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      Health disparities in chronic liver disease

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          Abstract

          The syndemic of hazardous alcohol consumption, opioid use, and obesity has led to important changes in liver disease epidemiology that have exacerbated health disparities. Health disparities occur when plausibly avoidable health differences are experienced by socially disadvantaged populations. Highlighting health disparities, their sources, and consequences in chronic liver disease is fundamental to improving liver health outcomes. There have been large increases in alcohol use disorder in women, racial and ethnic minorities, and those experiencing poverty in the context of poor access to alcohol treatment, leading to increasing rates of alcohol‐associated liver diseases. Rising rates of NAFLD and associated fibrosis have been observed in Hispanic persons, women aged > 50, and individuals experiencing food insecurity. Access to viral hepatitis screening and linkage to treatment are suboptimal for racial and ethnic minorities and individuals who are uninsured or underinsured, resulting in greater liver‐related mortality and later‐stage diagnoses of HCC. Data from more diverse cohorts on autoimmune and cholestatic liver diseases are lacking, supporting the need to study the contemporary epidemiology of these disorders in greater detail. Herein, we review the existing literature on racial and ethnic, gender, and socioeconomic disparities in chronic liver diseases using a social determinants of health framework to better understand how social and structural factors cause health disparities and affect chronic liver disease outcomes. We also propose potential solutions to eliminate disparities, outlining health‐policy, health‐system, community, and individual solutions to promote equity and improve health outcomes.

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          Most cited references179

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          Update on prevention, diagnosis, and treatment of chronic hepatitis B: AASLD 2018 hepatitis B guidance.

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            Burden of liver diseases in the world

            Liver disease accounts for approximately 2 million deaths per year worldwide, 1 million due to complications of cirrhosis and 1million due to viral hepatitis and hepatocellular carcinoma. Cirrhosis is currently the 11th most common cause of death globally and liver cancer is the 16th leading cause of death; combined, they account for 3.5% of all deaths worldwide. Cirrhosis is within the top 20 causes of disability-adjusted life years and years of life lost, accounting for 1.6% and 2.1% of the worldwide burden. About 2 billion people consume alcohol worldwide and upwards of 75 million are diagnosed with alcohol-use disorders and are at risk of alcohol-associated liver disease. Approximately 2 billion adults are obese or overweight and over 400 million have diabetes; both of which are risk factors for non-alcoholic fatty liver disease and hepatocellular carcinoma. The global prevalence of viral hepatitis remains high, while drug-induced liver injury continues to increase as a major cause of acute hepatitis. Liver transplantation is the second most common solid organ transplantation, yet less than 10% of global transplantation needs are met at current rates. Though these numbers are sobering, they highlight an important opportunity to improve public health given that most causes of liver diseases are preventable.
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              Genetic variation in PNPLA3 confers susceptibility to nonalcoholic fatty liver disease

              Nonalcoholic fatty liver disease (NAFLD) is a burgeoning health problem of unknown etiology that varies in prevalence among ethnic groups. To identify genetic variants contributing to differences in hepatic fat content, we performed a genome-wide association scan of nonsynonymous sequence variations (n=9,229) in a multiethnic population. An allele in PNPLA3 (rs738409; I148M) was strongly associated with increased hepatic fat levels (P=5.9×10−10) and with hepatic inflammation (P=3.7×10−4). The allele was most common in Hispanics, the group most susceptible to NAFLD; hepatic fat content was > 2-fold higher in PNPLA3-148M homozygotes than in noncarriers. Resequencing revealed another allele associated with lower hepatic fat content in African-Americans, the group at lowest risk of NAFLD. Thus, variation in PNPLA3 contributes to ethnic and inter-individual differences in hepatic fat content and susceptibility to NAFLD.
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                Author and article information

                Contributors
                Journal
                Hepatology
                Hepatology
                HEP
                Hepatology (Baltimore, Md.)
                Lippincott Williams & Wilkins (Hagerstown, MD )
                0270-9139
                1527-3350
                April 2023
                04 September 2022
                : 77
                : 4
                : 1382-1403
                Affiliations
                [1 ] Division of Gastrointestinal and Liver Diseases , University of Southern California , Los Angeles, California, USA
                [2 ] Division of Gastroenterology and Hepatology , University of Pennsylvania Perelman School of Medicine , Philadelphia, Pennsylvania, USA
                [3 ] Corporal Michael J. Crescenz VA Medical Center , Philadelphia, Pennsylvania, USA
                [4 ] Leonard Davis Institute of Health Economics , University of Pennsylvania , Philadelphia, Pennsylvania, USA
                [5 ] Division of Gastroenterology and Hepatology, Department of Medicine , Indiana University School of Medicine , Indianapolis, Indiana, USA
                [6 ] Indiana University Simon Comprehensive Cancer Center , Indianapolis, Indiana, USA
                Author notes
                Correspondence Lauren D. Nephew, Division of Gastroenterology and Hepatology, Department of Medicine, Indiana University School of Medicine, 702 Rotary Circle, Indianapolis, IN 46202, USA. Email: lnephew@ 123456iu.edu
                Article
                00030
                10.1002/hep.32743
                10026975
                35993341
                19bb32a1-5162-430a-a853-7bf0a6774b16
                Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc.

                This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0/

                History
                : 14 June 2022
                : 15 March 2022
                : 16 June 2022
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                Gastroenterology & Hepatology
                Gastroenterology & Hepatology

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