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Sherlock等首先报告了肝癌与HBsAg的关系。而后很多国家报导了肝细胞癌(HCC)病人HBsAg的高发生率、其滴度存在差别,e抗体阳性率有增高的倾向。HCC的发生率虽有种族差异,但在HBsAg携带者中发生HCC的危险性是正常人的50倍至350倍,其死亡率相差28.3倍。 有人提出HBsAg和HCC之间的关系可能是互为因果关系的假说,其病程的发展模式为:幼年的HBV感染→HBV携带状态→慢性活动性感染→肝硬变→肝癌。 论证上述假说的根据有:(1)在培养的人肝癌细胞中产生HBsAg;(2)肝癌患者癌细胞染色体组中有HBV的DNA整合;(3)肝癌患者95％以上有乙型肝炎病毒感染;(4)肝癌患者血清中含有
Sherlock et al. first reported the relationship between liver cancer and HBsAg. Then many countries reported that the high incidence of HBsAg in patients with hepatocellular carcinoma (HCC), the difference in their titers, and the e-antibody positive rate tend to increase. Although there is a racial difference in the incidence of HCC, the risk of developing HCC in HBsAg carriers is 50 to 350 times that of normal people, and the mortality rate differs by 28.3 times. It has been suggested that the relationship between HBsAg and HCC may be a hypothesis of mutual causality. The development pattern of the disease course is: juvenile HBV infection → HBV carrier status → chronic active infection → liver cirrhosis → liver cancer. The basis for the above hypothesis is as follows: (1) HBsAg production in cultured human hepatoma cells; (2) HBV DNA integration in cancer cell genomes of liver cancer patients; (3) Hepatitis B virus infection in more than 95% of liver cancer patients (4) serum from patients with liver cancer