Intrahepatic expression of HBcAg and delta antigen in anti‐HBe positive HBsAg carriers with acute exacerbation or chronic active liver disease

Intrahepatic expression of HBcAg and hepatitis delta antigen (HDAg) was studied in 43 patients with acute exacerbation AE and 37 with chronic active liver disease CALD, in order to evaluate the role of hepatitis B virus (HBV) replication and hepatitis delta virus (HDV) superinfection in development of AE or CALD in anti‐HBe positive HBsAg carriers in Taiwan, and the results were compared with 37 patients with only minor hepatitic activity. Only 8.1% of patients with minor hepatitic activity were HBcAg positive and none were HDAg positive. In contrast, 41.8% and 32.6% of patients with AE were positive for HBcAg and HDAg, respectively, and the other 25.6% were negative for both. The clinical features of AE showed no difference in relation to HBcAg and HDAg activity in the liver except that patients without HBcAg and HDAg were predominantly older adults. These patients might be supposed to have non‐A, non‐B hepatitis (NANB) virus superinfection, as many reports have shown a predominance of older patients in acute NANB hepatitis. Of the patients with CALD, 40.5% were HBcAg positive, 27.0% were HDAg positive, and 32.5% were positive for neither. Histological features of CALD were identified in 83.3% and 100% of patients with HBcAg and HDAg activity, respectively, but only in 26.1% of those without HBcAg and HDAg. The etiology of CALD in the latter group remains unclear. Furthermore, some of the anti‐delta seropositive patients with AE or CALD expressed HBcAg rather than HDAg in the liver. In conclusion, the majority of AE or CALD instances in anti‐HBe carriers in Taiwan could be attributed to HBV replication or HDV superinfection. Studies of HBcAg and HDAg activity in the liver are thus of great importance in the diagnosis and management of HBsAg/anti‐HBe positive chronic liver disease.