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Antiviral therapy and hepatocellular carcinoma risk in hepatitis B patients with cirrhosis
Gao, Xuesonga,,b; Yang, Hwai-Ic; Trinh, Huyd; Jeong, Donghaka; Li, Jiayie; Zhang, Jianf; Le, Ana; Hoang, Josepha; Nguyen, Paulinea; Henry, Lindaa; Nguyen, Mindie H.aAuthor Information
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.
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