Division of Gastroenterology and Hepatology, Stanford University Medical Center, Stanford, California, USA.
Department of General Medicine, Beijing Ditan Hospital, Capital Medical University, Beijing.
Eur J Gastroenterol Hepatol. 2020 Sep;32(9):1207-1211. doi: 10.1097/MEG.0000000000001639.
Our goal was to evaluate the effect of antiviral therapy on hepatocellular carcinoma incidence for cirrhotic patients with lower hepatitis B virus DNA levels.
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.
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.
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.
我们旨在评估低乙型肝炎病毒 DNA 水平的肝硬化患者接受抗病毒治疗对肝细胞癌发病率的影响。
我们纳入了来自美国队列的 381 例肝硬化患者和来自台湾队列的 408 例患者。患者被分为低（<20IU/ml）和高乙型肝炎病毒 DNA 组（≥20IU/ml），并进一步分为治疗和未治疗亚组。
除乙型肝炎 e 抗原外，两组乙型肝炎病毒 DNA 患者的基线特征相似。抗病毒治疗可显著降低乙型肝炎病毒 DNA≥20IU/ml 的肝硬化患者 5 年（12.2%对 22.8%）和 10 年（23.3%对 37.2%）的肝细胞癌发病率（P=0.0018）。对于乙型肝炎病毒 DNA<20IU/ml 的肝硬化患者，治疗组与未治疗组之间的累积肝细胞癌发生率无统计学差异。在校正年龄、性别和乙型肝炎 e 抗原状态后，抗病毒治疗是乙型肝炎病毒 DNA≥20IU/ml 患者肝细胞癌风险降低的独立预测因素（风险比 0.43，P<0.0001）。
抗病毒治疗与乙型肝炎病毒 DNA 低至 20IU/ml（但不更低）的肝硬化慢性乙型肝炎患者肝细胞癌发病率降低 57%相关。然而，无论乙型肝炎病毒 DNA 水平和治疗状态如何，肝细胞癌的发生率仍然很高，这突出表明需要对所有乙型肝炎病毒肝硬化患者进行持续的肝细胞癌监测。
