Eur J Gastroenterol Hepatol. 2019 Dec 24. doi: 10.1097/MEG.0000000000001639. [Epub ahead of print]
Antiviral therapy and hepatocellular carcinoma risk in hepatitis B patients with cirrhosis.
Gao X1,2, Yang HI3, Trinh H4, Jeong D1, Li J5, Zhang J6, Le A1, Hoang J1, Nguyen P1, Henry L1, Nguyen MH1.
Author information
1
Division of Gastroenterology and Hepatology, Stanford University Medical Center, Stanford, California, USA.
2
Department of General Medicine, Beijing Ditan Hospital, Capital Medical University, Beijing.
3
Genomics Research Center, Academia Sinica, Taipei, Taiwan, Republic of China.
4
San Jose Gastroenterology, San Jose.
5
Gastroenterology Department, Palo Alto Medical Foundation, Mountain View.
6
Primary Care, Chinese Hospital, San Francisco, California, USA.
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.
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在5年时（12.2％对22.8％）和10年时（23.3％对37.2％）的乙肝病毒DNA≥20 IU / ml的肝硬化患者的肝细胞癌发生率（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，性别和乙型肝炎e抗原状态后，抗病毒治疗是降低乙型肝炎病毒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水平和治疗状态如何，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。