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首页> 外文期刊>Journal of Clinical Microbiology >Evaluation of Impact of Serial Hepatitis B Virus DNA Levels on Development of Hepatocellular Carcinoma
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Evaluation of Impact of Serial Hepatitis B Virus DNA Levels on Development of Hepatocellular Carcinoma

机译:评估系列乙型肝炎病毒DNA水平对肝细胞癌发展的影响

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We aimed to investigate the impact of hepatitis B virus (HBV) DNA on the development of hepatocellular carcinoma (HCC). We conducted a case/control study based on 506 chronic HBV patients followed up since 1997. Forty-one patients developed HCC, and each of them was age and gender matched with two simultaneously recruited controls without HCC. HBV DNA was measured at the initial visit, at yearly intervals, and at the last visit. Patient age at the time of HCC development was 55 ± 9 years. Forty-nine (40%) patients experienced antiviral treatment. The median time from diagnosis to the development of HCC was 17 months, and the control patients were followed for 92 months. At the trough level (defined as lowest level among all studied visits), more (27 patients; 66%) HCC patients had HBV DNA levels of >10,000 copies/ml than the controls (17 patients; 21%). The area under the receiver operating characteristic curve of the trough log HBV DNA level for HCC was 0.79 (95% confidence interval [CI], 0.69 to 0.89). Trough log HBV DNA (odds ratio, 11.4; 95% CI, 3.6 to 37.6; P < 0.0001) and liver cirrhosis (odds ratio, 11.4; 95% CI, 3.6 to 36.2; P < 0.0001) levels were independently associated with HCC after an adjustment for age, gender, antiviral treatment, and HBV genotype. The difference in the trough HBV DNA level was more obvious among untreated patients (5.7 ± 1.4 log copies/ml in HCC patients versus 3.2 ± 1.3 log copies/ml in control patients; P < 0.0001) than among those who had received antiviral treatment (3.0 ± 1.4 log copies/ml in HCC patients versus 2.5 ± 0.9 log copies/ml in control patients; P = 0.38). A high trough HBV DNA level was associated with a higher risk of HCC. Whether antiviral treatment could prevent HCC was uncertain.
机译:我们旨在调查乙型肝炎病毒(HBV)DNA对肝细胞癌(HCC)发展的影响。自1997年以来,我们对506例慢性HBV患者进行了病例/对照研究。有41例患者发展为HCC,每个患者的年龄和性别均与同时招募的两个没有HCC的对照匹配。在初次就诊,每年间隔和最后一次就诊时测量HBV DNA。肝癌发生时的患者年龄为55±9岁。四十九(40%)名患者经历了抗病毒治疗。从诊断到发展为HCC的中位时间为17个月,对照组接受随访92个月。在低谷水平(定义为所有研究访视中最低水平),比对照组(17例患者; 21%)更多(27例患者; 66%)的HCC患者HBV DNA水平> 10,000拷贝/ ml。 HCC的低谷对数HBV DNA水平的接受者工作特征曲线下的面积为0.79(95%置信区间[CI],0.69至0.89)。低谷对数HBV DNA(比值比为11.4; 95%CI为3.6至37.6; P <0.0001)和肝硬化(比值比数为11.4; 95%CI为3.6至36.2; P <0.0001)水平在调整了年龄,性别,抗病毒治疗和HBV基因型后与HCC相关。与未经治疗的患者相比,低谷HBV DNA水平的差异更为明显(HCC患者为5.7±1.4 log拷贝/ ml,对照组为3.2±1.3 log拷贝/ ml; P <0.0001)接受抗病毒治疗的患者(HCC患者为3.0±1.4 log拷贝/ ml,对照组为2.5±0.9 log拷贝/ ml; P = 0.38)。高谷HBV DNA水平与更高的HCC风险相关。抗病毒治疗是否可以预防HCC尚不确定。

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