Rong Fan1, George Papatheodoridis2, Jian Sun1, Hamish Innes3, Hidenori Toyoda4, Qing Xie5, Shuyuan Mo6, Vana Sypsa7, Indra Neil Guha8, Takashi Kumada9, Junqi Niu10, George Dalekos11, Satoshi Yasuda4, Eleanor Barnes12, Jianqi Lian13, Vithika Suri6, Ramazan Idilman14, Stephen T Barclay15, Xiaoguang Dou16, Thomas Berg17, Peter C Hayes18, John F Flaherty6, Yuanping Zhou1, Zhengang Zhang19, Maria Buti20, Sharon J Hutchinson3, Yabing Guo1, Jose Luis Calleja21, Lanjia Lin6, Longfeng Zhao22, Yongpeng Chen1, Harry L A Janssen23, Chaonan Zhu24, Lei Shi24, Xiaoping Tang25, Anuj Gaggar6, Lai Wei26, Jidong Jia27, William L Irving8, Philip J Johnson28, Pietro Lampertico29, Jinlin Hou30. 1. State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China. 2. Department of Gastroenterology, Medical School of National and Kapodistrian University of Athens, Laiko General Hospital, Athens, Greece. 3. Glasgow Caledonian University, School of Health and Life Sciences, Glasgow, UK. 4. Department of Gastroenterology and Hepatology, Ogaki Municipal Hospital, Ogaki, Japan. 5. Department of Infectious Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. 6. Gilead Sciences, Foster City, CA, USA. 7. Department of Hygiene, Epidemiology & Medical Statistics, Medical School of National and Kapodistrian University of Athens, Athens, Greece. 8. NIHR Nottingham Biomedical Research Centre, Nottingham University Hospitals NHS Trust and the University of Nottingham, Nottingham, UK. 9. Department of Nursing, Gifu Kyoritsu University, Ogaki, Japan. 10. Department of Hepatology, First Hospital, Jilin University, Changchun, China. 11. Department of Internal Medicine, Thessalia University Medical School, Larissa, Greece. 12. Peter Medawar Building for Pathogen Research, Nuffield Department of Medicine and the Oxford NIHR Biomedical Research Centre, Oxford University, Oxford, UK. 13. Centers of Infectious Diseases, Tangdu Hospital, the Fourth Military Medical University, Xi'an, China. 14. Department of Gastroenterology, University of Ankara Medical School, Ankara, Turkey. 15. Glasgow Royal Infirmary, Glasgow, UK. 16. Department of Infectious Diseases, Shengjing Hospital of China Medical University, Shenyang, China. 17. Division of Hepatology, Clinic and Polyclinic for Gastroenterology, Hepatology Infectious Disease and Pneumology, University Clinic Leipzig, Leipzig, Germany. 18. Royal Infirmary of Edinburgh, Edinburgh, UK. 19. Department of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. 20. Hospital General Universitario Valle Hebron and Ciberehd, Barcelona, Spain. 21. Hospital U Puerta de Hierro, IDIPHIM CIBERehd, Madrid, Spain. 22. Department of Infectious Diseases, First Hospital of Shanxi Medical University, Taiyuan, China. 23. Liver Clinic, Toronto Western & General Hospital, University Health Network, Toronto, ON, Canada. 24. Big Data Research and Biostatistics Center, Hangzhou YITU Healthcare Technology Co. Ltd., Hangzhou, China. 25. Guangzhou Eighth People's Hospital, Guangzhou, China. 26. Peking University Hepatology Institute, Peking University People's Hospital, Beijing, China. 27. Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, China. 28. Department of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, UK. Electronic address: Philip.Johnson@liverpool.ac.uk. 29. Foundation IRCCS Ca' Granda Ospedale Maggiore Policlinico - Division of Gastroenterology and Hepatology - CRC 'A.M. and A. Migliavacca' Center for Liver Disease, Milan, Italy; Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy. Electronic address: pietro.lampertico@unimi.it. 30. State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China. Electronic address: jlhousmu@163.com.
Abstract
BACKGROUND & AIMS: Hepatocellular carcinoma (HCC) is the leading cause of death in patients with chronic hepatitis. In this international collaboration, we sought to develop a global universal HCC risk score to predict the HCC development for patients with chronic hepatitis. METHODS: A total of 17,374 patients, comprising 10,578 treated Asian patients with chronic hepatitis B (CHB), 2,510 treated Caucasian patients with CHB, 3,566 treated patients with hepatitis C virus (including 2,489 patients with cirrhosis achieving a sustained virological response) and 720 patients with non-viral hepatitis (NVH) from 11 international prospective observational cohorts or randomised controlled trials, were divided into a training cohort (3,688 Asian patients with CHB) and 9 validation cohorts with different aetiologies and ethnicities (n = 13,686). RESULTS: We developed an HCC risk score, called the aMAP score (ranging from 0 to 100), that involves only age, male, albumin-bilirubin and platelets. This metric performed excellently in assessing HCC risk not only in patients with hepatitis of different aetiologies, but also in those with different ethnicities (C-index: 0.82-0.87). Cut-off values of 50 and 60 were best for discriminating HCC risk. The 3- or 5-year cumulative incidences of HCC were 0-0.8%, 1.5-4.8%, and 8.1-19.9% in the low- (n = 7,413, 43.6%), medium- (n = 6,529, 38.4%), and high-risk (n = 3,044, 17.9%) groups, respectively. The cut-off value of 50 was associated with a sensitivity of 85.7-100% and a negative predictive value of 99.3-100%. The cut-off value of 60 resulted in a specificity of 56.6-95.8% and a positive predictive value of 6.6-15.7%. CONCLUSIONS: This objective, simple, reliable risk score based on 5 common parameters accurately predicted HCC development, regardless of aetiology and ethnicity, which could help to establish a risk score-guided HCC surveillance strategy worldwide. LAY SUMMARY: In this international collaboration, we developed and externally validated a simple, objective and accurate prognostic tool (called the aMAP score), that involves only age, male, albumin-bilirubin and platelets. The aMAP score (ranged from 0 to 100) satisfactorily predicted the risk of hepatocellular carcinoma (HCC) development among over 17,000 patients with viral and non-viral hepatitis from 11 global prospective studies. Our findings show that the aMAP score had excellent discrimination and calibration in assessing the 5-year HCC risk among all the cohorts irrespective of aetiology and ethnicity.
BACKGROUND & AIMS: Hepatocellular carcinoma (HCC) is the leading cause of death in patients with chronic hepatitis. In this international collaboration, we sought to develop a global universal HCC risk score to predict the HCC development for patients with chronic hepatitis. METHODS: A total of 17,374 patients, comprising 10,578 treated Asian patients with chronic hepatitis B (CHB), 2,510 treated Caucasian patients with CHB, 3,566 treated patients with hepatitis C virus (including 2,489 patients with cirrhosis achieving a sustained virological response) and 720 patients with non-viral hepatitis (NVH) from 11 international prospective observational cohorts or randomised controlled trials, were divided into a training cohort (3,688 Asian patients with CHB) and 9 validation cohorts with different aetiologies and ethnicities (n = 13,686). RESULTS: We developed an HCC risk score, called the aMAP score (ranging from 0 to 100), that involves only age, male, albumin-bilirubin and platelets. This metric performed excellently in assessing HCC risk not only in patients with hepatitis of different aetiologies, but also in those with different ethnicities (C-index: 0.82-0.87). Cut-off values of 50 and 60 were best for discriminating HCC risk. The 3- or 5-year cumulative incidences of HCC were 0-0.8%, 1.5-4.8%, and 8.1-19.9% in the low- (n = 7,413, 43.6%), medium- (n = 6,529, 38.4%), and high-risk (n = 3,044, 17.9%) groups, respectively. The cut-off value of 50 was associated with a sensitivity of 85.7-100% and a negative predictive value of 99.3-100%. The cut-off value of 60 resulted in a specificity of 56.6-95.8% and a positive predictive value of 6.6-15.7%. CONCLUSIONS: This objective, simple, reliable risk score based on 5 common parameters accurately predicted HCC development, regardless of aetiology and ethnicity, which could help to establish a risk score-guided HCC surveillance strategy worldwide. LAY SUMMARY: In this international collaboration, we developed and externally validated a simple, objective and accurate prognostic tool (called the aMAP score), that involves only age, male, albumin-bilirubin and platelets. The aMAP score (ranged from 0 to 100) satisfactorily predicted the risk of hepatocellular carcinoma (HCC) development among over 17,000 patients with viral and non-viral hepatitis from 11 global prospective studies. Our findings show that the aMAP score had excellent discrimination and calibration in assessing the 5-year HCC risk among all the cohorts irrespective of aetiology and ethnicity.
Authors: Jérémy Dana; Aïna Venkatasamy; Antonio Saviano; Joachim Lupberger; Yujin Hoshida; Valérie Vilgrain; Pierre Nahon; Caroline Reinhold; Benoit Gallix; Thomas F Baumert Journal: Hepatol Int Date: 2022-02-09 Impact factor: 9.029