<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Blaya D</submitter><funding>National Institute on Alcohol Abuse and Alcoholism</funding><funding>Instituto de Salud Carlos III</funding><funding>NIDDK NIH HHS</funding><funding>NIAAA NIH HHS</funding><funding>Ministerio de Educación, Cultura y Deporte</funding><funding>ERAB: The European Foundation for Alcohol Research</funding><pagination>1006-1017</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10113804</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(4)</volume><pubmed_abstract>&lt;h4>Objectives&lt;/h4>Alcoholic hepatitis (AH) is a severe condition characterized by a marked inflammatory response and high short-term mortality. Endothelial dysfunction (ED) is an early event in vascular and inflammatory disorders. The aim of this study is to evaluate ED in AH patients.&lt;h4>Methods&lt;/h4>Prognostic value of ED biomarkers was evaluated in patients with severe AH (n = 67), compensated alcoholic cirrhosis (n = 15), heavy drinkers without liver disease (n = 15) and controls (n = 9), and in a validation cohort of 50 patients with AH. Gene expression of ED markers was analyzed in liver tissue.&lt;h4>Results&lt;/h4>Plasma levels of ED markers such as vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), E-selectin and von Willebrand factor (vWF) increased</pubmed_abstract><journal>Hepatology international</journal><pubmed_title>Endothelial dysfunction markers predict short-term mortality in patients with severe alcoholic hepatitis.</pubmed_title><pmcid>PMC10113804</pmcid><funding_grant_id>P30 DK120531</funding_grant_id><funding_grant_id>FIS PI12/01265</funding_grant_id><funding_grant_id>CPII16/00041</funding_grant_id><funding_grant_id>U01 AA026972</funding_grant_id><funding_grant_id>FIS PI17/00673</funding_grant_id><funding_grant_id>PI20/00765</funding_grant_id><funding_grant_id>EA1653</funding_grant_id><funding_grant_id>1U01AA021908</funding_grant_id><funding_grant_id>U01 AA021908</funding_grant_id><funding_grant_id>FPU</funding_grant_id><funding_grant_id>1U01AA021908-01-33490</funding_grant_id><pubmed_authors>Tanguy M</pubmed_authors><pubmed_authors>Altamirano J</pubmed_authors><pubmed_authors>Pose E</pubmed_authors><pubmed_authors>Bataller R</pubmed_authors><pubmed_authors>Sancho-Bru P</pubmed_authors><pubmed_authors>Rubio-Tomas T</pubmed_authors><pubmed_authors>Argemi J</pubmed_authors><pubmed_authors>Issoufaly T</pubmed_authors><pubmed_authors>Caballeria J</pubmed_authors><pubmed_authors>Lozano J</pubmed_authors><pubmed_authors>Morales-Ibanez O</pubmed_authors><pubmed_authors>Blaya D</pubmed_authors><pubmed_authors>Rodrigo-Torres D</pubmed_authors><pubmed_authors>Affo S</pubmed_authors><pubmed_authors>Gratacos-Gines J</pubmed_authors><pubmed_authors>Coll M</pubmed_authors><pubmed_authors>Rautou PE</pubmed_authors></additional><is_claimable>false</is_claimable><name>Endothelial dysfunction markers predict short-term mortality in patients with severe alcoholic hepatitis.</name><description>&lt;h4>Objectives&lt;/h4>Alcoholic hepatitis (AH) is a severe condition characterized by a marked inflammatory response and high short-term mortality. Endothelial dysfunction (ED) is an early event in vascular and inflammatory disorders. The aim of this study is to evaluate ED in AH patients.&lt;h4>Methods&lt;/h4>Prognostic value of ED biomarkers was evaluated in patients with severe AH (n = 67), compensated alcoholic cirrhosis (n = 15), heavy drinkers without liver disease (n = 15) and controls (n = 9), and in a validation cohort of 50 patients with AH. Gene expression of ED markers was analyzed in liver tissue.&lt;h4>Results&lt;/h4>Plasma levels of ED markers such as vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), E-selectin and von Willebrand factor (vWF) increased</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Aug</publication><modification>2025-04-04T00:03:46.213Z</modification><creation>2025-04-04T00:03:46.213Z</creation></dates><accession>S-EPMC10113804</accession><cross_references><pubmed>33954832</pubmed><doi>10.1007/s12072-021-10165-y</doi></cross_references></HashMap>