Characterization of inflammatory response in acute-on-chronic liver failure and relationship with prognosis

ACLF is characterized by a systemic inflammatory response, but the cytokines involved in this process have not been well studied. The aim of this study was to characterize the systemic inflammatory response in patients with cirrhosis and ACLF and its relationship with prognosis. Fifty-five patients...

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Detalles Bibliográficos
Autores: Solé Padullés, Cristina, Solà, Elsa, Morales Ruiz, Manuel, Fernàndez, Guerau, Huelin, Patricia, Graupera, Isabel, Moreira, Rebeca, de la Prada, Gloria, Ariza Piquer, Xavier, Pose Méndez, Elisa, Fabrellas i Padrès, Núria, Kalko, Susana, Jiménez Povedano, Wladimiro, Ginès i Gibert, Pere
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2016
País:España
Institución:Universidad de Barcelona
Repositorio:Dipòsit Digital de la UB
OAI Identifier:oai:diposit.ub.edu:2445/116922
Acceso en línea:https://hdl.handle.net/2445/116922
Access Level:acceso abierto
Palabra clave:Inflamació
Insuficiència hepàtica
Malalties del fetge
Pronòstic mèdic
Cirrosi hepàtica
Inflammation
Liver failure
Liver diseases
Prognosis
Hepatic cirrhosis
Descripción
Sumario:ACLF is characterized by a systemic inflammatory response, but the cytokines involved in this process have not been well studied. The aim of this study was to characterize the systemic inflammatory response in patients with cirrhosis and ACLF and its relationship with prognosis. Fifty-five patients with cirrhosis, 26 with ACLF, were studied prospectively. Systemic inflammatory response was analyzed by measuring a large array of plasma cytokines by using a multiplex kit. A principal component analysis show noticeable differences between ACLF and decompensated cirrhosis without ACLF. Patients with ACLF had significant abnormal levels of 12 cytokines compared to those without ACLF, including: VCAM-1, VEGF-A, Fractalkine, MIP-1α, Eotaxin, IP-10, RANTES, GM-CSF, IL-1β, IL-2, ICAM-1, and MCP-1. Cytokines showing the most marked relationship with ACLF were VCAM-1 and VEGF-A (AUCROC 0.77; p = 0.001). There was a significant relationship between some of inflammatory mediators and 3-month mortality, particularly VCAM-1, ICAM-1, and GM-CSF (AUCROC>0.7; p < 0.05). Functional Enrichment Analysis showed that inflammatory markers differentially expressed in ACLF patients were enriched in leukocyte migration, particularly monocytes and macrophages, and chemotaxis pathways. In conclusion, ACLF is characterized by a marked inflammatory reaction with activation of mediators of adhesion and migration of leukocytes. The intensity of the inflammatory reaction correlates with prognosis.