Evidence map›Paper›PMID 41495100›Full record

Trial reportScientific reports2026

Plasma growth differentiation factor-15 is associated with cardiovascular events in patients hospitalized for acute exacerbation of COPD.

Pradeesh Sivapalan, Daniel Alexander Ackermann, Anna Kubel Vognsen, Ruth Frikke-Schmidt, Jens P Goetze, Thérèse Lappere, Christina Christoffersen, Jon Torgny Wilcke, Charlotte S Ulrik, Niklas Dyrby Johansen and 6 more

Abstract readRandomized Controlled Trial
In one paragraph

Trial report in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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

16 authors.

Pradeesh SivapalanCopenhagen Respiratory Research, Department of Medicine, Copenhagen University Hospital- Herlev and Gentofte, Copenhagen, Denmark. pradeesh.sivapalan.02@regionh.dk.
Daniel Alexander AckermannCopenhagen Respiratory Research, Department of Medicine, Copenhagen University Hospital- Herlev and Gentofte, Copenhagen, Denmark.
Anna Kubel VognsenCopenhagen Respiratory Research, Department of Medicine, Copenhagen University Hospital- Herlev and Gentofte, Copenhagen, Denmark.
Ruth Frikke-SchmidtDepartment of Clinical Medicine, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark.
Jens P GoetzeDepartment of Clinical Biochemistry, Rigshospitalet, Copenhagen University Hospital, 2100, Copenhagen, Denmark.
Thérèse LappereDepartment of Respiratory Medicine, Antwerp University Hospital, 2650, Edegem, Belgium.
Christina ChristoffersenDepartment of Clinical Biochemistry, Rigshospitalet, Copenhagen University Hospital, 2100, Copenhagen, Denmark.
Jon Torgny WilckeCopenhagen Respiratory Research, Department of Medicine, Copenhagen University Hospital- Herlev and Gentofte, Copenhagen, Denmark.
Charlotte S UlrikDepartment of Clinical Medicine, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark.
Niklas Dyrby JohansenDepartment of Cardiology, Copenhagen University Hospital - Herlev and Gentofte, Gentofte, Denmark.
Mats C Højbjerg AndersenDepartment of Cardiology, Copenhagen University Hospital - Herlev and Gentofte, Gentofte, Denmark.
Alexander G MathioudakisDivision of Immunology, Immunity to Infection and Respiratory Medicine, School of Bio-Logical Science, The University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.
Jørgen VestboCopenhagen Respiratory Research, Department of Medicine, Copenhagen University Hospital- Herlev and Gentofte, Copenhagen, Denmark.
Manan PareekDepartment of Cardiology, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark.
Tor Biering-SørensenDepartment of Cardiology, Copenhagen University Hospital - Herlev and Gentofte, Gentofte, Denmark.
Jens-Ulrik JensenCopenhagen Respiratory Research, Department of Medicine, Copenhagen University Hospital- Herlev and Gentofte, Copenhagen, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) are at increased risk of major adverse cardiovascular events (MACE) and death. Growth differentiation factor-15 (GDF-15), a marker of cellular stress and inflammation, and Syndecan-1, a marker of endothelial dysfunction, have been suggested as prognostic biomarkers in plasma for MACE. We aimed to assess their association with a combined outcome of MACE or all-cause mortality over a 5-year period. This sub-study was embedded within the randomized controlled trial CORTICOsteroid reduction in COPD (CORTICO-COP), which investigated the effects of eosinophil-guided corticosteroid therapy in patients hospitalized with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). A total of 299 patients hospitalized with AECOPD were included in this analysis. Baseline plasma concentrations of growth differentiation factor 15 (GDF-15) and Syndecan-1 were measured and stored in a biobank for later analysis. The primary outcome was MACE or all-cause mortality, secondary outcomes included heart failure, re-AECOPD, and all-cause mortality. Hazard ratios (HRs) between low and high biomarker levels were adjusted for age, smoking, sex, GOLD class, and kidney insufficiency. The area under the receiver operating curve (AUC) was reported for each model after 6 months and two years respectively. Among the 299 hospitalized AECOPD patients included in this sub-study of the randomized controlled trial CORTICOsteroid reduction in COPD (CORTICO-COP), higher baseline concentrations of GDF-15 were associated with an increased risk of the combined outcome of MACE or all-cause mortality (hazard ratio [HR] 1.68, 95% confidence interval [CI] 1.16-2.44, p = 0.007), as well as all-cause mortality alone (HR 1.5, 95% CI 1.07-2.19, p = 0.02). GDF-15 showed moderate discriminative ability for survival, with an AUC of 64% at 6 months and 60% at 2 years. No significant associations were observed between GDF-15 and heart failure or hospital re-admission due to respiratory disease. Syndecan-1 concentrations were not associated with the combined endpoint or any of the secondary outcomes. GDF-15 may identify AECOPD patients at risk of MACE and all-cause mortality. Syndecan-1 has no predictive value in AECOPD patients.

Indexed as

Cardiovascular DiseasesGrowth Differentiation Factor 15Pulmonary Disease, Chronic ObstructiveAgedBiomarkersDisease ProgressionFemaleHospitalizationHumansMaleMiddle AgedPrognosisRisk FactorsSyndecan-1BiomarkersGDF15 protein, humanGrowth Differentiation Factor 15Syndecan-1AECOPDBiomarkerCardiovascular RiskCOPDGDF-15Syndecan-1

Identifiers

PMID41495100
PMCPMC12783264

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.