HBeAg status implicated in liver pathology in chronic hepatitis B
Patients with chronic hepatitis B (CHB) virus infection who are HBeAg-negative are more likely to have advanced liver fibrosis than those with a positive HBeAg status, a study has found.
Researchers reviewed the medical records of 683 treatment-naïve CHB patients who had undergone liver biopsy. They applied the propensity score-matching (PSM) method to adjust the imbalance of baseline confounders between HBeAg-positive (n=345) and HBeAg-negative (n=338) CHB patients, with 123 patients included in each group.
Compared with HBeAg-positive CHB patients, those who were HBeAg-negative showed significantly advanced liver fibrosis (p=0.03). Moreover, the latter had more severe liver inflammation (p=0.037).
In multivariate regression models, significant liver fibrosis was associated with platelets (PLT; odds ratio [OR], 0.994, 95 percent confidence interval [CI], 0.991–0.997; p<0.001), gamma-glutamyl transpeptidase (GGT; OR, 1.007, 95 percent CI, 1.003–1.011; p<0.001) and HBeAg-negative status (OR, 1.887, 95 percent CI, 1.157–3.077; p=0.011).
Meanwhile, predictors of significant liver inflammation were PLT (OR, 0.993, 95 percent CI, 0.990–0.996; p<0.001), GGT (OR, 1.006, 95 percent CI, 1.001–1.011; p<0.017) and HBV DNA (OR, 1.138, 95 percent CI, 1.030–1.257; p=0.011).
While the exact mechanism underlying the association between HBeAg-negative hepatitis and advanced liver fibrosis is unknown, it may involve the core promoter mutation found in HBeAg-negative CHB patients. Its presence may increase hepatitis B virus replication ability, resulting in enhanced viral level in the hepatocyte, therefore causing liver damage by the host immune, the researchers explained. Furthermore, liver fibrogenesis may not be solely caused by hepatitis activity but also other influencing factors. [Cell Immunol 2012;276:35-41; Liver Int 2007;27:1356-1363]