Impact of HBeAg on Hepatocellular Carcinoma Risk During Oral Antiviral Treatment in Patients With Chronic Hepatitis B
- Authors
- Jang, Heejoon; Yoon, Jun Sik; Park, Soo Young; Lee, Han Ah; Jang, Myoung-Jin; Kim, Seung Up; Sinn, Dong Hyun; Seo, Yeon Seok; Kim, Hwi Young; Kim, Sung Eun; Jun, Dae Won; Yoon, Eileen L.; Sohn, Joo Hyun; Ahn, Sang Bong; Shim, Jae-Jun; Jeong, Soung Won; Cho, Yong Kyun; Kim, Hyoung Su; Nam, Joon Yeul; Lee, Yun Bin; Kim, Yoon Jun; Yoon, Jung-Hwan; Zoulim, Fabien; Lampertico, Pietro; Dalekos, George N.; Idilman, Ramazan; Sypsa, Vana; Berg, Thomas; Buti, Maria; Calleja, Jose Luis; Goulis, John; Manolakopoulos, Spilios; La Janssen, Harry; Papatheodoridis, George, V; Lee, Jeong-Hoon
- Issue Date
- Jun-2022
- Publisher
- ELSEVIER SCIENCE INC
- Keywords
- Cumulative Incidence; DNA; Hepatitis B Virus; Liver Cancer; Neoplasm
- Citation
- CLINICAL GASTROENTEROLOGY AND HEPATOLOGY, v.20, no.6, pp.1343 - 1353
- Indexed
- SCIE
SCOPUS
- Journal Title
- CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
- Volume
- 20
- Number
- 6
- Start Page
- 1343
- End Page
- 1353
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/184776
- DOI
- 10.1016/j.cgh.2021.09.001
- ISSN
- 1542-3565
- Abstract
- BACKGROUND & AIMS: Antiviral treatment from hepatitis B envelope antigen (HBeAg)-positive status may attenuate the integration of hepatitis B virus DNA into the host genome causing hepatocellular carcinoma (HCC). We investigated the impact of HBeAg status at the onset of antiviral treatment on the risk of HCC.
METHODS: The incidence of HCC was evaluated in Korean patients with chronic hepatitis B who started entecavir or tenofovir in either HBeAg-positive or HBeAg-negative phase. The results in the Korean cohort were validated in a Caucasian PAGE-B cohort.
RESULTS: A total of 9143 Korean patients (mean age, 49.2 years) were included: 49.1% were HBeAg-positive and 49.2% had cirrhosis. During follow-up (median, 5.1 years), 916 patients (10.0%) developed HCC. Baseline HBeAg positivity was not associated with the risk of HCC in the entire cohort or cirrhotic subcohort. However, in the non-cirrhotic subcohort, HBeAg positivity was independently associated with a lower risk of HCC in multivariable (adjusted hazard ratio [aHR], 0.41; 95% confidence interval [CI], 0.26-0.66), propensity score-matching (aHR, 0.46; 95% CI, 0.28-0.76), and inverse probability weighting analyses (aHR, 0.44; 95% CI, 0.28-0.70). In the Caucasian cohort (n = 719; mean age, 51.8 years; HBeAg-positive, 20.3%; cirrhosis, 34.8%), HBeAg-positivity was not associated with the risk of HCC either in the entire cohort or cirrhotic subcohort. In the non-cirrhotic subcohort, none of the HBeAg-positive group developed HCC, although the difference failed to reach statistical significance (aHR, 0.21; 95% CI, 0.00-1.67).
CONCLUSIONS: This multinational cohort study implies that HBeAg positivity at the onset of antiviral treatment seems to be an independent factor associated with a lower risk of HCC in patients with chronic hepatitis B without cirrhosis, but not in those with cirrhosis.
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