Acute exacerbations in Chinese patients with chronic hepatitis B virus (HBV) infection. Incidence, predisposing factors and etiology

Abstract

Three hundred and eighty-six Chinese patients (262 men and 124 women), age 5-74 years, with chronic hepatitis B virus (HBV) infection were prospectively followed for 1-5 years to determine the incidence, predisposing factors and etiology of acute exacerbations that occurred during the course of chronic HBV infection. Group I consisted of 334 patients with serum alanine aminotransferase (ALT) levels below 200 IU/l at presentation. Of these, 29 (8.7%) patients developed 32 episodes of acute exacerbation during follow-up., The cumulative probabilities of developing exacerbations were 6.3% and 15% at the end of 1 and 4 years, respectively. Group II included 52 patients with ALT levels above 200 IU/l at presentation. Of these, 19 (37%) patients developed 26 episodes of exacerbation during follow-up. The cumulative probabilities of developing exacerbations were 24% and 47% at the end of 1 and 4 years, respectively. In both groups, the probability of developing exacerbations was slightly higher in men and significantly higher in those above the age of 20 and those who were HBeAg positive. Logistic regression analysis showed that HBeAg positivity (p < 0.00001), elevated ALT levels (> 200 IU/l) at presentation (p < 0.0001) and male sex (p = 0.03) were associated with a significantly higher probability of developing exacerbations. Twenty eight (48%) episodes of exacerbation were accompanied by symptoms of acute hepatitis. Thirty-three (57%) episodes of exacerbation were associated with inactivation and seven (12%) episodes with reactivation of HBV replication, one (2%) episode was due to superimposed acute hepatitis A, two episodes may be secondary to post-transfusion non-A, non-B hepatitis. None of the exacerbations was related to superinfection with hepatitis D virus. An understanding of the factors that trigger these exacerbations will help to delineate the mechanism(s) of immune clearance of HBV and the pathogenesis of HBV-induced liver diseases.