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Hepatology. 2016 Oct;64(4):1249-64. doi: 10.1002/hep.28740. Epub 2016 Aug 25.

Systemic inflammation in decompensated cirrhosis: Characterization and role in acute-on-chronic liver failure.

Author information

1
Department of Biochemistry and Molecular Genetics, Hospital Clínic, IDIBAPS and CIBERehd, Barcelona, Spain.
2
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
3
Department of Gastroenterology and Hepatology, Leiden University Medical Center, Leiden, The Netherlands.
4
Inserm, U1149, Centre de Recherche sur l'Inflammation (CRI), UMRS1149; Université Paris Diderot-Paris 7, Département Hospitalo-Universitaire (DHU) UNITY; Service d'Hépatologie, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Laboratoire d'Excellence Inflamex, ComUE Sorbonne Paris Cité, Paris, France.
5
Liver Failure Group, Institute for Liver Disease Health, University College London, Royal Free Hospital, London, United Kingdom.
6
EF-CLIF and EASL-CLIF Consortium, Barcelona, Spain.
7
Institute of Physiological Chemistry, Medical University of Graz, Graz, Austria.
8
Unit of Internal Medicine and Hepatology, Department of Medicine, DIMED, University of Padova, Padova, Italy.
9
Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy.
10
Division of Gastroenterology and Hepatology, San Giovanni Battista Hospital, Torino, Italy.
11
Department of Medicine II, University Hospital LMU Munich, Liver Center Munich, Munich, Germany.
12
Kings College London, London, United Kingdom.
13
University Hospital Gasthuisberg, KU Leuven, Leuven, Belgium.
14
Department of Internal Medicine I, University of Bonn, Bonn, Germany.
15
Hôpital Paul Brousse, Université Paris-Sud, Villejuif, France.
16
J.W. Goethe University Hospital, Frankfurt, Germany.
17
Hospital Ramón y Cajal, Madrid, Spain.
18
Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium.
19
University Hospital Hamburg-Eppendorf, Hamburg, Germany.
20
Liver Unit, Hospital Clínic, IDIBAPS and CIBERehd, Barcelona, Spain. pgines@clinic.ub.es.

Abstract

Acute-on-chronic liver failure (ACLF) in cirrhosis is characterized by acute decompensation (AD), organ failure(s), and high short-term mortality. Recently, we have proposed (systemic inflammation [SI] hypothesis) that ACLF is the expression of an acute exacerbation of the SI already present in decompensated cirrhosis. This study was aimed at testing this hypothesis and included 522 patients with decompensated cirrhosis (237 with ACLF) and 40 healthy subjects. SI was assessed by measuring 29 cytokines and the redox state of circulating albumin (HNA2), a marker of systemic oxidative stress. Systemic circulatory dysfunction (SCD) was estimated by plasma renin (PRC) and copeptin (PCC) concentrations. Measurements were performed at enrollment (baseline) in all patients and sequentially during hospitalization in 255. The main findings of this study were: (1) Patients with AD without ACLF showed very high baseline levels of inflammatory cytokines, HNA2, PRC, and PCC. Patients with ACLF showed significantly higher levels of these markers than those without ACLF; (2) different cytokine profiles were identified according to the type of ACLF precipitating event (active alcoholism/acute alcoholic hepatitis, bacterial infection, and others); (3) severity of SI and frequency and severity of ACLF at enrollment were strongly associated. The course of SI and the course of ACLF (improvement, no change, or worsening) during hospitalization and short-term mortality were also strongly associated; and (4) the strength of association of ACLF with SI was higher than with SCD.

CONCLUSION:

These data support SI as the primary driver of ACLF in cirrhosis. (Hepatology 2016;64:1249-1264).

PMID:
27483394
DOI:
10.1002/hep.28740
[Indexed for MEDLINE]
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