Transition to decompensation and acute-on-chronic liver failure: Role of predisposing factors and precipitating events.


Journal

Journal of hepatology
ISSN: 1600-0641
Titre abrégé: J Hepatol
Pays: Netherlands
ID NLM: 8503886

Informations de publication

Date de publication:
07 2021
Historique:
received: 23 09 2020
revised: 08 12 2020
accepted: 08 12 2020
entrez: 27 5 2021
pubmed: 28 5 2021
medline: 8 2 2022
Statut: ppublish

Résumé

The transition from compensated to decompensated cirrhosis results from a complex interplay of predisposing and precipitating factors and represents an inflection point in the probability of a patient surviving. With the progression of cirrhosis, patients accumulate multiple disorders (e.g. altered liver architecture, portal hypertension, local and systemic inflammation, bacterial translocation, gut dysbiosis, kidney vasoconstriction) that predispose them to decompensation. On the background of these factors, precipitating events (e.g. bacterial infection, alcoholic hepatitis, variceal haemorrhage, drug-induced liver injury, flare of liver disease) lead to acute decompensation (ascites, hepatic encephalopathy, variceal bleeding, jaundice) and/or organ failures, which characterise acute-on-chronic liver failure. In this review paper, we will discuss the current hypotheses and latest evidences regarding predisposing and precipitating factors associated with the transition to decompensated liver disease.

Identifiants

pubmed: 34039491
pii: S0168-8278(20)33842-3
doi: 10.1016/j.jhep.2020.12.005
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

S36-S48

Informations de copyright

Copyright © 2020 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of interest TG gives advice to Promethera Biosciences, Martin Pharmaceuticals, Goliver therapeutics, and Abbvie and has received grants from Gilead. VS has received speaker’s honoraria/travel expenses from Astellas, Institut Allergosan, Fresenius, MSD, Gilead and research support: Institut Allergosan, Fresenius, Winclove Probiotics. MT received a grant from Novartis. CA and WL have nothing to disclose. Please refer to the accompanying ICMJE disclosure forms for further details.

Auteurs

Thierry Gustot (T)

Dept. Gastroenterology and Hepato-Pancreatology, C.U.B. Erasme Hospital, Brussels, Belgium; Laboratory of Experimental Gastroenterology, Université Libre de Bruxelles, Brussels, Belgium; Inserm Unité 1149, Centre de Recherche sur l'inflammation (CRI), Paris, France; UMR S_1149, Université Paris Diderot, Paris, France; The EASL-CLIF Consortium, European Foundation-CLIF, Barcelona, Spain. Electronic address: thierry.gustot@erasme.ulb.ac.be.

Vanessa Stadlbauer (V)

Department of Internal Medicine, Division of Gastroenterology and Hepatology, Medical University of Graz, Auenbruggerplatz 15, 8036, Graz, Austria; Center of Biomarker Research in Medicine (CBmed), Graz, Austria.

Wim Laleman (W)

Department of Gastroenterology and Hepatology, Section of Liver and Biliopancreatic disorders, University Hospitals Leuven, KULeuven, Belgium.

Carlo Alessandria (C)

Division of Gastroenterology and Hepatology, Città della Salute e della Scienza Hospital, University of Turin, Turin, Italy.

Mark Thursz (M)

Division of Digestive Diseases, Imperial College, London, UK.

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