Serum miR-181b-5p predicts ascites onset in patients with compensated cirrhosis.

Ascites CSPH, clinically significant portal hypertension Ct, cycle threshold HVPG, hepatic venous pressure gradient NSBBs, non-selective beta-blockers ROC, receiver-operating characteristic beta-blockers cirrhosis miRNAs, microRNAs microRNA portal hypertension

Journal

JHEP reports : innovation in hepatology
ISSN: 2589-5559
Titre abrégé: JHEP Rep
Pays: Netherlands
ID NLM: 101761237

Informations de publication

Date de publication:
Dec 2021
Historique:
received: 05 07 2021
revised: 19 08 2021
accepted: 08 09 2021
entrez: 29 10 2021
pubmed: 30 10 2021
medline: 30 10 2021
Statut: epublish

Résumé

Treatment with non-selective beta-blockers (NSBBs) reduces the risk of ascites, which is the most common decompensating event in cirrhosis. This study aimed to assess the ability of a serum microRNA (miRNA) signature to predict ascites formation and the hemodynamic response to NSBBs in compensated cirrhosis. Serum levels of miR-452-5p, miR-429, miR-885-5p, miR-181b-5p, and miR-122-5p were analyzed in patients with compensated cirrhosis (N = 105). Hepatic venous pressure gradient (HVPG) was measured at baseline, after intravenous propranolol, and 1 year after randomization to NSBBs (n = 52) or placebo (n = 53) (PREDESCI trial). miRNAs were analyzed at baseline and at 1 year. Nineteen patients (18%) developed ascites, of whom 17 developed ascites after 1 year. miR-181b-5p levels at 1 year, but not at baseline, were higher in patients that developed ascites. The AUC of miR-181b-5p at 1 year to predict ascites was 0.7 (95% CI 0.59-0.78). miR-429 levels were lower at baseline in acute HVPG responders to NSBBs (AUC 0.65; 95% CI, 0.53-0.76), but levels at baseline and at 1 year were not associated with the HVPG response to NSBBs at 1 year. Serum miR-181b-5p is a promising non-invasive biomarker to identify patients with compensated cirrhosis at risk of ascites development. Ascites marks the transition from the compensated to decompensated stage in cirrhosis and indicates a worsening in prognosis. There are currently no easily accessible tools to identify patients with compensated cirrhosis at risk of developing ascites. We evaluated the levels of novel molecules termed microRNAs in the blood of patients with compensated cirrhosis and observed that miR-181b-5p can predict which patients are going to develop ascites.

Sections du résumé

BACKGROUND & AIMS OBJECTIVE
Treatment with non-selective beta-blockers (NSBBs) reduces the risk of ascites, which is the most common decompensating event in cirrhosis. This study aimed to assess the ability of a serum microRNA (miRNA) signature to predict ascites formation and the hemodynamic response to NSBBs in compensated cirrhosis.
METHODS METHODS
Serum levels of miR-452-5p, miR-429, miR-885-5p, miR-181b-5p, and miR-122-5p were analyzed in patients with compensated cirrhosis (N = 105). Hepatic venous pressure gradient (HVPG) was measured at baseline, after intravenous propranolol, and 1 year after randomization to NSBBs (n = 52) or placebo (n = 53) (PREDESCI trial). miRNAs were analyzed at baseline and at 1 year.
RESULTS RESULTS
Nineteen patients (18%) developed ascites, of whom 17 developed ascites after 1 year. miR-181b-5p levels at 1 year, but not at baseline, were higher in patients that developed ascites. The AUC of miR-181b-5p at 1 year to predict ascites was 0.7 (95% CI 0.59-0.78). miR-429 levels were lower at baseline in acute HVPG responders to NSBBs (AUC 0.65; 95% CI, 0.53-0.76), but levels at baseline and at 1 year were not associated with the HVPG response to NSBBs at 1 year.
CONCLUSIONS CONCLUSIONS
Serum miR-181b-5p is a promising non-invasive biomarker to identify patients with compensated cirrhosis at risk of ascites development.
LAY SUMMARY BACKGROUND
Ascites marks the transition from the compensated to decompensated stage in cirrhosis and indicates a worsening in prognosis. There are currently no easily accessible tools to identify patients with compensated cirrhosis at risk of developing ascites. We evaluated the levels of novel molecules termed microRNAs in the blood of patients with compensated cirrhosis and observed that miR-181b-5p can predict which patients are going to develop ascites.

Identifiants

pubmed: 34712934
doi: 10.1016/j.jhepr.2021.100368
pii: S2589-5559(21)00144-0
pmc: PMC8531668
doi:

Types de publication

Journal Article

Langues

eng

Pagination

100368

Informations de copyright

© 2021 The Authors.

Déclaration de conflit d'intérêts

The authors have declared that no personal or financial competing interests exist. Please refer to the accompanying ICMJE disclosure forms for further details.

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Auteurs

Ana Garcia Garcia de Paredes (A)

Gastroenterology and Hepatology Department, Hospital Universitario Ramon y Cajal, Instituto Ramon y Cajal de Investigacion Sanitaria (IRYCIS), Universidad de Alcala, Madrid, Spain.

Càndid Villanueva (C)

Hospital of Santa Creu and Sant Pau, Autonomous University of Barcelona, Hospital Sant Pau Biomedical Research Institute (IIB Sant Pau) Barcelona, Spain.
Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Spain.

Carolina Blanco (C)

Biomarkers and Therapeutic Targets Group, Instituto Ramon y Cajal de Investigacion Sanitaria (IRYCIS), Madrid, Spain.

Joan Genescà (J)

Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Spain.
Liver Unit, Vall d'Hebron University Hospital, Vall d'Hebron Institute of Research (VHIR), Vall d'Hebron Barcelona Hospital campus, Autonomous University of Barcelona, Barcelona, Spain.

Nicolo Manicardi (N)

Liver Vascular Biology Research Group, IDIBAPS Biomedical Research Institute, Barcelona, Spain.

Juan Carlos Garcia-Pagan (JC)

Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Spain.
Barcelona Hepatic Haemodynamic Laboratory, Liver Unit, Institute of Digestive and Metabolic Diseases, August Pi i Sunyer Institute of Biomedical Research, Hospital Clínic, Barcelona, Spain.

Jose Luis Calleja (JL)

Gastroenterology and Hepatology Department, Hospital Universitario Puerta de Hierro, Puerta de Hierro Hospital Research Institute, Autonomous University of Madrid, Madrid, Spain.

Carlos Aracil (C)

Institute of Biomedical Research, Arnau de Vilanova University Hospital (IRB Lleida), Lleida, Spain.

Rosa M Morillas (RM)

Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Spain.
Liver Section, Hospital Universitari Germans Trias i Pujol, IGTP, Badalona, Spain.
Universitat Autònoma de Barcelona, Spain.

Maria Poca (M)

Hospital of Santa Creu and Sant Pau, Autonomous University of Barcelona, Hospital Sant Pau Biomedical Research Institute (IIB Sant Pau) Barcelona, Spain.

Beatriz Peñas (B)

Gastroenterology and Hepatology Department, Hospital Universitario Ramon y Cajal, Instituto Ramon y Cajal de Investigacion Sanitaria (IRYCIS), Universidad de Alcala, Madrid, Spain.

Salvador Augustin (S)

Liver Unit, Vall d'Hebron University Hospital, Vall d'Hebron Institute of Research (VHIR), Vall d'Hebron Barcelona Hospital campus, Autonomous University of Barcelona, Barcelona, Spain.

Juan G Abraldes (JG)

Barcelona Hepatic Haemodynamic Laboratory, Liver Unit, Institute of Digestive and Metabolic Diseases, August Pi i Sunyer Institute of Biomedical Research, Hospital Clínic, Barcelona, Spain.
Liver Unit, Division of Gastroenterology, University of Alberta, Edmonton, Canada.

Eldimar Alvarado (E)

Hospital of Santa Creu and Sant Pau, Autonomous University of Barcelona, Hospital Sant Pau Biomedical Research Institute (IIB Sant Pau) Barcelona, Spain.

Félix Royo (F)

Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Spain.
Exosomes Laboratory, Center for Cooperative Research in Biosciencies (CIC bioGUNE), Basque Research and Technology Alliance (BRTA), Derio, Bizkaia, 48160, Spain.

Maria Laura Garcia-Bermejo (ML)

Biomarkers and Therapeutic Targets Group, Instituto Ramon y Cajal de Investigacion Sanitaria (IRYCIS), Madrid, Spain.

Juan Manuel Falcon-Perez (JM)

Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Spain.
Exosomes Laboratory, Center for Cooperative Research in Biosciencies (CIC bioGUNE), Basque Research and Technology Alliance (BRTA), Derio, Bizkaia, 48160, Spain.

Rafael Bañares (R)

Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Spain.
Gastroenterology and Hepatology Department, Hospital Universitario Gregorio Marañon, Instituto de Investigacion Sanitaria Gregorio Marañon (IiSGM), Universidad Complutense de Madrid, Madrid, Spain.

Jaime Bosch (J)

Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Spain.
Barcelona Hepatic Haemodynamic Laboratory, Liver Unit, Institute of Digestive and Metabolic Diseases, August Pi i Sunyer Institute of Biomedical Research, Hospital Clínic, Barcelona, Spain.
Department of Biomedical Research and University Clinic for Visceral Medicine and Surgery, Inselspital, Bern, Switzerland.

Jordi Gracia-Sancho (J)

Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Spain.
Liver Vascular Biology Research Group, IDIBAPS Biomedical Research Institute, Barcelona, Spain.

Agustin Albillos (A)

Gastroenterology and Hepatology Department, Hospital Universitario Ramon y Cajal, Instituto Ramon y Cajal de Investigacion Sanitaria (IRYCIS), Universidad de Alcala, Madrid, Spain.
Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Spain.

Classifications MeSH