Immunogenicity of hepatitis A vaccination in decompensated cirrhotic patients
Article first published online: 30 DEC 2003
Copyright © 2001 American Association for the Study of Liver Diseases
Volume 34, Issue 1, pages 28–31, July 2001
How to Cite
Arguedas, M. R., Johnson, A., Eloubeidi, M. A. and Fallon, M. B. (2001), Immunogenicity of hepatitis A vaccination in decompensated cirrhotic patients. Hepatology, 34: 28–31. doi: 10.1053/jhep.2001.25883
- Issue published online: 30 DEC 2003
- Article first published online: 30 DEC 2003
- Manuscript Accepted: 30 APR 2001
- Manuscript Received: 28 FEB 2001
- Walter B. Frommeyer Jr. Fellowship in Investigative Medicine (1999)
- Department of Medicine, University of Alabama at Birmingham
- AASLD/Schering Advanced Hepatology Fellowship (2000).
Hepatitis A virus (HAV) vaccination is recommended in chronic liver disease because of an increased morbidity and mortality associated with HAV superinfection. However, data regarding the efficacy of HAV vaccination in patients with advanced chronic liver disease is limited. We assessed the efficacy of a standard HAV vaccination schedule in decompensated chronic liver disease in comparison with compensated disease and defined clinical predictors associated with seroconversion. Eighty-four anti-HAV antibody–negative patients, 49 with compensated liver disease, and 35 with decompensated disease were enrolled. Seroconversion was measured by qualitative and quantitative anti-HAV antibody measurements 1 month after each vaccine dose, and univariate/multivariate analysis was performed to define clinical predictors associated with seroconversion. One month after the primary dose, 71.4% of patients with compensated liver disease had detectable anti-HAV antibody compared with 37.1% with decompensated liver disease (P < .05). One month after the booster dose, 98% of compensated patients seroconverted compared with 65.7% with decompensated disease (P < .05). The median serum antibody concentration in compensated liver disease was 76.4 mIU/mL at month 1 and 327.91 mIU/mL at month 7 compared with 20.0 mIU/mL and 102.57 mIU/mL, respectively, in decompensated disease. On multivariate analysis, Child-Pugh class was the only factor predicting response to vaccination. Seroconversion after HAV vaccination was significantly less common in decompensated liver disease and the presence of advanced disease (Child-Pugh class B/C) predicted a lower response rate. These findings indicate that the response to HAV vaccination in chronic liver disease is optimal when targeted to patients before the development of hepatic decompensation.