Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/130741
Title: Addressing profiles of systemic inflammation across the different clinical phenotypes of acutely decompensated cirrhosis
Author: Trebicka, Jonel
Amorós, Àlex
Pitarch Abaigar, Carla
Titos Rodríguez, Esther
Alcaraz-Quiles, José
Schierwagen, Robert
Deulofeu, Carme
Fernández Gómez, Javier
Piano, Salvatore
Caraceni, Paolo
Oettl, Karl
Sola, Elsa
Laleman, Wim
McNaughtan, Jane
Mookerjee, Rajeshwar P.
Coenraad, Minneke J.
Welzel, Tania
Steib, Christian
García, Rita
Gustot, Thierry
Rodríguez Gandia, Miguel A.
Bañares, Rafael
Albillos, Agustín
Zeuzem, Stefan
Vargas, Víctor
Saliba, Faouzi
Nevens, Frederik
Alessandria, Carlo
Gottardi, Andrea de
Zoller, Heinz
Ginès i Gibert, Pere
Sauerbruch, Tilman
Gerbes, Alexander
Stauber, Rudolf E.
Bernardi, Mauro
Angeli, Paolo
Pavesi, Marco
Moreuau, Richard
Clària i Enrich, Joan
Arroyo, Vicente
Jalan, Rajiv
Keywords: Cirrosi hepàtica
Inflamació
Malalties del fetge
Hepatic cirrhosis
Inflammation
Liver diseases
Issue Date: 19-Mar-2019
Publisher: Frontiers Media
Abstract: Background: Patients with acutely decompensated cirrhosis (AD) may or may not develop acute-on-chronic liver failure (ACLF). ACLF is characterized by high-grade systemic inflammation, organ failures (OF) and high short-term mortality. Although patients with AD cirrhosis exhibit distinct clinical phenotypes at baseline, they have low short-term mortality, unless ACLF develops during follow-up. Because little is known about the association of profile of systemic inflammation with clinical phenotypes of patients with AD cirrhosis, we aimed to investigate a battery of markers of systemic inflammation in these patients. Methods: Upon hospital admission baseline plasma levels of 15 markers (cytokines, chemokines, and oxidized albumin) were measured in 40 healthy controls, 39 compensated cirrhosis, 342 AD cirrhosis, and 161 ACLF. According to EASL-CLIF criteria, AD cirrhosis was divided into three distinct clinical phenotypes (AD-1: Creatinine<1.5, no HE, no OF; AD-2: creatinine 1.5-2, and or HE grade I/II, no OF; AD-3: Creatinine<1.5, no HE, non-renal OF). Results: Most markers were slightly abnormal in compensated cirrhosis, but markedly increased in AD. Patients with ACLF exhibited the largest number of abnormal markers, indicating "full-blown" systemic inflammation (all markers). AD-patients exhibited distinct systemic inflammation profiles across three different clinical phenotypes. In each phenotype, activation of systemic inflammation was only partial (30% of the markers). Mortality related to each clinical AD-phenotype was significantly lower than mortality associated with ACLF (p < 0.0001 by gray test). Among AD-patients baseline systemic inflammation (especially IL-8, IL-6, IL-1ra, HNA2 independently associated) was more intense in those who had poor 28-day outcomes (ACLF, death) than those who did not experience these outcomes. Conclusions: Although AD-patients exhibit distinct profiles of systemic inflammation depending on their clinical phenotypes, all these patients have only partial activation of systemic inflammation. However, those with the most extended baseline systemic inflammation had the highest the risk of ACLF development and death.
Note: Reproducció del document publicat a: https://doi.org/10.3389/fimmu.2019.00476
It is part of: Frontiers in Immunology, 2019, vol. 10, p. 476
URI: http://hdl.handle.net/2445/130741
Related resource: https://doi.org/10.3389/fimmu.2019.00476
ISSN: 1664-3224
Appears in Collections:Articles publicats en revistes (IDIBAPS: Institut d'investigacions Biomèdiques August Pi i Sunyer)
Articles publicats en revistes (Biomedicina)

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