Evidence map›Paper›PMID 39959584›Full record

ArticleFrontiers in immunology2024

Analysis of fatty acid-derived lipids in critically ill patients after cardiac surgery yields novel pathophysiologically relevant mediators with possible relevance for systemic inflammatory reactions.

Holger Neb, Verena Roth, Jessica Roos, Tom Bauer, Anja Urbschat, Ulrike Heinicke, Carlo Angioni, Dieter Steinhilber, Matthias Piesche, Nerea Ferreirós and 8 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Clinical lipidomics in bacterial sepsis: a systematic review of serum and plasma evaluations.Metabolomics : Official journal of the Metabolomic Society · 2026
    Pooled it
  2. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors.

Holger NebDepartment of Anesthesiology, Intensive Care Medicine and Pain Therapy, Frankfurt University Hospital, Goethe University Frankfurt, Frankfurt, Germany.
Verena RothDepartment of Immunology, Paul-Ehrlich-Institute (Federal Institute for Vaccines and Biomedicines), Langen, Germany.
Jessica RoosDepartment of Anesthesiology, Intensive Care Medicine and Pain Therapy, Frankfurt University Hospital, Goethe University Frankfurt, Frankfurt, Germany.
Tom BauerDepartment of Immunology, Paul-Ehrlich-Institute (Federal Institute for Vaccines and Biomedicines), Langen, Germany.
Anja UrbschatDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Ulrike HeinickeDepartment of Anesthesiology, Intensive Care Medicine and Pain Therapy, Frankfurt University Hospital, Goethe University Frankfurt, Frankfurt, Germany.
Carlo AngioniInstitute of Clinical Pharmacology, Frankfurt University Hospital, Frankfurt, Germany.
Dieter SteinhilberInstitute of Pharmaceutical Chemistry, Goethe University Frankfurt, Frankfurt, Germany.
Matthias PiescheBiomedical Research Laboratories, Medicine Faculty, Universidad Católica del Maule, Talca, Chile.
Nerea FerreirósInstitute of Clinical Pharmacology, Frankfurt University Hospital, Frankfurt, Germany.
Robert GurkeInstitute of Clinical Pharmacology, Frankfurt University Hospital, Frankfurt, Germany.
Gerd GeisslingerInstitute of Clinical Pharmacology, Frankfurt University Hospital, Frankfurt, Germany.
Edith UtechDepartment of Anesthesiology, Intensive Care Medicine and Pain Therapy, Frankfurt University Hospital, Goethe University Frankfurt, Frankfurt, Germany.
Kai ZacharowskiDepartment of Anesthesiology, Intensive Care Medicine and Pain Therapy, Frankfurt University Hospital, Goethe University Frankfurt, Frankfurt, Germany.
Patrick MeybohmDepartment of Anesthesiology, Intensive Care Medicine and Pain Therapy, Frankfurt University Hospital, Goethe University Frankfurt, Frankfurt, Germany.
Patrick Paulus *Laboratory for Experimental Anesthesiology, Johannes Kepler University (JKU), Linz, Austria, Department of Anesthesiology and Operative Intensive Care Medicine, Kepler University Hospital Linz, Linz, Austria.
Elke Schmitt *Department of Anesthesiology, Intensive Care Medicine and Pain Therapy, Frankfurt University Hospital, Goethe University Frankfurt, Frankfurt, Germany.
Thorsten Jürgen Maier *Department of Anesthesiology, Intensive Care Medicine and Pain Therapy, Frankfurt University Hospital, Goethe University Frankfurt, Frankfurt, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: 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-PGF 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.

Indexed as

Cardiac Surgical ProceduresFatty AcidsInflammationInflammation MediatorsLipidsSystemic Inflammatory Response SyndromeAgedBiomarkersChromatography, LiquidCritical IllnessFemaleHumansIntensive Care UnitsMaleMiddle AgedTandem Mass SpectrometryBiomarkersFatty AcidsInflammation MediatorsLipidsbiomarkerceramideseicosanoidsendocannabinoidsprostaglandinssphingolipidssystemic inflammation

Identifiers

PMID39959584
PMCPMC11826806

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.