TY - JOUR
T1 - HCC risk post-SVR with DAAs in East Asians
T2 - findings from the REAL-C cohort
AU - For the REAL-C Investigators
AU - Tanaka, Yasuhito
AU - Ogawa, Eiichi
AU - Huang, Chung Feng
AU - Toyoda, Hidenori
AU - Jun, Dae Won
AU - Tseng, Cheng Hao
AU - Hsu, Yao Chun
AU - Enomoto, Masaru
AU - Takahashi, Hirokazu
AU - Furusyo, Norihiro
AU - Yeh, Ming Lun
AU - Iio, Etsuko
AU - Yasuda, Satoshi
AU - Lam, Carla Pui Mei
AU - Lee, Dong Hyun
AU - Haga, Hiroaki
AU - Yoon, Eileen L.
AU - Ahn, Sang Bong
AU - Wong, Grace
AU - Nakamuta, Makoto
AU - Nomura, Hideyuki
AU - Tsai, Pei Chien
AU - Jung, Jang Han
AU - Song, Do Seon
AU - Dang, Hansen
AU - Maeda, Mayumi
AU - Henry, Linda
AU - Cheung, Ramsey
AU - Yuen, Man Fung
AU - Ueno, Yoshiyuki
AU - Eguchi, Yuichiro
AU - Tamori, Akihiro
AU - Yu, Ming Lung
AU - Hayashi, Jun
AU - Nguyen, Mindie H.
AU - Azuma, Koichi
AU - Chuang, Wan Long
AU - Dai, Chia Yen
AU - Dohmen, Kazufumi
AU - Huang, Jee Fu
AU - Jun, Mi Jung
AU - Kajiwara, Eiji
AU - Kato, Masaki
AU - Kawano, Akira
AU - Koyanagi, Toshimasa
AU - Lee, Mei Hsuan
AU - Ooho, Aritsune
AU - Satoh, Takeaki
AU - Shimoda, Shinji
AU - Takahashi, Kazuhiro
N1 - Funding Information:
YT: Research support: Janssen, Gilead, Speaker: Gilead. CFH: Speaker: AbbVie, BMS, Gilead, Merck. YCH: Research support: Gilead, Consultation: Gilead, Speaker: AbbVie, Bristol-Myers Squibb and Gilead. ME: Speaker: AbbVie. DHL: Research support: Gilead Sciences Korea, Korea Pharma. GW: Research support: Gilead, Consultation: Gilead, Speaker: Abbott, AbbVie, BMS, Echosens, Furui, Gilead, Janssen and Roche, Research grant: Gilead. MFY: Consultation: AbbVie, Arbutus Biopharma, Assembly Biosciences, Bristol Myer Squibb, Dicerna Pharmaceuticals, GlaxoSmithKline, Gilead Sciences, Janssen, Merck Sharp and Dohme, Clear B Therapeutics, Springbank Pharmaceutical. YU: Research support: Gilead, AbbVie, Governmental funding for research: AMED. YE: Speaker: Gilead. MLY: Research support: Abbott, BMS, Gilead and Merck, Consultant and/or an advisory board: Abbvie, Abbott, Ascletis, BMS, Gilead and Merck, Speaker: Abbvie, Abbott, BMS, Gilead, Merck, and IPSEN. WLC: Consultation: Gilead, AbbVie, BMS, MSD, PharmaEssentia, Speaker: Gilead, AbbVie, BMS, MSD, PharmaEssentia. CYD: Consultation: Abbvie, Speaker: AbbVie, Merck, BMS, and Gilead. MHL: Research support: The Ministry of Science and Technology, Taipei, Taiwan (105-2628-B010-003-MY4, 107-2314-B-010-004-MY2 and 107-2918-I-010-004), Consultation: Gilead. MHN: Research support: Enanta, Gilead, Pfizer, B.K. Kee Foundation, National Cancer Institute. Consultant and/or an advisory board: Novartis, Bayer, Eisai, Intercept, Gilead, Janssen, Laboratory of Advanced Medicine, Exact Sciences, and Intercept. All other authors have nothing to disclose.
Funding Information:
This study was supported in part by an investigator-initiated research grant to Stanford University by Gilead Sciences and ML Yu wishes to acknowledge partial support for work performed at Kaohsiung Medical University by Kaohsiung Medical University Grant KMUDK109002, Research Center Grant, Cohort Research Center KMU-TC108B07 and Center of Cancer Research KMU-TCA04-3.
Funding Information:
The members of the REAL-C Investigators are: Koichi Azuma: Department of Medicine, Kyushu Central Hospital, Fukuoka, Japan; Wan-Long Chuang: Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital; Hepatitis Research Center, College of Medicine and Cohort Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan; Chia-Yen Dai: Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital; Hepatitis Research Center, College of Medicine and Cohort Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan; Kazufumi Dohmen: Department of Internal Medicine, Chihaya Hospital, Fukuoka, Japan; Jee-Fu Huang: Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital; Hepatitis Research Center, College of Medicine and Cohort Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan; Mi Jung Jun: Department of Gastroenterology, Good Gang-An Hospital, Busan, Korea; Eiji Kajiwara: Kajiwara Clinic, Kitakyushu, Japan; Masaki Kato: Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan; Akira Kawano: Department of Medicine, Kitakyushu Municipal Medical Center, Kitakyushu, Japan; Toshimasa Koyanagi: Department of Medicine, Fukuoka City Hospital, Fukuoka, Japan; Mei-Hsuan Lee: Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan; Aritsune Ooho: Department of Hepatology, Steel Memorial Yawata Hospital, Kitakyushu, Japan; Takeaki Satoh: Center for Liver Disease, National Hospital Organization Kokura Medical Center, Kitakyushu, Japan; Shinji Shimoda: Department of Medicine and Biosystemic Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan; Kazuhiro Takahashi: Department of Medicine, Hamanomachi Hospital, Fukuoka, Japan; Hwai-I Yang: Genomics Research Center, Academia Sinica, Taipei, Taiwan.
Publisher Copyright:
© 2020, Asian Pacific Association for the Study of the Liver.
PY - 2020/12
Y1 - 2020/12
N2 - Background: Despite HCV cure, patients remain at risk for HCC, but risk factor data for HCC following SVR are limited for Asian patients. Methods: To address this gap, we analyzed 5814 patients (5646 SVR, 168 non-SVR) from the Real-World Evidence from the Asia Liver Consortium for HCV (REAL-C) who did not have HCC or a history of HCC at baseline (pre-DAA treatment) and did not develop HCC within 6 months of baseline. To assess the effect of SVR on HCC incidence, we used 1:4 propensity score matching [(PSM), age, sex, baseline cirrhosis, and baseline AFP] to balance the SVR and non-SVR groups. Results: In the PSM cohort (160 non-SVR and 612 SVR), the HCC incidence rate per 100 person years was higher in the non-SVR compared to the SVR group (5.26 vs. 1.94, p < 0.001). Achieving SVR was independently associated with decreased HCC risk (adjusted HR [aHR]: 0.41, p = 0.002). Next, we stratified the SVR cohort of 5646 patients to cirrhotic and noncirrhotic subgroups. Among cirrhotic SVR patients, aged ≥ 60, having an albumin bilirubin grade (ALBI) of 2 or 3 (aHR: 2.5, p < 0.001), and baseline AFP ≥ 10 ng/mL (aHR: 1.6, p = 0.001) were associated with higher HCC risk, while among the non-cirrhotic SVR group, only baseline AFP ≥ 10 ng/mL was significant (aHR: 4.26, p = 0.005). Conclusions: Achieving SVR decreases HCC risk; however, among East Asians, patients with elevated pretreatment AFP remained at risk. Pretreatment AFP, an easily obtained serum marker, may provide both prognostic and surveillance value for HCC in East Asian patients who obtained SVR.
AB - Background: Despite HCV cure, patients remain at risk for HCC, but risk factor data for HCC following SVR are limited for Asian patients. Methods: To address this gap, we analyzed 5814 patients (5646 SVR, 168 non-SVR) from the Real-World Evidence from the Asia Liver Consortium for HCV (REAL-C) who did not have HCC or a history of HCC at baseline (pre-DAA treatment) and did not develop HCC within 6 months of baseline. To assess the effect of SVR on HCC incidence, we used 1:4 propensity score matching [(PSM), age, sex, baseline cirrhosis, and baseline AFP] to balance the SVR and non-SVR groups. Results: In the PSM cohort (160 non-SVR and 612 SVR), the HCC incidence rate per 100 person years was higher in the non-SVR compared to the SVR group (5.26 vs. 1.94, p < 0.001). Achieving SVR was independently associated with decreased HCC risk (adjusted HR [aHR]: 0.41, p = 0.002). Next, we stratified the SVR cohort of 5646 patients to cirrhotic and noncirrhotic subgroups. Among cirrhotic SVR patients, aged ≥ 60, having an albumin bilirubin grade (ALBI) of 2 or 3 (aHR: 2.5, p < 0.001), and baseline AFP ≥ 10 ng/mL (aHR: 1.6, p = 0.001) were associated with higher HCC risk, while among the non-cirrhotic SVR group, only baseline AFP ≥ 10 ng/mL was significant (aHR: 4.26, p = 0.005). Conclusions: Achieving SVR decreases HCC risk; however, among East Asians, patients with elevated pretreatment AFP remained at risk. Pretreatment AFP, an easily obtained serum marker, may provide both prognostic and surveillance value for HCC in East Asian patients who obtained SVR.
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U2 - 10.1007/s12072-020-10105-2
DO - 10.1007/s12072-020-10105-2
M3 - Article
C2 - 33277685
AN - SCOPUS:85097134034
VL - 14
SP - 1023
EP - 1033
JO - Hepatology International
JF - Hepatology International
SN - 1936-0533
IS - 6
ER -