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dc.contributor.authorNeb, Holger
dc.contributor.authorRoth, Verena
dc.contributor.authorRoos, Jessica
dc.contributor.authorBauer, Tom
dc.contributor.authorUrbschat, Anja
dc.contributor.authorHeinicke, Ulrike
dc.contributor.authorAngioni, Carlo
dc.contributor.authorSteinhilber, Dieter
dc.contributor.authorPiesche, Matthias
dc.contributor.authorFerreirós, Nerea
dc.contributor.authorGurke, Robert
dc.contributor.authorGeisslinger, Gerd
dc.contributor.authorUtech, Edith
dc.contributor.authorZacharowski, Kai D.
dc.contributor.authorMeybohm, Patrick
dc.contributor.authorPaulus, Patrick
dc.contributor.authorSchmitt, Elke
dc.contributor.authorJürgen Maier, Thorsten
dc.date.accessioned2025-04-28T18:39:18Z
dc.date.available2025-04-28T18:39:18Z
dc.date.issued2025
dc.identifier.urihttp://repositorio.ucm.cl/handle/ucm/6013
dc.description.abstractIntroduction: Critically ill patients suffer from a wide variety of clinical events, most of them leading to pro-inflammatory states such as sepsis or simply as consequence of major surgery. Many of these patients develop forms of acute kidney injury, heart or acute liver failure during intensive care. Lipid signaling is critically involved in triggering systemic inflammation processes, pain and vascular tone. We therefore hypothesized that fatty-acid-derived lipid mediators might be regulated during inflammatory stages and other clinical events in critically ill patients and might serve as potential biomarker candidates. Methods and study design: Using liquid chromatography-tandem mass spectrometry (LC-MS/MS), we determined the levels of 53 lipid mediators in plasma from nine patients. These patients were hospitalized at Frankfurt University Hospital’s intensive care unit (ICU) after cardiac surgery. Inflammatory stages were illustrated over time using clinically established biomarkers such as interleukin-6 (IL-6) and leukocyte count. Normal range values of the lipids were obtained from healthy volunteers. Results: Plasma levels clearly outside the normal range were observed for 22 of 53 lipid mediators, of which 13 were increased (including ceramides Cer (d18:0/18:0), Cer (d18:1/16:0), Cer (d18:1/18:1), glucosyl-ceramide GluCer (d18:1/24:1), lactosylceramide LacCer (d18:1/18:0), and LacCer (d18:1/24:1), 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha), 11,12- and 14,15-DHET and 1- and 2-arachidonoyl glycerol (1-AG and 2-AG), Sphingosine SPH (d18:1) and 20-HETE. Furthermore, nine lipids were decreased (Cer (d18:1/24:0), LacCer (d18:1/16:0), LacCer (d18:1/24:0), sphingosine-1-phosphate S1P (d18:1), S1P (d18:0), the lysophosphatidic acids LPA (16:0), LPA (18:0), LPA (18:1) and 9-HODE. Among increased lipids, the remarkable changes in 1-AG, 2-AG, and to a lower extent of 6-keto-PGF1-alpha plasma levels showed a certain agreement with inflammatory phases. Furthermore, 6-keto-PGF1alpha had its peak shortly before initiation of continuous veno-venous hemodialysis (at least in 5 of the observed patients), 2-AG was elevated in all our nine patients during (right) heart failure in the context of either re-opening patient’s chest, implementation of veno-arterial ECMO or at least while significantly increasing the amount of catecholamines. Discussion: In this pilot trial we identified several evaluated lipids in critically ill patients representing either potentially (patho-) physiologically relevant mediators of the pro-inflammatory processes and during heart failure or possible markers preceding veno-venous hemodialysis.es_CL
dc.language.isoenes_CL
dc.rightsAtribución-NoComercial-SinDerivadas 3.0 Chile*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
dc.sourceFrontiers in Immunology, 15, 1148806es_CL
dc.subjectEicosanoidses_CL
dc.subjectProstaglandinses_CL
dc.subjectSphingolipidses_CL
dc.subjectCeramideses_CL
dc.subjectEndocannabinoidses_CL
dc.subjectSystemic inflammationes_CL
dc.subjectBiomarkeres_CL
dc.titleAnalysis of fatty acid-derived lipids in critically ill patients after cardiac surgery yields novel pathophysiologically relevant mediators with possible relevance for systemic inflammatory reactionses_CL
dc.typeArticlees_CL
dc.ucm.facultadFacultad de Medicinaes_CL
dc.ucm.indexacionScopuses_CL
dc.ucm.indexacionIsies_CL
dc.ucm.urifrontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1148806/fulles_CL
dc.ucm.doidoi.org/10.3389/fimmu.2024.1148806es_CL


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