Obata H, Hayashi N, Motoike Y, Hisamitsu T, Okuda H, Kobayashi S, Nishioka K
Institute of Gastroenterology, Tokyo Women's Medical College, 10 Kawada Cho, Ichigaya, Shinjuku Ward, Tokyo, Japan.
Int J Cancer. 1980 Jun 15;25(6):741-7. doi: 10.1002/ijc.2910250609.
We made a prospective study on the development of hepatocellular carcinoma (HCC) in patients with liver cirrhosis with hepatitis B virus infection from April, 1973 to December, 1977. Seven out of 30 patients (23%) with hepatitis B surface antigen (HBsAg)-positive cirrhosis developed HCC. On the other hand, only 5.9% of the patients with HBsAg-negative liver cirrhosis developed HCC. These patients were classified into three groups according to their anti-HB core (anti-HBc) titers. When the anti-HBc titer, expressed as a dilution of serum, was 2(10) or more (Group I), 20-24% of the liver cirrhosis patients developed HCC either with or without a detectable amount of HBs Ag present in the sera. When the anti-HBc titer was 2(9) or less (Group II), only 0-5.7% developed HCC. There was no significant difference between this and the anti-HBc and HBsAg-negative group (Group III), which was 4.4%. In five individual cases from group I, HBsAg was detected in serum, and in biopsies of liver cells, before HCC could be detected by angiography and/or rising levels of alphafetoprotein (AFP). In all of these cases, the anti-HBc titer was higher than 2(10) throughout the observation period, even before the development of HCC. These findings indicate that active virus proliferation in chronic hepatitis B virus infection precedes the development of HCC as indicated by a higher anti-HBc titer. Therefore we have prepared these studies to show the pathogenic role of hepatitis B virus in the development of hepatocellular carcinoma.
我们对1973年4月至1977年12月期间乙型肝炎病毒感染所致肝硬化患者肝细胞癌（HCC）的发生情况进行了前瞻性研究。30例乙型肝炎表面抗原（HBsAg）阳性肝硬化患者中有7例（23%）发生了HCC。另一方面，HBsAg阴性肝硬化患者中只有5.9%发生了HCC。这些患者根据其抗-HB核心（抗-HBc）滴度分为三组。当以血清稀释度表示的抗-HBc滴度为2（10）或更高时（第一组），无论血清中是否可检测到HBsAg，20%-24%的肝硬化患者发生了HCC。当抗-HBc滴度为2（9）或更低时（第二组），只有0%-5.7%的患者发生了HCC。这与抗-HBc和HBsAg阴性组（第三组，发生率为4.4%）之间没有显著差异。在第一组的5例个体病例中，在通过血管造影和/或甲胎蛋白（AFP）水平升高检测到HCC之前，血清和肝细胞活检中检测到了HBsAg。在所有这些病例中，即使在HCC发生之前，整个观察期内抗-HBc滴度均高于2（10）。这些发现表明，慢性乙型肝炎病毒感染中活跃的病毒增殖先于HCC的发生，表现为抗-HBc滴度升高。因此，我们进行了这些研究以显示乙型肝炎病毒在肝细胞癌发生中的致病作用。
