Chung-Feng Huang1,2,3, Ming-Lun Yeh1,2, Ching-I Huang1, Po-Cheng Liang1, Yi-Hung Lin1, Zu-Yau Lin1,2, Shinn-Cherng Chen1,2, Jee-Fu Huang1,2, Chia-Yen Dai1,2,4, Wan-Long Chuang1,2, Ming-Lung Yu5,6,7,8,9. 1. Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan. 2. Faculty of Internal Medicine, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan. 3. Department of Occupational Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan. 4. Department of Preventive Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan. 5. Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan. fish6069@gmail.com. 6. Faculty of Internal Medicine, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan. fish6069@gmail.com. 7. Division of Gastroenterology and Hepatology, Chi-Mei Medical Center Liouying, Tainan, Taiwan. fish6069@gmail.com. 8. Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan. fish6069@gmail.com. 9. College of Biological Science and Technology, National Chiao Tung University, Hsin-Chu, Taiwan. fish6069@gmail.com.
Abstract
BACKGROUND/AIMS: Liver fibrosis determined hepatocellular carcinoma (HCC) occurrence in chronic hepatitis C patients with sustained virological response (SVR). We aimed to determine whether post-treatment fibrotic modification overwhelmed pretreatment fibrotic status in terms of long-term HCC prediction. METHODS: 265 SVR patients with paired biopsies before and after antiviral therapy were enrolled for analysis of the association of fibrotic changes with HCC. RESULTS: Eighteen (6.8%) of the 265 patients developed HCC over 1931 person-years. Cox regression analysis without post-treatment fibrosis as a covariant revealed that factors predicted HCC included age (hazard ratio [HR]/confidence intervals [CI] 1.07/1.01-1.13, p = 0.01), male gender (HR/CI 4.57/1.45-14.36, p = 0.009), diabetes (HR/CI 3.60/1.32-9.85, p = 0.01) and pretreatment advanced fibrosis (HR/CI 2.73/1.05-7.07, p = 0.039). Advanced fibrosis in post-treatment status replaced pretreatment fibrosis as the most critical determinant of HCC when it was included for analysis (HR/CI 3.53/1.34-9.30, p = 0.01). The incidences of HCC among patients with fibrotic modification from F0-2 to F0-2, F34 to F0-2, F0-2 to F34 and F34 to F34 were 0.41%, 0.84%, 1.68%, and 3.05%, respectively (p = 0.004). Compared to patients whose fibrotic stage remained at F0-2 before and after treatment, the HCC risk decreased and did not differ among those whose fibrotic stage improved from F34 to F0-2. However, HCC risk increased significantly and gradually in patients whose fibrotic stages changed from F0-2 to F34 (HR/CI 4.13/1.11-15.36, p = 0.035) and whose fibrotic stages remained at F34 before and after treatment (HR/CI 7.47/2.37-23.55, p = 0.001) (trend p = 0.003). CONCLUSIONS: Post-treatment fibrotic modifications overwhelmed pretreatment fibrotic statuses in predicting HCC.
BACKGROUND/AIMS: Liver fibrosis determined hepatocellular carcinoma (HCC) occurrence in chronic hepatitis Cpatients with sustained virological response (SVR). We aimed to determine whether post-treatment fibrotic modification overwhelmed pretreatment fibrotic status in terms of long-term HCC prediction. METHODS: 265 SVR patients with paired biopsies before and after antiviral therapy were enrolled for analysis of the association of fibrotic changes with HCC. RESULTS: Eighteen (6.8%) of the 265 patients developed HCC over 1931 person-years. Cox regression analysis without post-treatment fibrosis as a covariant revealed that factors predicted HCC included age (hazard ratio [HR]/confidence intervals [CI] 1.07/1.01-1.13, p = 0.01), male gender (HR/CI 4.57/1.45-14.36, p = 0.009), diabetes (HR/CI 3.60/1.32-9.85, p = 0.01) and pretreatment advanced fibrosis (HR/CI 2.73/1.05-7.07, p = 0.039). Advanced fibrosis in post-treatment status replaced pretreatment fibrosis as the most critical determinant of HCC when it was included for analysis (HR/CI 3.53/1.34-9.30, p = 0.01). The incidences of HCC among patients with fibrotic modification from F0-2 to F0-2, F34 to F0-2, F0-2 to F34 and F34 to F34 were 0.41%, 0.84%, 1.68%, and 3.05%, respectively (p = 0.004). Compared to patients whose fibrotic stage remained at F0-2 before and after treatment, the HCC risk decreased and did not differ among those whose fibrotic stage improved from F34 to F0-2. However, HCC risk increased significantly and gradually in patients whose fibrotic stages changed from F0-2 to F34 (HR/CI 4.13/1.11-15.36, p = 0.035) and whose fibrotic stages remained at F34 before and after treatment (HR/CI 7.47/2.37-23.55, p = 0.001) (trend p = 0.003). CONCLUSIONS: Post-treatment fibrotic modifications overwhelmed pretreatment fibrotic statuses in predicting HCC.