Hsu H C, Lin W S, Tsai M J
Cancer. 1983 Nov 15;52(10):1825-32. doi: 10.1002/1097-0142(19831115)52:10<1825::aid-cncr2820521011>3.0.co;2-m.
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.
采用间接免疫过氧化物酶技术，通过检测1970年至1979年间获取的284例肝癌活检和手术标本石蜡切片上的组织乙肝表面抗原（HBsAg），从免疫病理学角度评估了乙肝病毒（HBV）感染与肝细胞癌（HCC）之间的关系，无论有无肝硬化。在190例有非肿瘤性肝组织可供组织学和病因学分析的病例中，针吸活检组肝硬化的发生率为69.8%（53例中的37例），楔形切除组为67.4%（46例中的31例），切除或肝叶切除组为30.8%（91例中的28例）。整个系列中非肿瘤性肝实质中检测到HBsAg的比例为85.7%，肝硬化病例中为90.6%（楔形切除组为96.8%，切除病例组为100%）。切除组非肝硬化病例中HBsAg阳性率为84.1%（63例中的53例），而该组10例阴性病例均为非肝硬化病例。这清楚地表明，台湾地区肝硬化和非肝硬化患者中HBsAg与HCC之间存在密切关联，尤其是在肝硬化组，楔形切除和切除系列中HBsAg的高流行率证明了这一点。另一方面，HBsAg阴性且非肝硬化组的病因，该组男性优势也不太明显（男:女 = 3.3:1，而其他组为6 − 19.5:1），且肝细胞发育异常明显少于HBsAg阳性或肝硬化组，仍有待解释。在223例肿瘤组织满足最低分析要求的病例中，27例（12.1%）肿瘤细胞中检测到HBsAg（切除组为15%）。这项研究表明HBV在肝细胞癌发生中具有重要的病因学作用，并且在台湾地区HCC的发生并不依赖于肝硬化的共存。
