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

Clària, Joan; Stauber, Rudolf E; Coenraad, Minneke J; Moreau, Richard; Jalan, Rajiv; Pavesi, Marco; Amorós, Àlex; Titos, Esther; Alcaraz-Quiles, José; Oettl, Karl; Morales-Ruiz, Manuel; Angeli, Paolo; Domenicali, Marco; Alessandria, Carlo; Gerbes, Alexander; Wendon, Julia; Nevens, Frederik; Trebicka, Jonel; Laleman, Wim; Saliba, Faouzi; ... (2016). Systemic inflammation in decompensated cirrhosis: Characterization and role in acute-on-chronic liver failure. Hepatology, 64(4), pp. 1249-1264. Wiley Interscience 10.1002/hep.28740

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UNLABELLED 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).

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > BioMedical Research (DBMR) > DBMR Forschung Mu35 > Forschungsgruppe Hepatologie
04 Faculty of Medicine > Pre-clinic Human Medicine > BioMedical Research (DBMR) > DBMR Forschung Mu35 > Forschungsgruppe Hepatologie

04 Faculty of Medicine > Department of Gastro-intestinal, Liver and Lung Disorders (DMLL) > Clinic of Visceral Surgery and Medicine > Hepatology

UniBE Contributor:

De Gottardi, Andrea

Subjects:

600 Technology > 610 Medicine & health

ISSN:

0270-9139

Publisher:

Wiley Interscience

Language:

English

Submitter:

Lilian Karin Smith-Wirth

Date Deposited:

05 Apr 2017 12:49

Last Modified:

05 Apr 2017 12:49

Publisher DOI:

10.1002/hep.28740

PubMed ID:

27483394

BORIS DOI:

10.7892/boris.93573

URI:

https://boris.unibe.ch/id/eprint/93573

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