Evidence map›Paper›PMID 18316629›Full record

Trial reportBlood2008

Hyperglycemia enhances coagulation and reduces neutrophil degranulation, whereas hyperinsulinemia inhibits fibrinolysis during human endotoxemia.

Michiel E Stegenga, Saskia N van der Crabben, Regje M E Blümer, Marcel Levi, Joost C M Meijers, Mireille J Serlie, Michael W T Tanck, Hans P Sauerwein, Tom van der Poll

Open access · bronzeAbstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed, 5 pooled it
7.4field-weighted citation impact, top 2% 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

160 citing papers in PubMed, 5 syntheses or guidelines pooled it, 357 citations in OpenAlex.

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100 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 3 countries.

Michiel E StegengaCenter for Infection and Immunity Amsterdam, Bioinformatics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. m.e.stegenga@amc.uva.nl
Saskia N van der Crabben
Regje M E Blümer
Marcel Levi
Joost C M Meijers
Mireille J Serlie
Michael W T Tanck
Hans P Sauerwein
Tom van der Poll
Center for Vascular Biology Research · USAcademic Medical Center · NLCenter for Molecular Medicine and Immunology · USInstitute of Infection and Immunity · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes is associated with altered immune and hemostatic responses. We investigated the selective effects of hyperglycemia and hyperinsulinemia on innate immune, coagulation, and fibrinolytic responses during systemic inflammation. Twenty-four healthy humans were studied for 8 hours during clamp experiments in which either plasma glucose, insulin, both, or none was increased, depending on randomization. Target plasma concentrations were 5 versus 12 mM for glucose, and 100 versus 400 pmol/L for insulin. After 3 hours, 4 ng/kg Escherichia coli endotoxin was injected intravenously to induce a systemic inflammatory and procoagulant response. Endotoxin administration induced cytokine release, activation of neutrophils, endothelium and coagulation, and inhibition of fibrinolysis. Hyperglycemia reduced neutrophil degranulation (plasma elastase levels, P < .001) and exaggerated coagulation (plasma concentrations of thrombin-antithrombin complexes and soluble tissue factor, both P < .001). Hyperinsulinemia attenuated fibrinolytic activity due to elevated plasminogen activator-inhibitor-1 levels (P < .001). Endothelial cell activation markers and cytokine concentrations did not differ between clamps. We conclude that in humans with systemic inflammation induced by intravenous endotoxin administration hyperglycemia impairs neutrophil degranulation and potentiates coagulation, whereas hyperinsulinemia inhibits fibrinolysis. These data suggest that type 2 diabetes patients may be especially vulnerable to prothrombotic events during inflammatory states.

Indexed as

AdultBlood CoagulationCell DegranulationCytokinesDiabetes Mellitus, Type 2Endothelial CellsEndotoxemiaEndotoxinsFibrinolysisGlucose Clamp TechniqueHumansHyperglycemiaHyperinsulinismImmunity, InnateInflammation MediatorsMaleCytokinesEndotoxinsInflammation Mediators

Identifiers

PMID18316629
PMCPMC2435690
OpenAlexW2027627028

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.