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Nucleos(t)ide Analogue Treatment for Patients With Hepatitis B Virus (HBV) e Antigen–Positive Chronic HBV Genotype C Infection: A Nationwide, Multicenter, Retrospective Study
Young Chang Won Hyeok Choe Dong Hyun Sinn Jeong-Hoon Lee Sang Hoon Ahn Hyewon Lee Jae-Jun Shim Dae Won Jun Soo Young Park Joon Yeul Nam ... Show more
The Journal of Infectious Diseases, Volume 216, Issue 11, 12 December 2017, Pages 1407–1414, https://doi.org/10.1093/infdis/jix506
Published:
23 September 2017
Abstract
Background
Antiviral treatment for hepatitis B virus (HBV) e antigen (HBeAg)–positive chronic HBV infection is still controversial. We assessed whether antiviral treatment reduces the risk of liver disease progression in these patients.
Methods
This study included consecutive patients in 8 large-volume hospitals in Korea who tested positive for HBeAg and had an HBV DNA level of >20000 IU/mL, an alanine aminotransferase (ALT) level of <40 IU/L, and no evidence of cirrhosis. The primary end point was the development of hepatocellular carcinoma (HCC), and the secondary end point was the development of cirrhosis.
Results
A total of 484 patients were included: 87 were in the antiviral treatment group, and 397 were in the control group. Baseline liver function was significantly more favorable for the control group. After matching for propensity score to overcome those differences, the antiviral treatment group had a significantly reduced risk for HCC (hazard ratio [HR], 0.234; log-rank P = .046) and cirrhosis (HR, 0.235; log-rank P = .015), compared with the control group. After balancing the baseline characteristics by using inverse probability weighting, antiviral therapy significantly decreased the risk of HCC (HR, 0.189; log-rank P = .004) and cirrhosis (HR, 0.347; log-rank P = .036).
Conclusion
Antiviral therapy for patients with HBeAg-positive chronic HBV infection and have a high HBV load reduces the risk of HCC, even if the ALT level is below the upper limit of normal.
Issue Section:
Viruses
© The Author 2017. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: [email protected].
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