University of North Carolina, Chapel Hill, NC, USA.; Division of Gastroenterology, Hepatology, and Nutrition, Virginia Commonwealth University, Richmond, VA, USA.; Toronto Centre for Liver Disease, Toronto General Hospital, University of Toronto, Toronto, ON, Canada.; Graduate School of Public, Health University of Pittsburgh, Pittsburgh, PA, USA.; Johns Hopkins University, Baltimore, MD, USA.; California Pacific Medical Center & Research Institute, San Francisco, CA, USA.; Saint Louis University Liver Center, Saint Louis University, Saint Louis, MO, USA.
Authors
Lee William M., King Wendy C., Janssen Harry L.A., Ghany Marc G., Fontana Robert J., Fried Michael, Sterling Richard K., Feld Jordan J., Wang Junyao, Mogul Douglas B., Cooper Stewart L., Di Bisceglie Adrian M.
Studies
Abstract
Hepatitis B e antigen (HBeAg) is a soluble viral protein in plasma of patients with hepatitis B virus infection. HBeAg loss is an important first stage of viral antigen clearance. We determined the rate and predictors of HBeAg loss in a North American cohort with chronic hepatitis B viral infection (CHB). Among children and adults with CHB and without HIV, HCV or HDV co-infection enrolled in the Hepatitis B Research Network prospective cohort studies, 819 were HBeAg positive at their first assessment (treatment naïve or >24 weeks since treatment). Of these, 577 (200 children, 377 adults) were followed every 24–48 weeks. HBeAg loss was defined as first HBeAg negative value; sustained HBeAg loss was defined as ≥2 consecutive HBeAg negative values ≥24 weeks apart. During a median follow-up of 1.8 years, 164 participants experienced HBeAg loss, a rate of 11.4 (95% CI, 9.8–13.3) per 100 person-years. After adjustment for confounders, HBeAg loss rate was significantly higher in males than females, in older than younger individuals, in Whites or Blacks than Asians, in those with genotype A2 or B versus C, and in those with basal core promoter/precore mutations versus wildtype. Additionally, during follow-up, an ALT flare and a lower quantitative HBsAg, quantitative HBeAg or HBV DNA level predicted higher rates of HBeAg loss. The majority (88%) with HBeAg loss had sustained HBeAg loss. In conclusion, a number of specific demographic, clinical and viral characteristics impacted rate of HBeAg loss and may prove useful in design and interpretation of future therapeutic studies.