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Hepatocellular carcinoma risk in chronic hepatitis B virus-infected compensated cirrhosis patients with low viral load
Dong Hyun Sinn1, Junggyu Lee1, Juna Goo2, Kyunga Kim2, Geum-Youn Gwak1, Yong-Han Paik1, Moon Seok Choi1, Joon Hyeok Lee1, Kwang Cheol Koh1, Byung Chul Yoo1 andSeung Woon Paik1,*
DOI: 10.1002/hep.27889
© 2015 by the American Association for the Study of Liver Diseases
Issue
Cover image for Vol. 61 Issue 5
Hepatology
Accepted Article (Accepted, unedited articles published online and citable. The final edited and typeset version of record will appear in future.)
Article has an altmetric score of 5
1 Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
2 Biostatistics and Clinical Epidemiology Center, Samsung Medical Center, Seoul, Korea
*Corresponding author: Seung Woon Paik, MD, PhD, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-ro, Gangnam-Gu, 135-710, Seoul, South Korea, Tel: +82-2-3410-3409; Fax: +82-2-3410-6983; E-mail: [email protected]
Keywords:
Liver cancer;antiviral therapy;alanine aminotransferase;treatment;virus
Abstract
Controversy exists about whether antiviral therapy (AVT) should be recommended for compensated cirrhosis patients with chronic hepatitis B virus (HBV) infection and detectable but low serum HBV DNA levels. A retrospective cohort of 385 treatment-naïve, HBV-related compensated cirrhosis patients (mean age 51.1 ± 9.7 years; 66% male) with low HBV DNA levels (<2,000 IU/mL) was assessed for the development of hepatocellular carcinoma (HCC). During median of 5.6 years of follow-up, HCC had developed in 37 (9.6%) patients. The 5-year cumulative HCC incidence rate was 2.2%, 8.0% and 14.0% for patients with undetectable HBV DNA (<12 IU/mL), low HBV DNA levels plus normal alanine aminotransferase (ALT) levels, and low HBV DNA levels plus elevated ALT levels at baseline (p = 0.011). During follow-up, 71 patients maintained undetectable HBV DNA levels, and 126 patients experienced HBV DNA elevation over 2,000 IU/mL. AVT was initiated in 77 patients. In patients without AVT, the 5-year cumulative HCC incidence rates were 13.3%, 8.8% and 1.4% for patients who experienced HBV DNA elevation, patients who maintained detectable but low HBV DNA levels, and patients who maintained undetectable HBV DNA levels, respectively. The 5-year cumulative HCC incidence rate was 5.9% for patients who started AVT; longer AVT duration and longer complete virological response (< 12 IU/mL) duration was associated with lower HCC risk. Conclusion: Compensated cirrhosis patients with detectable but low viral load were not at low risk for HCC, and AVT was associated with lower HCC risk, suggesting that prompt AVT should be considered for these patients. This article is protected by copyright. All rights reserved.
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发表于 2015-5-16 12:49
