Department of Internal Medicine, National Taiwan University College of Medicine and Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan.
Hepatol Res. 2007 Sep;37 Suppl 2:S101-5. doi: 10.1111/j.1872-034X.2007.00170.x.
Hepatocellular carcinoma (HCC) is common in Taiwan. The age-adjusted incidence rates have been increasing, from approxiimately 15/100 000 in the 1980s to approximately 30/100 000 recently. The main causes are chronic hepatitis B and C infections, with >90% of patients positive for hepatitis B surface antigen (HBsAg) or antibody to hepatitis C virus (anti-HCV). Before 1990, approximately 80% of patients with HCC were positive for HBsAg. The infection is mainly from perinatal mother-to-infant transmission. HCV is the second important cause, accounting for approximately 70% of HBsAg negative patients. Overall, 5-10% patients have infections of both viruses. In HBsAg negative-anti-HCV negative patients, polymerase chain reaction assay still reveals the key role of HBV. Epidemiologic studies also reveal the important role of HBV. In a nested case-control study, cumulative incidence of HCC was 10% after nine years of follow-up in hepatitis B e-antigen (HBeAg) positive carriers, with a relative risk of 60.2 compared to 9.6 in HBeAg negative carriers. The role of high viral load was confirmed when another community-based prospective study of 3644 HBsAg carriers stratified by serum hepatitis B virus (HBV) DNA levels correlated well with the occurrence of HCC, especially in carriers with levels >10(5) copies/mL. Genotype C infection contributed more to hepatocarcinogenesis than genotype B. Although HBV is dominant in causing HCC, in the last two decades the relative importance of HCV has changed. The proportion of anti-HCV positive cases has increased. In some areas of southern Taiwan where HCV infection is rampant, HCV-associated HCC have surpassed HBV-associated cases. To control hepatitis B, a mass neonatal vaccination program against hepatitis B was launched in 1984. The HBsAg carrier rate decreased from the historical 15-20% to < 1% after vaccination. Most importantly, annual incidence of childhood HCC has decreased from 0.67 to 0.19/100 000 children. To control hepatitis C, besides interrupting the transmission routes and screening blood donors with anti-HCV, treatment with interferon and ribavirin was implemented on a national basis in 2003. Through these efforts, virally-induced HCC will be controlled in 20-30 years, and a decrease of approximately 85% is anticipated by 2040. Then, HCC will not be commonly seen in Taiwanese people, and the major cause of HCC will be non-viral factors that lead to cirrhosis, such as non-alcoholic steatohepatitis.
在台湾,肝细胞癌(HCC)较为常见。经年龄调整后的发病率一直在上升,从 20 世纪 80 年代的约 15/100000 上升至最近的约 30/100000。主要病因是慢性乙型肝炎和丙型肝炎感染,>90%的患者乙型肝炎表面抗原(HBsAg)或丙型肝炎病毒抗体(抗-HCV)阳性。1990 年前,约 80%的 HCC 患者 HBsAg 阳性。感染主要来自围产期母婴传播。HCV 是第二大重要病因,约占 HBsAg 阴性患者的 70%。总体而言,5-10%的患者同时感染两种病毒。在 HBsAg 阴性-抗-HCV 阴性患者中,聚合酶链反应检测仍显示 HBV 起关键作用。流行病学研究也揭示了 HBV 的重要作用。在一项巢式病例对照研究中,乙型肝炎 e 抗原(HBeAg)阳性携带者在 9 年的随访后 HCC 的累积发病率为 10%,相对风险为 60.2,而 HBeAg 阴性携带者的相对风险为 9.6。当对 3644 名 HBsAg 携带者进行基于血清乙型肝炎病毒(HBV)DNA 水平的社区前瞻性研究分层时,高病毒载量的作用得到了证实,该研究与 HCC 的发生密切相关,尤其是在病毒载量>10(5)拷贝/mL 的携带者中。C 基因型感染比 B 基因型更易导致肝癌发生。尽管 HBV 是导致 HCC 的主要因素,但在过去的二十年中,HCV 的相对重要性发生了变化。抗-HCV 阳性病例的比例有所增加。在台湾南部一些 HCV 感染猖獗的地区,HCV 相关性 HCC 已超过 HBV 相关性 HCC。为了控制乙型肝炎,1984 年启动了一项大规模新生儿乙型肝炎疫苗接种计划。HBsAg 携带率从历史上的 15-20%下降至接种后的<1%。最重要的是,儿童 HCC 的年发病率已从 0.67 降至 0.19/100000 儿童。为了控制丙型肝炎,除了阻断传播途径和筛查抗-HCV 献血者外,2003 年在全国范围内实施了干扰素和利巴韦林治疗。通过这些努力,病毒引起的 HCC 将在 20-30 年内得到控制,预计到 2040 年将减少约 85%。届时,台湾人将不再常见 HCC,导致肝硬化的主要原因将是非病毒因素,如非酒精性脂肪性肝炎。