Hepatitis-B surface antigen and hepatocellular carcinoma in Taiwan. With special reference to types and localization of HBsAg in the tumor cells.

The relationship between hepatitis B virus (HBV) infection and hepatocellular carcinoma (HCC), with or without cirrhosis, was assessed immunopathologically through the detection of tissue hepatitis B surface antigen (HBsAg) on paraffin sections of 284 biopsy and surgical specimens of HCC, which were performed from 1970 to 1979, by the indirect immunoperoxidase technique. In 190 cases with nontumorous liver tissue available for histologic and etiologic analyses, cirrhosis was identified in 69.8% (37 of 53) in needle biopsy, 67.4% (31/46) in wedge, and 30.8% (28/91) in the resection or lobectomy group. HBsAg was detected in the nontumorous liver parenchyma in 85.7% in the whole series, and 90.6% in the cirrhotic cases (96.8% in wedge and 100% in resection cases). The HBsAg positivity in the noncirrhotic cases of the resection group was 84.1% (53/63), whereas the 10 negative cases in this group were all noncirrhotic. This clearly demonstrates a strong association of HBsAg and HCC in both cirrhotic and noncirrhotic patients in Taiwan, particularly in the cirrhotic group, as evidenced by the high prevalence of HBsAg in wedge and resection series. On the other hand, the etiology in the HBsAg-negative and noncirrhotic group, which also had a less evident male predominance (male:female = 3.3:1 versus 6-19.5:1) and significantly less liver cell dysplasia than HBsAg-positive or cirrhotic groups, remains to be explained. In 223 cases where tumor tissue met the minimal requirement for analysis, HBsAg was demonstrated in 27 cases (12.1%) in the tumor cells (15% in the resection group). This investigation indicates an important etiologic role of HBV in hepatocellular carcinogenesis, and the development of HCC does not depend on the coexistence of cirrhosis in Taiwan.