Systemic inflammation in decompensated cirrhosis Characterization and role in acute-on-chronic liver failure
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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; Welzel, Tania M; Albillos, Agustin; Gustot, Thierry; Benten, Daniel; Durand, François; Ginès, Pere; Bernardi, Mauro; Arroyo, Vicente; CANONIC Study Investigators of the EASL-CLIF Consortium and the European Foundation for the Study of Chronic Liver Failure (EF-CLIF).
in: HEPATOLOGY, Jahrgang 64, Nr. 4, 10.2016, S. 1249-64.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Systemic inflammation in decompensated cirrhosis Characterization and role in acute-on-chronic liver failure
AU - Clària, Joan
AU - Stauber, Rudolf E
AU - Coenraad, Minneke J
AU - Moreau, Richard
AU - Jalan, Rajiv
AU - Pavesi, Marco
AU - Amorós, Àlex
AU - Titos, Esther
AU - Alcaraz-Quiles, José
AU - Oettl, Karl
AU - Morales-Ruiz, Manuel
AU - Angeli, Paolo
AU - Domenicali, Marco
AU - Alessandria, Carlo
AU - Gerbes, Alexander
AU - Wendon, Julia
AU - Nevens, Frederik
AU - Trebicka, Jonel
AU - Laleman, Wim
AU - Saliba, Faouzi
AU - Welzel, Tania M
AU - Albillos, Agustin
AU - Gustot, Thierry
AU - Benten, Daniel
AU - Durand, François
AU - Ginès, Pere
AU - Bernardi, Mauro
AU - Arroyo, Vicente
AU - CANONIC Study Investigators of the EASL-CLIF Consortium and the European Foundation for the Study of Chronic Liver Failure (EF-CLIF)
AU - Lohse, Ansgar Wilhelm
AU - Wege, Henning
N1 - © 2016 by the American Association for the Study of Liver Diseases.
PY - 2016/10
Y1 - 2016/10
N2 - 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).
AB - 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).
KW - Journal Article
U2 - 10.1002/hep.28740
DO - 10.1002/hep.28740
M3 - SCORING: Journal article
C2 - 27483394
VL - 64
SP - 1249
EP - 1264
JO - HEPATOLOGY
JF - HEPATOLOGY
SN - 0270-9139
IS - 4
ER -
