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α区T1653突变增加了基因C型HBV慢性感染患者发生肝细胞癌的危险性
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Clin Infect Dis. 2006 Jan 1;42(1):1-7. T1653 mutation in the box alpha increases the risk of hepatocellular carcinoma in patients with chronic hepatitis B virus genotype C infection. Ito K, Tanaka Y, Orito E, Sugiyama M, Fujiwara K, Sugauchi F, Kato T, Tokita H, Izumi N, Kato M, Yuen MF, Lai CL, Gish RG, Ueda R, Mizokami M. Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan. BACKGROUND: Most patients with chronic hepatitis B virus infection become carriers of inactive virus after hepatitis B e antigen seroconversion; however, a subgroup of patients have persistent abnormal transaminase levels and develop hepatocellular carcinoma after seroconversion. METHODS: In an age-matched case-control study, 40 carriers of inactive virus (mean age+/-standard deviation [SD], 50.9 +/- 11.1 years), 40 patients with chronic hepatitis (mean age+/-SD, 50.2 +/- 8.9 years), and 40 patients with hepatocellular carcinoma (mean age+/-SD, 50.7 +/- 9.4 years) who were infected with hepatitis B virus genotype C and had test results positive for antibody to hepatitis B e antigen were analyzed. RESULTS: The prevalence of T1653 in the box alpha was significantly higher among patients with hepatocellular carcinoma than among carriers of inactive virus who did not have hepatocellular carcinoma (70% vs. 25%; P < .0001) or chronic hepatitis (70% vs. 35%; P = .003). Mutations in the basic core promoter region (T1762/A1764) were frequently found in all groups, regardless of clinical status (in 77.5% of carriers of inactive virus, 77.5% of patients with chronic hepatitis, and 90% of patients with hepatocellular carcinoma). In the multivariate analysis, the presence of T1653, an alanine aminotransferase level of > or = 37 U/L, and a platelet count of < 18 x 10(4) platelets/mm3 were independent predictive values for hepatocellular carcinoma (odds ratio [95% confidence interval], 5.05 [1.56-16.35], 12.56 [3.05-51.77], and 11.5 [3.47-38.21], respectively). High alpha -fetoprotein level was the only independent predictive value for T1653 in patients with hepatocellular carcinoma (odds ratio, 12.67; 95% confidence interval, 1.19-134.17]). Among patients with test results positive for antibody to hepatitis B e antigen who had hepatocellular carcinoma and were infected with different genotypes of hepatitis B virus, the prevalence of T1653 was 40%, 15%, 25%, 25%, 67%, and 23% in patients infected with hepatitis B virus genotypes Aa, Ae, Ba, Bj, C, and D, respectively (P<.05 for genotype C vs. genotypes Ae, Ba, Bj, or D). CONCLUSIONS: Our data indicate that the addition of T1653 mutation in the box alpha to the basic core promoter mutation increases the risk of hepatocellular carcinoma in patients with hepatitis B virus genotype C. 背景：大多数感染乙型肝炎病毒的患者在发生HBeAg血清学转换后变成了无活动性病毒复制的慢性乙型肝炎携带者；然而，一部分患者在发生血清学转换后一直具有持续的血清学转氨酶水平异常和发生肝细胞肝癌。 方法：在一项年龄匹配的病例对照研究中，40位无病毒活动的慢性乙肝携带者（平均年龄±标准差：50.2±8.9岁），和40位慢性肝炎患者（平均年龄±标准差：50.9±11.1岁），和40位感染基因C型乙型肝炎病毒且HBeAb阳性的肝细胞肝癌的患者（平均年龄±标准差：50.7±9.4岁）纳入分析。 结果：肝细胞肝癌患者中发生α区T1653突变者较那些无病毒复制活性且无肝细胞肝癌的慢性携带者（70% vs 25%；P<0.0001）或慢性肝炎患者（70% vs 35%；P＝0.003）相比明显为高。在基本核心启动子区域的T1762/A1764突变在各组均十分常见，且于临床状态没有相关性（77.5%的无病毒复制活性的慢性携带者，77.5%的慢性肝炎患者，和90%具有肝细胞肝癌的患者具有这一突变）。在多因素分析中，T1653的发生率、丙氨酸氨基转移酶水平≥37IU/L、和血小板计数<18×10E4/mm3是肝细胞肝癌发生的独立预测因素，比数比分别是（95%的可信区间）：5.05（1.56～16.35）、12.56（3.05～51.77）和11.5（3.47～38.21）。在所有检测HBeAb阳性的肝细胞肝癌且感染乙型肝炎病毒不同基因亚型患者中，T1653突变的发生率在基因亚型Aa、Ae、Ba、Bj、C、和D分别为40%、15%、25%、25%、67%和23%（P<0.05 对于基因C型 vs. 基因Ae、Ba、Bj、或D）。 结论：我们的数据提示在基础核心启动子α区发生的T1653突变增加了基因C型乙型肝炎病毒感染患者发生肝细胞肝癌的危险性。 |
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