Evidence map›Paper›PMID 39242108›Full record

ArticleLupus science & medicine2024

Learning from serum markers reflecting endothelial activation: longitudinal data in childhood-onset systemic lupus erythematosus.

Sandy C Bergkamp, Nick D Bergkamp, Mohamed Javad Wahadat, Mariken P Gruppen, Amara Nassar-Sheikh Rashid, Sander W Tas, Martine J Smit, Marjan A Versnel, J Merlijn van den Berg, Sylvia Kamphuis and 1 more

Abstract readMulticenter Study
In one paragraph

Article in Lupus science & medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

11 authors.

Sandy C BergkampDepartment of Paediatric Immunology, Rheumatology and Infectious Diseases, Emma Children's Hospital, Amsterdam University Medical Centres (AUMC), University of Amsterdam, Amsterdam, The Netherlands s.c.bergkamp@amsterdamumc.nl.ORCID 0000-0001-9737-3142
Nick D BergkampAmsterdam Institute for Molecular and Life Sciences (AIMMS), Division of Medicinal Chemistry, Faculty of Science, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Mohamed Javad WahadatDepartment of Paediatric Rheumatology, Sophia Children's Hospital, Erasmus University Medical Centre, Rotterdam, The Netherlands.ORCID 0000-0003-3961-1274
Mariken P GruppenDepartment of Paediatric Immunology, Rheumatology and Infectious Diseases, Emma Children's Hospital, Amsterdam University Medical Centres (AUMC), University of Amsterdam, Amsterdam, The Netherlands.
Amara Nassar-Sheikh RashidDepartment of Paediatric Immunology, Rheumatology and Infectious Diseases, Emma Children's Hospital, Amsterdam University Medical Centres (AUMC), University of Amsterdam, Amsterdam, The Netherlands.
Sander W TasAmsterdam Rheumatology and Immunology Centre, Department of Rheumatology and Clinical Immunology, and Laboratory for Experimental Immunology, Amsterdam University Medical Centres (AUMC), University of Amsterdam, Amsterdam, The Netherlands.
Martine J SmitAmsterdam Institute for Molecular and Life Sciences (AIMMS), Division of Medicinal Chemistry, Faculty of Science, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Marjan A VersnelDepartment of Immunology, Erasmus Medical Centre, Rotterdam, The Netherlands.ORCID 0000-0003-0245-5386
J Merlijn van den BergDepartment of Paediatric Immunology, Rheumatology and Infectious Diseases, Emma Children's Hospital, Amsterdam University Medical Centres (AUMC), University of Amsterdam, Amsterdam, The Netherlands.
Sylvia KamphuisDepartment of Paediatric Rheumatology, Sophia Children's Hospital, Erasmus University Medical Centre, Rotterdam, The Netherlands.ORCID 0000-0002-1964-352X
Dieneke Schonenberg-MeinemaDepartment of Paediatric Immunology, Rheumatology and Infectious Diseases, Emma Children's Hospital, Amsterdam University Medical Centres (AUMC), University of Amsterdam, Amsterdam, The Netherlands.ORCID 0000-0001-9416-6631

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesIn childhood-onset SLE (cSLE), patients have an increased risk of premature atherosclerosis. The pathophysiological mechanisms for this premature atherosclerosis are not yet completely understood, but besides traditional risk factors, the endothelium plays a major role. The first aim of this study was to measure levels of SLE-associated markers involved in endothelial cell (EC) function and lipids in a cSLE cohort longitudinally in comparison with healthy controls (HC). Next aim was to correlate these levels with Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) and nailfold capillaroscopic patterns.

methodsBlood serum samples, videocapillaroscopy images and patient characteristics were collected in a multicentre longitudinal cSLE cohort and from age and sex comparable HC. Disease activity was evaluated by SLEDAI. A total of 15 EC markers and six lipids were measured in two longitudinal cSLE samples (minimum interval of 6 months) and in HC. Nailfold videocapillaroscopy images were scored according to the guidelines from the EULAR Study Group on Microcirculation in Rheumatic Diseases.

resultsIn total, 47 patients with cSLE and 42 HCs were analysed. Median age at diagnosis was 15 years (IQR 12-16 years). Median time between t=1 and t=2 was 14.5 months (IQR 9-24 months). Median SLEDAI was 12 (IQR 6-18) at t=1 and 2 (IQR 1-4) at t=2. Serum levels of angiopoietin-2, CCL2, CXCL10, GAS6, pentraxin-3, thrombomodulin, VCAM-1 and vWF-A2 were elevated in cSLE compared with HC at t=1. While many elevated EC markers at t=1 normalised over time after treatment, several markers remained significantly increased compared with HC (angiopoietin-2, CCL2, CXCL10, GAS6, thrombomodulin and VCAM-1).

conclusionIn serum from patients with cSLE different markers of endothelial activation were dysregulated. While most markers normalised during treatment, others remained elevated in a subset of patients, even during low disease activity. These results suggest a role for the dysregulated endothelium in early and later phases of cSLE, possibly also during lower disease activity. TRIAL REGISTRATION NUMBER: NL60885.018.17.

Indexed as

BiomarkersLupus Erythematosus, SystemicMicroscopic AngioscopyAdolescentAge of OnsetAtherosclerosisCase-Control StudiesChildEndothelial CellsEndothelium, VascularFemaleHumansLipidsLongitudinal StudiesMaleSeverity of Illness IndexBiomarkersLipidsThrombomodulinAutoimmune DiseasesCardiovascular DiseasesLipidsLupus Erythematosus, Systemic

Identifiers

PMID39242108
PMCPMC11381702

What Socratic holds

Textmetadata
LicenceCC BY
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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.