HCV genotype 3 is associated with a higher hepatocellular carcinoma incidence in patients with ongoing viral C cirrhosis
HCV genotype 3 is associated with a higher hepatocellular carcinoma incidence in patients with ongoing viral C cirrhosis
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DOI：
10.1111/j.1365-2893.2011.01441.x
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发表时间：
2011-10-01
影响因子：
2.5
通讯作者：
Beaugrand, M.
中科院分区：
文献类型：
--
作者：
Nkontchou, G.;Ziol, M.;Beaugrand, M.
肝脏脂肪变性是丙型肝炎病毒感染的主要组织病理学特征。脂肪变性和/或脂肪形成的机制可能导致肝癌的发生。这项回顾性研究的目的是评估丙型肝炎病毒3型感染对持续的丙型肝炎肝硬变患者发生肝细胞癌的影响。连续353名患者(男性193人，平均年龄58+/-13岁)，经组织学证实为丙型肝炎肝硬变并持续病毒复制，在1994年至2007年期间进行了前瞻性的肝细胞癌随访和筛查。用对数等级检验和COX模型比较不同基因型亚组之间肝癌的精算发病率。3型感染者的凝血酶原活动度较低[78(四分位数区间60~85)vs 84(71~195)%，P=0.03]，饮酒率较高(48%vs 29%，P=0.046)。在中位随访5.54年[2.9-8.6]期间，分别有11/25(44%)和87/328(26%)的3型和非3型患者发生了肝细胞癌。不同基因型亚组间肝癌发病率差异有统计学意义(P=0.001)。3型组和非3型组的5年肝癌发生率分别为34%(95%CI 1.3~6.3)和17%(95%CI 5.7~9.2)(P=0.002)。在多因素分析中，即使在调整了凝血酶原活动度和酗酒因素后，感染3型仍与肝癌发生的风险增加独立相关[危险比3.54(95%可信区间1.84~6.81，P=0.0002)]。对于丙型肝炎肝硬变和持续感染的患者，3型感染独立地与肝癌发展的风险增加相关。
Liver steatosis is a main histopathological feature of Hepatitis C (HCV) infection because of genotype 3. Steatosis and/or mechanisms underlying steatogenesis can contribute to hepatocarcinogenesis. The aim of this retrospective study was to assess the impact of infection with HCV genotype 3 on hepatocellular carcinoma (HCC) occurrence in patients with ongoing HCV cirrhosis. Three hundred and fifty-three consecutive patients (193 men, mean age 58 +/- 13 years), with histologically proven HCV cirrhosis and persistent viral replication prospectively followed and screened for HCC between 1994 and 2007. Log-rank test and Cox model were used to compare the actuarial incidence of HCC between genotype subgroups. The patients infected with a genotype 3 (n = 25) as compared with those infected with other genotypes (n = 328) had a lower prothrombin activity [78 (interquartile range 60-85) vs 84 (71-195) %, P = 0.03] and higher rate of alcohol abuse (48% vs 29%, P = 0.046). During a median follow-up of 5.54 years [2.9-8.6], 11/25 patients (44%) and 87/328 patients (26%) with a genotype 3 and non-3 genotype, respectively, develop a HCC. HCC incidences were significantly different among the genotype subgroups (P = 0.001). The 5-year occurrence rate of HCC was 34% (95% CI, 1.3-6.3) and 17% (95% CI, 5.7-9.2) in genotype 3 and non-3 genotype groups, respectively (P = 0.002). In multivariate analysis, infection with a genotype 3 was independently associated with an increased risk of HCC occurrence [hazard ratio 3.54 (95% CI, 1.84-6.81), P = 0.0002], even after adjustment for prothrombin activity and alcohol abuse [3.58 (1.80-7.13); P = 0.003]. For patients with HCV cirrhosis and ongoing infection, infection with genotype 3 is independently associated with an increased risk of HCC development.