Evidence map›Paper›PMID 31019718›Full record

ArticleJournal of intensive care2019

Loss of sphingosine 1-phosphate (S1P) in septic shock is predominantly caused by decreased levels of high-density lipoproteins (HDL).

Martin Sebastian Winkler, Konstantin B Märtz, Axel Nierhaus, Günter Daum, Edzard Schwedhelm, Stefan Kluge, Markus H Gräler

Open access · goldAbstract read
In one paragraph

Article in Journal of intensive care, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
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

36 citing papers in PubMed, 47 citations in OpenAlex.

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  5. Blood-borne sphingosine 1-phosphate maintains vascular resistance, blood pressure, and cardiac function in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

7 authors at 2 institutions in 2 countries.

Martin Sebastian Winkler1Department of Anesthesiology, University Medical Center Hamburg-Eppendorf, Martinistr. 52, Hamburg, 20246 Germany.
Konstantin B Märtz2Department of Anesthesiology and Intensive Care Medicine, Center for Sepsis Control and Care (CSCC), and the Center for Molecular Biomedicine (CMB), Jena University Hospital, Hans-Knöll-Str. 2, 07745 Jena, Germany.
Axel Nierhaus3Department of Intensive Care Medicine, University Medical Center Hamburg-Eppendorf, Martinistr. 52, Hamburg, 20246 Germany.
Günter Daum4Clinic and Polyclinic for Vascular Medicine, University Heart Center, Martinistrasse 52, 20246 Hamburg, Germany.
Edzard Schwedhelm5Institute of Clinical Pharmacology and Toxicology, University Medical Center Hamburg-Eppendorf, Martinistr. 52, Hamburg, 20246 Germany.
Stefan Kluge3Department of Intensive Care Medicine, University Medical Center Hamburg-Eppendorf, Martinistr. 52, Hamburg, 20246 Germany.
Markus H Gräler2Department of Anesthesiology and Intensive Care Medicine, Center for Sepsis Control and Care (CSCC), and the Center for Molecular Biomedicine (CMB), Jena University Hospital, Hans-Knöll-Str. 2, 07745 Jena, Germany.ORCID 0000-0001-6650-7849
Universität Hamburg · DEJena University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSphingosine 1-phosphate (S1P) is a signaling lipid essential in regulating processes involved in sepsis pathophysiology, including endothelial permeability and vascular tone. Serum S1P is progressively reduced in sepsis patients with increasing severity. S1P function depends on binding to its carriers: serum albumin (SA) and high-density lipoproteins (HDL). The aim of this single-center prospective observational study was to determine the contribution of SA- and HDL-associated S1P (SA-S1P and HDL-S1P) to sepsis-induced S1P depletion in plasma with regard to identify future strategies to supplement vasoprotective S1P.

methodsSequential precipitation of lipoproteins was performed with plasma samples obtained from 100 ICU patients: surgical trauma (

resultsPlasma S1P levels significantly decreased with sepsis severity and showed a strong negative correlation with increased organ failure, quantified by the Sequential Organ Failure Assessment (SOFA) score (rho - 0.59,

conclusionsReduced plasma S1P was associated with sepsis-induced organ failure. A constant plasma S1P level during the acute phase after surgery was maintained with increased HDL-S1P and decreased SA-S1P, suggesting the redistribution of plasma S1P from SA to HDL. The decrease of plasma S1P levels in patients with increasing sepsis severity was mainly caused by decreasing HDL and HDL-S1P. Therefore, strategies to reconstitute HDL-S1P rather than SA-S1P should be considered for sepsis patients.

Indexed as

Endothelial cell barrierSepsisSequential Organ Failure AssessmentSerum albuminVolume resuscitation

Identifiers

PMID31019718
PMCPMC6472014
OpenAlexW2945041032

What Socratic holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.