TY  - JOUR
A1  - Trebicka, Jonel
A1  - Amoros, Alex
A1  - Pitarch, Carla
A1  - Titos, Esther
A1  - Alcaraz Quiles, Francisco José
A1  - Schierwagen, Robert
A1  - Deulofeu, Carmen
A1  - Fernandez-Gomez, Javier
A1  - Piano, Salvatore
A1  - Caraceni, Paolo
A1  - Öttl, Karl
A1  - Solà, Elsa
A1  - Laleman, Wim
A1  - McNaughtan, Jane
A1  - Mookerjee, Rajeshwar Prosad
A1  - Coenraad, Minneke J.
A1  - Welzel, Tania Mara
A1  - Steib, Christian Johannes
A1  - Garcia, Rita
A1  - Gustot, Thierry
A1  - Rodriguez Gandia, Miguel A.
A1  - Bañares, Rafael
A1  - Albillos, Agustin
A1  - Zeuzem, Stefan
A1  - Vargas Blasco, Victor Manuel
A1  - Saliba, Faouzi
A1  - Nevens, Frederic
A1  - Alessandria, Carlo
A1  - De Gottardi, Andrea
A1  - Zoller, Heinz
A1  - Ginès, Pere
A1  - Sauerbruch, Tilman
A1  - Gerbes, Alexander L.
A1  - Stauber, Rudolf E.
A1  - Bernardi, Mauro
A1  - Angeli, Paolo
A1  - Pavesi, Marco
A1  - Moreau, Richard
A1  - Clària, Joan
A1  - Jalan, Rajiv
A1  - Arroyo, Vicente
T1  - Addressing profiles of systemic inflammation across the different clinical phenotypes of acutely decompensated cirrhosis
T2  - Frontiers in immunology
N2  - 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.
KW  - acute decompensation
KW  - cirrhosis
KW  - signature
KW  - ACLF
KW  - organ failure
KW  - organ dysfunction
Y1  - 2019
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/52567
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-525677
SN  - 1664-3224
N1  - Copyright © 2019 Trebicka, Amoros, Pitarch, Titos, Alcaraz-Quiles, Schierwagen, Deulofeu, Fernandez-Gomez, Piano, Caraceni, Oettl, Sola, Laleman, McNaughtan, Mookerjee, Coenraad, Welzel, Steib, Garcia, Gustot, Rodriguez Gandia, Bañares, Albillos, Zeuzem, Vargas, Saliba, Nevens, Alessandria, de Gottardi, Zoller, Ginès, Sauerbruch, Gerbes, Stauber, Bernardi, Angeli, Pavesi, Moreau, Clària, Jalan and Arroyo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
VL  - 10
IS  - Art. 476
SP  - 1
EP  - 12
PB  - Frontiers Media
CY  - Lausanne
ER  -