TY - JOUR
T1 - Systematic review with meta-analysis
T2 - risk of hepatocellular carcinoma in non-alcoholic steatohepatitis without cirrhosis compared to other liver diseases
AU - Stine, Jonathan G.
AU - Wentworth, Brian J.
AU - Zimmet, Alex
AU - Rinella, Mary E.
AU - Loomba, Rohit
AU - Caldwell, Stephen H.
AU - Argo, Curtis K.
N1 - Funding Information:
Declaration of personal interests: Mary Rinella has served as a speaker, a consultant and an advisory board member for Intercept, Genfit, Echosens, and has received research funding from Novartis. Mary Rinella has served in an advisory role for Gilead, Novartis, Immuron, NGM Bio, NuSirt, Enanta Pharmaceuticals and BMS. Stephen Caldwell has served as a consultant and an advisory board member for Shionogi, and has received research funding from Gilead, GenFit, Conatus, Galmed, Taiwan J, Intercept, Vital Therapy and Mallinckrodt. Rohit Loomba has served as a consultant for Bird Rock Bio, BMS, Coh Bar, Celgene, Civi Bio, Conatus, Enanta, Gilead, GRI Bio, Ionis, Metacrine, NGM, Receptos, Sanofi, Salix, Kowa, Median technologies; he served as a consultant for Bird Rock Bio, BMS, Coh Bar, Celgene, Civi Bio, Conatus, Enanta, Gilead, GRI Bio, Ionis, Meta-crine, NGM, Receptos, Sanofi, Salix, Kowa, Median technologies; he also received grants from Nuisirt, Allergan, BMS, Boehringer Ingle-heim, Eli Lily, Galectin, Galmed, GE, Genfit, Gilead, Intercept, Jans-sen, Madrigal, NGM, Prometheus, Siemens, Shire, Pfizer; he is also a Co-Founder of Liponexus Inc.
Funding Information:
Declaration of funding interests: This work was supported in part by grant funding from the National Institutes of Health (grant 5T32DK007769‐15). This work was also supported by a Transplant Hepatology Fellowship Award from the American Association for the Study of Liver Diseases (AASLD).
Funding Information:
We would like to thank Puja M. Shah MD, MSc for their help with the systematic review search process. Declaration of personal interests: Mary Rinella has served as a speaker, a consultant and an advisory board member for Intercept, Genfit, Echosens, and has received research funding from Novartis. Mary Rinella has served in an advisory role for Gilead, Novartis, Immuron, NGM Bio, NuSirt, Enanta Pharmaceuticals and BMS. Stephen Caldwell has served as a consultant and an advisory board member for Shionogi, and has received research funding from Gilead, GenFit, Conatus, Galmed, Taiwan J, Intercept, Vital Therapy and Mallinckrodt. Rohit Loomba has served as a consultant for Bird Rock Bio, BMS, Coh Bar, Celgene, Civi Bio, Conatus, Enanta, Gilead, GRI Bio, Ionis, Metacrine, NGM, Receptos, Sanofi, Salix, Kowa, Median technologies; he served as a consultant for Bird Rock Bio, BMS, Coh Bar, Celgene, Civi Bio, Conatus, Enanta, Gilead, GRI Bio, Ionis, Metacrine, NGM, Receptos, Sanofi, Salix, Kowa, Median technologies; he also received grants from Nuisirt, Allergan, BMS, Boehringer Ingleheim, Eli Lily, Galectin, Galmed, GE, Genfit, Gilead, Intercept, Janssen, Madrigal, NGM, Prometheus, Siemens, Shire, Pfizer; he is also a Co-Founder of Liponexus Inc. Declaration of funding interests: This work was supported in part by grant funding from the National Institutes of Health (grant 5T32DK007769-15). This work was also supported by a Transplant Hepatology Fellowship Award from the American Association for the Study of Liver Diseases (AASLD).
Publisher Copyright:
© 2018 John Wiley & Sons Ltd
PY - 2018/10
Y1 - 2018/10
N2 - Background: Given the lack of long-term prospective studies, it is challenging for clinicians to make informed decisions about screening and treatment decisions regarding the risk of hepatocellular carcinoma (HCC) in patients with non-alcoholic steatohepatitis (NASH) who do not have cirrhosis. Aim: To characterise the pooled risk of HCC in the non-cirrhosis population. Methods: Published studies were identified through April 2016 in MEDLINE, Scopus, Science Citation Index, AMED and the Cochrane Library. Two independent reviewers screened citations and extracted data. Random effect odds ratios (OR) were calculated to obtain aggregate estimates of effect size between NASH and non-NASH groups. Between-study variability and heterogeneity were assessed. Results: Nineteen studies with 168 571 participants were included. Eighty-six per cent of included subjects had cirrhosis. The prevalence of HCC in non-cirrhotic NASH was 38.0%; among other aetiologies in non-cirrhotics, it was 14.2% (P < 0.001). Non-cirrhotic NASH subjects were at greater odds of developing HCC than non-cirrhotic subjects of other aetiologies (OR 2.61, 95% CI 1.27-5.35, P = 0.009). When examining all NASH subjects either with or without cirrhosis, those with NASH as the underlying liver disease did not have a significantly increased risk of HCC (OR 1.43, 95% CI 0.77-2.65, P = 0.250). Conclusions: In non-cirrhotic subjects, those with NASH have a higher risk of HCC compared to other aetiologies of liver disease. Further study investigating the risk factors of HCC among non-cirrhotic NASH patients is needed.
AB - Background: Given the lack of long-term prospective studies, it is challenging for clinicians to make informed decisions about screening and treatment decisions regarding the risk of hepatocellular carcinoma (HCC) in patients with non-alcoholic steatohepatitis (NASH) who do not have cirrhosis. Aim: To characterise the pooled risk of HCC in the non-cirrhosis population. Methods: Published studies were identified through April 2016 in MEDLINE, Scopus, Science Citation Index, AMED and the Cochrane Library. Two independent reviewers screened citations and extracted data. Random effect odds ratios (OR) were calculated to obtain aggregate estimates of effect size between NASH and non-NASH groups. Between-study variability and heterogeneity were assessed. Results: Nineteen studies with 168 571 participants were included. Eighty-six per cent of included subjects had cirrhosis. The prevalence of HCC in non-cirrhotic NASH was 38.0%; among other aetiologies in non-cirrhotics, it was 14.2% (P < 0.001). Non-cirrhotic NASH subjects were at greater odds of developing HCC than non-cirrhotic subjects of other aetiologies (OR 2.61, 95% CI 1.27-5.35, P = 0.009). When examining all NASH subjects either with or without cirrhosis, those with NASH as the underlying liver disease did not have a significantly increased risk of HCC (OR 1.43, 95% CI 0.77-2.65, P = 0.250). Conclusions: In non-cirrhotic subjects, those with NASH have a higher risk of HCC compared to other aetiologies of liver disease. Further study investigating the risk factors of HCC among non-cirrhotic NASH patients is needed.
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U2 - 10.1111/apt.14937
DO - 10.1111/apt.14937
M3 - Review article
C2 - 30136293
AN - SCOPUS:85052622554
SN - 0269-2813
VL - 48
SP - 696
EP - 703
JO - Alimentary Pharmacology and Therapeutics
JF - Alimentary Pharmacology and Therapeutics
IS - 7
ER -