Synergistic effects of family history of hepatocellular carcinoma and hepatitis B virus infection on risk for incident hepatocellular carcinoma.

Synergistic effects of family history of hepatocellular carcinoma and hepatitis B virus infection on risk for incident hepatocellular carcinoma.
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DOI:
10.1016/j.cgh.2013.04.043
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发表时间:
2013-12
影响因子:
12.6
通讯作者:
Chen, Chien-Jen
Chen, Chien-Jen
中科院分区:
医学1区
文献类型:
--
作者:
Loomba, Rohit;Liu, Jessica;Yang, Hwai-I.;Lee, Mei-Hsuan;Lu, Sheng-Nan;Wang, Li-Yu;Iloeje, Uchenna H.;You, San-Lin;Brenner, David;Chen, Chien-Jen

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关于肝细胞癌家族史对乙肝进展或患肝癌风险的影响,我们知之甚少。我们研究了家族肝细胞癌病史和存在或分期的乙肝病毒感染如何影响肝细胞癌的风险。我们对来自台湾7个乡镇的22,472名参与者进行了一项基于人群的队列研究,这些参与者从1991年到1992年接受了肝病评估。那些在1991年1月1日至2008年12月31日期间首次被诊断为肝细胞癌的患者,是从台湾癌症登记中心确认的。在362,268人年的随访评价中,共有374例肝癌发生。无肝细胞癌家族史的乙肝表面抗原(HBs)阴性患者发生肝细胞癌的累积风险为0.62%,有肝细胞癌家族史者为0.65%,无肝细胞癌家族史者为7.5%,有肝细胞癌家族史者为15.8%(P<.001)。与无肝细胞癌家族史的乙肝表面抗原血清阴性个体相比,有家族史的乙肝表面抗原阳性个体的多因素调整风险比为32.33(95%可信区间,20.8-50.3;P<.001)。交互作用的相对超额风险为19,归因比为0.59,协同指数值为2.54。这些发现表明,家族肝细胞癌病史和乙肝表面抗原血清状态之间存在协同作用。在HBeAg血清水平和血清HBVDNA水平的分层分析中,这些因素之间的协同作用仍然显著。在乙肝病毒感染的每个阶段,肝细胞癌家族史都会增加患肝细胞癌的风险。有肝细胞癌家族史的患者需要更严格的乙肝病毒感染管理和对肝癌的监测。
Little is known about the effects of family history of hepatocellular carcinoma (HCC) on hepatitis B progression or risk of HCC. We examined how family HCC history and presence or stage of hepatitis B virus (HBV) infection affect risk for HCC. We performed a population-based cohort study of 22,472 participants from 7 townships in Taiwan who underwent evaluation for liver disease from 1991 through 1992. Those who received a first diagnosis of HCC from January 1, 1991, to December 31, 2008, were identified from the Taiwanese cancer registry. There were 374 cases of incident HCC over 362,268 person-years of follow-up evaluation. The cumulative risk of HCC in hepatitis B surface antigen (HBsAg)-seronegative patients without a family history of HCC was 0.62%, in those with a family history of HCC the cumulative risk was 0.65%, in HBsAg-seropositive patients without a family history of HCC the cumulative risk was 7.5%, and in HBsAg-seropositive patients with a family history of HCC the cumulative risk was 15.8% (P < .001). The multivariate-adjusted hazard ratio for HBsAg-seropositive individuals with family history, compared with HBsAg-seronegative individuals without a family history of HCC, was 32.33 (95% confidence interval, 20.8–50.3; P < .001). The relative excess risk owing to interaction was 19, the attributable proportion was 0.59, and the synergy index value was 2.54. These findings indicate synergy between family HCC history and HBsAg serostatus. The synergy between these factors remained significant in stratification analyses by HBeAg serostatus and serum level of HBV DNA. Family history of HCC multiplies the risk of HCC at each stage of HBV infection. Patients with a family history of HCC require more intensive management of HBV infection and surveillance for liver cancer.
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