Global burden of disease: acute-on-chronic liver failure, a systematic review and meta-analysis.


Journal

Gut
ISSN: 1468-3288
Titre abrégé: Gut
Pays: England
ID NLM: 2985108R

Informations de publication

Date de publication:
01 2022
Historique:
received: 10 06 2020
revised: 22 12 2020
accepted: 23 12 2020
pubmed: 14 1 2021
medline: 11 1 2022
entrez: 13 1 2021
Statut: ppublish

Résumé

Acute-on-chronic liver failure (ACLF) is characterised by acute decompensation of cirrhosis associated with organ failures. We systematically evaluated the geographical variations of ACLF across the world in terms of prevalence, mortality, aetiology of chronic liver disease (CLD), triggers and organ failures. We searched EMBASE and PubMed from 3/1/2013 to 7/3/2020 using the ACLF-EASL-CLIF (European Association for the Study of the Liver-Chronic Liver Failure) criteria. Two investigators independently conducted the abstract selection/abstraction of the aetiology of CLD, triggers, organ failures and prevalence/mortality by presence/grade of ACLF. We grouped countries into Europe, East/South Asia and North/South America. We calculated the pooled proportions, evaluated the methodological quality using the Newcastle-Ottawa Scale and statistical heterogeneity, and performed sensitivity analyses. We identified 2369 studies; 30 cohort studies met our inclusion criteria (43 206 patients with ACLF and 140 835 without ACLF). The global prevalence of ACLF among patients admitted with decompensated cirrhosis was 35% (95% CI 33% to 38%), highest in South Asia at 65%. The global 90-day mortality was 58% (95% CI 51% to 64%), highest in South America at 73%. Alcohol was the most frequently reported aetiology of underlying CLD (45%, 95% CI 41 to 50). Infection was the most frequent trigger (35%) and kidney dysfunction the most common organ failure (49%). Sensitivity analyses showed regional estimates grossly unchanged for high-quality studies. Type of design, country health index, underlying CLD and triggers explained the variation in estimates. The global prevalence and mortality of ACLF are high. Region-specific variations could be explained by the type of triggers/aetiology of CLD or grade. Health systems will need to tailor early recognition and treatment of ACLF based on region-specific data.

Sections du résumé

BACKGROUND AND AIMS
Acute-on-chronic liver failure (ACLF) is characterised by acute decompensation of cirrhosis associated with organ failures. We systematically evaluated the geographical variations of ACLF across the world in terms of prevalence, mortality, aetiology of chronic liver disease (CLD), triggers and organ failures.
METHODS
We searched EMBASE and PubMed from 3/1/2013 to 7/3/2020 using the ACLF-EASL-CLIF (European Association for the Study of the Liver-Chronic Liver Failure) criteria. Two investigators independently conducted the abstract selection/abstraction of the aetiology of CLD, triggers, organ failures and prevalence/mortality by presence/grade of ACLF. We grouped countries into Europe, East/South Asia and North/South America. We calculated the pooled proportions, evaluated the methodological quality using the Newcastle-Ottawa Scale and statistical heterogeneity, and performed sensitivity analyses.
RESULTS
We identified 2369 studies; 30 cohort studies met our inclusion criteria (43 206 patients with ACLF and 140 835 without ACLF). The global prevalence of ACLF among patients admitted with decompensated cirrhosis was 35% (95% CI 33% to 38%), highest in South Asia at 65%. The global 90-day mortality was 58% (95% CI 51% to 64%), highest in South America at 73%. Alcohol was the most frequently reported aetiology of underlying CLD (45%, 95% CI 41 to 50). Infection was the most frequent trigger (35%) and kidney dysfunction the most common organ failure (49%). Sensitivity analyses showed regional estimates grossly unchanged for high-quality studies. Type of design, country health index, underlying CLD and triggers explained the variation in estimates.
CONCLUSIONS
The global prevalence and mortality of ACLF are high. Region-specific variations could be explained by the type of triggers/aetiology of CLD or grade. Health systems will need to tailor early recognition and treatment of ACLF based on region-specific data.

Identifiants

pubmed: 33436495
pii: gutjnl-2020-322161
doi: 10.1136/gutjnl-2020-322161
doi:

Types de publication

Journal Article Meta-Analysis Research Support, Non-U.S. Gov't Systematic Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

148-155

Commentaires et corrections

Type : CommentIn
Type : CommentIn
Type : CommentIn

Informations de copyright

© Author(s) (or their employer(s)) 2022. No commercial re-use. See rights and permissions. Published by BMJ.

Déclaration de conflit d'intérêts

Competing interests: AC is a consultant for Mallinckrodt Pharmaceuticals, Boston Scientific and Shionogi, has participated on advisory boards for Mallinckrodt Pharmaceuticals, and has received grant support from Mallinckrodt and Boston Scientific. PG declares that he has received research funding from Mallinckrodt, Grifols and Gilead. He has participated on advisory boards for Novartis, Promethera, Sequana, Gilead and Martin Pharmaceuticals.

Auteurs

Gabriel Mezzano (G)

Liver Unit, Hospital Clinic de Barcelona, Barcelona, Catalunya, Spain.
Gastroenterología - Hepatología, Hospital del Salvador. Universidad de Chile, Santiago, Chile.

Adria Juanola (A)

Liver Unit, Hospital Clinic de Barcelona, Barcelona, Catalunya, Spain.
Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
Centro de Investigacion Biomedica en Red Enfermedades Hepaticas y Digestivas (CIBERehd), Madrid, Spain.

Andres Cardenas (A)

Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
Centro de Investigacion Biomedica en Red Enfermedades Hepaticas y Digestivas (CIBERehd), Madrid, Spain.
Institute of Digestive Disease and Metabolism, Hospital Clinic de Barcelona, Barcelona, Catalunya, Spain.

Esteban Mezey (E)

Division of Gastroenterology and Hepatology. Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

James P Hamilton (JP)

Division of Gastroenterology and Hepatology. Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Elisa Pose (E)

Liver Unit, Hospital Clinic de Barcelona, Barcelona, Catalunya, Spain.
Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
Centro de Investigacion Biomedica en Red Enfermedades Hepaticas y Digestivas (CIBERehd), Madrid, Spain.

Isabel Graupera (I)

Liver Unit, Hospital Clinic de Barcelona, Barcelona, Catalunya, Spain.
Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
Centro de Investigacion Biomedica en Red Enfermedades Hepaticas y Digestivas (CIBERehd), Madrid, Spain.
Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Catalunya, Spain.

Pere Ginès (P)

Liver Unit, Hospital Clinic de Barcelona, Barcelona, Catalunya, Spain.
Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
Centro de Investigacion Biomedica en Red Enfermedades Hepaticas y Digestivas (CIBERehd), Madrid, Spain.
Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Catalunya, Spain.

Elsa Solà (E)

Liver Unit, Hospital Clinic de Barcelona, Barcelona, Catalunya, Spain.
Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
Centro de Investigacion Biomedica en Red Enfermedades Hepaticas y Digestivas (CIBERehd), Madrid, Spain.
Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Catalunya, Spain.

Ruben Hernaez (R)

Gastroenterology and Hepatology, Depatment of Medicine, Baylor College of Medicine, Houston, Texas, USA ruben.hernaez@bcm.edu.
Section of Gastroenterology, Michael E DeBakey Veterans Affairs Medical Center, Houston, Texas, USA.
Center for Innovation in Quality, Effectiveness and Safety (IQuESt), Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas, USA.

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