Progressive systemic inflammation precedes decompensation in compensated cirrhosis
Sánchez-Aldehuelo, Rubén (Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas)
Villanueva, Càndid (Institut de Recerca Sant Pau)
Genescà Ferrer, Joan (Hospital Universitari Vall d'Hebron)
García-Pagán, JC (Hospital Clínic i Provincial de Barcelona)
Castillo, Elisa (Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas)
Calleja, Jose Luis (Hospital Universitario Puerta de Hierro Majadahonda (Madrid))
Aracil, Carlos (Hospital Universitari Arnau de Vilanova)
Bañares, Rafael (Hospital General Universitario Gregorio Marañón)
Téllez, Luis (Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas)
Paule, Lorena (Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas)
Morillas Cunill, Rosa Ma (Institut Germans Trias i Pujol. Hospital Universitari Germans Trias i Pujol)
Poca Sans, Maria (Institut de Recerca Sant Pau)
Peñas, Beatriz (Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas)
Augustin Recio, Salvador (Hospital Universitari Vall d'Hebron)
Abraldes, Juan G. (University of Alberta)
Alvarado-Tapias, Edilmar (Institut de Recerca Sant Pau)
Bosch, Jaume (University of Bern)
Albillos, Agustín (Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas)
Universitat Autònoma de Barcelona

Data:	2024
Resum:	Systemic inflammation is a driver of decompensation in cirrhosis with unclear relevance in the compensated stage. We evaluated inflammation and bacterial translocation markers in compensated cirrhosis and their dynamics in relation to the first decompensation. This study is nested within the PREDESCI trial, which investigated non-selective beta-blockers for preventing decompensation in compensated cirrhosis and clinically significant portal hypertension (CSPH: hepatic venous pressure gradient ≥10 mmHg). Blood biomarkers were measured at baseline and at 1 and 2 years in patients who remained compensated and had available samples (n = 164). Values of patients with CSPH were split at each time point by decompensation development in the next time interval after sampling. We also included 54 patients with cirrhosis and subclinical portal hypertension (PH) and 35 controls. We assessed markers of inflammation (interleukin-6 [IL-6], tumor necrosis factor-alpha, von Willebrand factor [vWF], C-reactive protein), macrophage activation (CD14, CD163), intestinal barrier integrity (fatty acid-binding protein [FABP], haptoglobin), and bacterial translocation (lipopolysaccharide [LPS]). IL-6, CD163, and vWF were higher (p < 0. 01) at baseline in patients with cirrhosis and CSPH compared to those with subclinical PH and controls. IL-6 increased (p < 0. 05) at 1 year in patients with CSPH, with a greater rise in those who developed decompensation. CD163 was higher (p < 0. 01) in patients who decompensated at baseline and 1 and 2 years. FABP was elevated (p < 0. 01) in patients with CSPH compared to subclinical PH and controls at baseline and 1 year, while haptoglobin was lower (p < 0. 01). LPS was higher (p < 0. 01) in patients with CSPH than in those with subclinical PH and controls and increased at 1 year regardless of decompensation development. Inflammation and bacterial products are present in the systemic circulation in patients with compensated cirrhosis and CSPH. Progressive inflammation precedes the first decompensation. Systemic inflammation drives cirrhosis progression during the decompensated stage, but its role in the compensated stage is unclear. We evaluated biomarkers of systemic inflammation, intestinal barrier integrity and bacterial translocation in patients with compensated cirrhosis and their dynamics in relation to the first decompensation. We demonstrate that low-grade inflammation and bacterial products are present in the systemic circulation in compensated cirrhosis, provided clinically significant portal hypertension has developed. We also show that worsening of systemic inflammation precedes the development of first clinical decompensation.
Drets:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Llengua:	Anglès
Document:	Article ; recerca ; Versió publicada
Matèria:	Cytokine ; Bacterial translocation ; Portal hypertension ; Chronic advanced liver disease ; Immunity
Publicat a:	JHEP Reports, Vol. 7 (october 2024) , ISSN 2589-5559

DOI: 10.1016/j.jhepr.2024.101231
PMID: 39850960

7 p, 582.3 KB

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Documents de recerca > Documents dels grups de recerca de la UAB > Centres i grups de recerca (producció científica) > Ciències de la salut i biociències > Institut d'Investigació en Ciencies de la Salut Germans Trias i Pujol (IGTP)
Documents de recerca > Documents dels grups de recerca de la UAB > Centres i grups de recerca (producció científica) > Ciències de la salut i biociències > Institut de Recerca Sant Pau
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