aDivision of Gastroenterology and Hepatology, Stanford University Medical Center, Stanford, California, USA
bDepartment of General Medicine, Beijing Ditan Hospital, Capital Medical University, Beijing
cGenomics Research Center, Academia Sinica, Taipei, Taiwan, Republic of China
dSan Jose Gastroenterology, San Jose
eGastroenterology Department, Palo Alto Medical Foundation, Mountain View
fPrimary Care, Chinese Hospital, San Francisco, California, USA
Received 19 June 2019 Accepted 22 August 2019
Correspondence to Mindie H. Nguyen, MD, MAS, Division of Gastroenterology and Hepatology, Stanford University Medical Center, 750 Welch Road, Suite 210, Palo Alto, CA 94304, USA, Tel: +650 498 5691; fax: +650 498 5692; e-mail: [email protected]
European Journal of Gastroenterology & Hepatology: September 2020 - Volume 32 - Issue 9 - p 1207-1211
doi: 10.1097/MEG.0000000000001639
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Abstract
Objectives:
Our goal was to evaluate the effect of antiviral therapy on hepatocellular carcinoma incidence for cirrhotic patients with lower hepatitis B virus DNA levels.
Methods:
Consecutive cirrhosis patients from a US cohort (n = 381) and 408 patients from a Taiwan cohort were enrolled. Patients were classified into a low (<20 IU/ml) and high hepatitis B virus DNA group (≥20 IU/ml), and each was further stratified into treated and untreated subgroups.
Results:
Except for hepatitis B e antigen, baseline characteristics were similar for both hepatitis B virus DNA groups. Antiviral therapy significantly reduced hepatocellular carcinoma incidence in cirrhotic patients with hepatitis B virus DNA ≥20 IU/ml at 5-years (12.2% vs. 22.8%) and 10-years (23.3% vs. 37.2%) (P = 0.0018). For cirrhotic patients with hepatitis B virus DNA <20 IU/ml, there was no statistically significant difference in cumulative hepatocellular carcinoma incidence between the treated and untreated groups. After adjusting for age, sex, and hepatitis B e antigen status, antiviral therapy was an independent predictor (hazard ratio 0.43, P < 0.0001) for reduced hepatocellular carcinoma risk in patients with hepatitis B virus DNA ≥20 IU/ml.
Conclusion:
Antiviral therapy was associated with a 57% reduction in hepatocellular carcinoma incidence in chronic hepatitis B patients with cirrhosis and hepatitis B virus DNA as low as 20 IU/ml (but no lower). However, hepatocellular carcinoma incidence remained substantial, regardless of hepatitis B virus DNA levels and treatment status, highlighting the need for ongoing hepatocellular carcinoma surveillance for all cirrhotic hepatitis B virus patients. 作者: StephenW 时间: 2020-8-4 09:26
美国队列（n = 381）的连续性肝硬化患者和台湾队列的408例患者入组。将患者分为低（<20 IU / ml）和高乙型肝炎病毒DNA组（≥20IU / ml），然后将患者进一步分为治疗组和未治疗组。
结果：
除乙肝e抗原外，两个乙肝病毒DNA组的基线特征均相似。抗病毒治疗显着降低了乙肝病毒DNA≥20 IU / ml的肝硬化患者在5年（12.2％对22.8％）和10年（23.3％对37.2％）时的肝细胞癌发生率（P = 0.0018）。对于乙型肝炎病毒DNA <20 IU / ml的肝硬化患者，治疗组和未治疗组之间累积肝细胞癌发生率无统计学差异。在调整了年龄，性别和乙肝e抗原状态后，抗病毒治疗是降低乙肝病毒DNA≥20 IU / ml的肝细胞癌风险的独立预测因子（危险比0.43，P <0.0001）。
结论：
在慢性乙型肝炎肝硬化和乙型肝炎病毒DNA低至20 IU / ml（但不更低）的患者中，抗病毒治疗可使肝细胞癌的发生率降低57％。但是，无论乙肝病毒DNA的水平和治疗状况如何，肝细胞癌的发生率仍然很高，这凸显了对所有肝硬化乙肝病毒患者进行持续肝细胞癌监测的必要性。作者: 健康平安猫 时间: 2020-8-4 10:47
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乙型肝炎病毒DNA <20 IU / ml的肝硬化患者，5年和10年的肝癌发生率有吗？
病毒DNA <20 IU 的话，治疗与否都区别不大，是这样理解的吗？作者: StephenW 时间: 2020-8-4 21:13