한빛사논문
Won-Mook Choi MD 1†, Terry Cheuk-Fung Yip PhD 2†, Grace Lai-Hung Wong MD 2, W. Ray Kim MD 3, Leland J. Yee PhD 4, Craig Brooks-Rooney MA 5, Tristan Curteis MSc 6, Laura J. Clark PhD 6, Zarena Jafry MPH 5, Chien-Hung Chen MD 7, Chi-Yi Chen MD 8, Yi-Hsiang Huang MD 9,10, Young-Joo Jin MD 11, Dae Won Jun MD 12, Jin-Wook Kim MD 13,14, Neung Hwa Park MD 15,16, Cheng-Yuan Peng MD 17,18, Hyun Phil Shin MD 19, Jung Woo Shin MD 15, Yao-Hsu Yang MD 20,21, Young-Suk Lim MD 1
1Department of Gastroenterology, Liver Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, The Republic of Korea
2CUHK Medical Data Analytics Centre, Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China
3Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, California, U.S.A
4Gilead Sciences, Foster City, California, U.S.A
5Costello Medical Inc, Boston Massachusetts, U.S.A
6Costello Medical Consulting Ltd, Cambridge, U.K
7Division of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine Kaohsiung, Taiwan
8Division of Hepatogastroenterology, Department of Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chia-Yi, Taiwan
9Division of Gastroenterology and Hepatology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
10Institute of Clinical Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
11Digestive Disease Center, Department of Internal Medicine, Inha University Hospital, Inha University School of Medicine, Incheon, South Korea
12Department of Internal Medicine, Hanyang University Hospital, Hanyang University College of Medicine, Seoul, Republic of Korea
13Department of Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of Korea
14Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea
15Department of Internal Medicine, University of Ulsan College of Medicine, Ulsan University Hospital, Ulsan, Republic of Korea
16Biomedical Research Center, University of Ulsan College of Medicine, Ulsan University Hospital, Ulsan, Republic of Korea
17Center for Digestive Medicine, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan
18School of Medicine, China Medical University, Taichung, Taiwan
19Department of Gastroenterology and Hepatology, Kyung Hee University Hospital at Gangdong, Kyung Hee University School of Medicine, Seoul, Republic of Korea
20Department of Traditional Chinese Medicine, Chiayi Chang Gung Memorial Hospital, Chiayi, Taiwan
21Health Information and Epidemiology Laboratory, Chang Gung Memorial Hospital, Chiayi, Taiwan
†Co-first authors
CORRESPONDENCE: Young-Suk Lim
Abstract
Background and aims: Hepatocellular carcinoma (HCC) risk persists in chronic hepatitis B (CHB) patients despite antiviral therapy. The relationship between pre-treatment baseline hepatitis B virus (HBV) viral load and HCC risk during antiviral treatment remains uncertain.
Methods: This multinational cohort study aimed to investigate the association between baseline HBV viral load and on-treatment HCC risk in 20,826 noncirrhotic, hepatitis B e antigen (HBeAg)-positive and HBeAg-negative patients with baseline HBV DNA levels ≥2,000 IU/mL (3.30 log10 IU/mL) who initiated entecavir or tenofovir treatment. The primary outcome was on-treatment HCC incidence, stratified by baseline HBV viral load as a categorical variable.
Results: In total, 663 patients developed HCC over a median follow-up of 4.1 years, with an incidence rate of 0.81 per 100 person-years (95% confidence interval [CI], 0.75-0.87). Baseline HBV viral load was significantly associated with HCC risk in a non-linear parabolic pattern, independent of other factors. Patients with baseline viral load between 6.00 and 7.00 log10 IU/mL had the highest on-treatment HCC risk (adjusted hazard ratio, 4.28; 95% CI, 2.15-8.52; P < .0001) compared to those with baseline viral load ≥8.00 log10 IU/mL, who exhibited the lowest HCC risk.
Conclusion: Baseline viral load showed a significant, non-linear, parabolic association with HCC risk during antiviral treatment in noncirrhotic CHB patients. Early initiation of antiviral treatment based on HBV viral load may help prevent irreversible HCC risk accumulation in CHB patients.
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