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Published on: February 19, 2019
Seroepidemiology of hepatitis A in patients with chronic liver disease
1Division of Digestive Diseases, Department of Medicine, University of California Los Angeles, Los Angeles, CA, USA. ssaab@mednet.ucla.edu
Hepatitis A virus (HAV) rarely causes fulminant hepatic failure in the general population. Yet it is a cause of significant morbidity and mortality in patients with chronic liver disease (CLD), in whom routine HAV vaccination is recommended. However, studies of HAV seroprevalence and exposure predictors in populations with CLD are scarce. We have studied a cohort of 473 patients with various causes of CLD between July 2000 and June 2002. Patients were stratified on the basis of age, gender, ethnicity and aetiology of liver disease. The HAV seroprevalence in patients with CLD was compared with that in the general population. We used a logistic regression analysis to identify independent predictors of HAV exposure. Of the 473 patients studied, HAV seroprevalence was available for 454 individuals. HCV, HBV, alcohol, and HCV and alcohol were the causes of CLD in 337, 72, 37 and eight patients, respectively. The overall HAV seroprevalence was 55% in the studied cohort. The age-stratified HAV prevalence for ages 21-30, 31-40, 41-50, 51-60, 61-70 and greater than 70 years was 44, 51, 44, 63, 65 and 64%, respectively. Hispanic ethnicity, Asian ethnicity, alcohol use and ages of 51-70 years were found to be independent predictive variables of prior exposure to HAV. HAV infection in patients with CLD causes considerable morbidity and mortality. We demonstrated that age-stratified seroprevalence of HAV in patients with CLD of various aetiologies is significantly higher than that of the general population, and identified several independent predictors of HAV prior exposure.
Hepatitis A virus (HAV) rarely causes fulminant hepatic failure in the general population. Yet it is a cause of significant morbidity and mortality in patients with chronic liver disease (CLD), in whom routine HAV vaccination is recommended. However, studies of HAV seroprevalence and exposure predictors in populations with CLD are scarce. We have studied a cohort of 473 patients with various causes of CLD between July 2000 and June 2002. Patients were stratified on the basis of age, gender, ethnicity and aetiology of liver disease. The HAV seroprevalence in patients with CLD was compared with that in the general population. We used a logistic regression analysis to identify independent predictors of HAV exposure. Of the 473 patients studied, HAV seroprevalence was available for 454 individuals. HCV, HBV, alcohol, and HCV and alcohol were the causes of CLD in 337, 72, 37 and eight patients, respectively. The overall HAV seroprevalence was 55% in the studied cohort. The age-stratified HAV prevalence for ages 21-30, 31-40, 41-50, 51-60, 61-70 and greater than 70 years was 44, 51, 44, 63, 65 and 64%, respectively. Hispanic ethnicity, Asian ethnicity, alcohol use and ages of 51-70 years were found to be independent predictive variables of prior exposure to HAV. HAV infection in patients with CLD causes considerable morbidity and mortality. We demonstrated that age-stratified seroprevalence of HAV in patients with CLD of various aetiologies is significantly higher than that of the general population, and identified several independent predictors of HAV prior exposure.
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