Evidence map›Paper›PMID 36038904›Full record

ArticleJournal of translational medicine2022

Markers of endothelial glycocalyx dysfunction in Clarkson disease.

Zhihui Xie, Magne Børset, Kjell Svéen, Ole Wilhelm Bøe, Eunice C Chan, Justin B Lack, Katherine M Hornick, Franco Verlicchi, A Robin Eisch, Remo Melchio and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Systemic capillary leak syndrome.Nature reviews. Disease primers · 2024
    Review
  3. Article
  4. Article
  5. 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

12 authors at 5 institutions in 3 countries.

Zhihui XieLung and Vascular Inflammation Section, Laboratory of Allergic Diseases, National, Institute of Allergy and Infectious Diseases/National Institutes of Health, (NIAID/NIH), 10 Center Drive, Room 11N238A, Bethesda, MD, 20892, USA.
Magne BørsetDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Kjell SvéenDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Ole Wilhelm BøeDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Eunice C ChanLung and Vascular Inflammation Section, Laboratory of Allergic Diseases, National, Institute of Allergy and Infectious Diseases/National Institutes of Health, (NIAID/NIH), 10 Center Drive, Room 11N238A, Bethesda, MD, 20892, USA.
Justin B LackNIAID Collaborative Bioinformatics Resource, NIAID/NIH, Health, Bethesda, MD, 20892, USA.
Katherine M HornickNIAID Collaborative Bioinformatics Resource, NIAID/NIH, Health, Bethesda, MD, 20892, USA.
Franco VerlicchiTransfusion Medicine Faenza-Lugo, Transfusion Service Ravenna, Romagna Health Unit, Ravenna, Italy.
A Robin EischLung and Vascular Inflammation Section, Laboratory of Allergic Diseases, National, Institute of Allergy and Infectious Diseases/National Institutes of Health, (NIAID/NIH), 10 Center Drive, Room 11N238A, Bethesda, MD, 20892, USA.
Remo MelchioDepartment of Internal Medicine, Santa Croce E Carle' Hospital, Via Michele Coppino 26, Cuneo, Italy.
Arkadiusz Z DudekHealthPartners Neuroscience Center, St. Paul, MN, USA.
Kirk M DrueyLung and Vascular Inflammation Section, Laboratory of Allergic Diseases, National, Institute of Allergy and Infectious Diseases/National Institutes of Health, (NIAID/NIH), 10 Center Drive, Room 11N238A, Bethesda, MD, 20892, USA. kdruey@niaid.nih.gov.ORCID 0000-0002-5834-6501
National Institutes of Health · USNorwegian University of Science and Technology · NOAzienda Sanitaria Ospedaliera S.Croce e Carle Cuneo · ITAzienda Unità Sanitaria Locale Della Romagna · ITHealthPartners · US

Funding

Division of Intramural Research, National Institute of Allergy and Infectious Diseases Z01-AI-001083
6 · The paper itself

Abstract

backgroundClarkson disease (monoclonal gammopathy-associated idiopathic systemic capillary leak syndrome, ISCLS) is a rare idiopathic condition marked by transient, relapsing-remitting episodes of systemic microvascular hyper-permeability, which liberates plasma fluid and macromolecules into the peripheral tissues. This pathology manifests clinically as the abrupt onset of hypotensive shock, hemoconcentration, and hypoalbuminemia.

methodsWe analysed endothelial glycocalyx (eGCX)-related markers in plasma from patients with ISCLS during acute disease flares and convalescence by ELISA and comprehensive proteomic profiling. We evaluated eGCX-related components and gene expression in cultured endothelial cells using RNA-sequencing, real-time PCR, and fluorescence staining.

resultsSerum levels of eGCX-related core components including hyaluronic acid (HA) and the core proteoglycan soluble syndecan-1 (sCD138) were elevated at baseline and during acute ISCLS flares. Serial measurements demonstrated that sCD138 levels peaked during the recovery (post-leak) phase of the illness. Proteomic analysis of matched acute and convalescent ISCLS plasma revealed increased abundance of eGCX-related proteins, including glypicans, thrombospondin-1 (TSP-1), and eGCX-degrading enzymes in acute compared to remission plasma. Abundance of endothelial cell damage markers did not differ in acute and baseline plasma. Expression of several eGCX-related genes and surface carbohydrate content in endothelial cells from patients with ISCLS did not differ significantly from that observed in healthy control cells.

conclusionseGCX dysfunction, but not endothelial injury, may contribute to clinical symptoms of acute ISCLS. Serum levels of of eGCX components including sCD138 may be measured during acute episodes of ISCLS to monitor clinical status and therapeutic responses.

Indexed as

Capillary Leak SyndromeBiomarkersEndothelial CellsGlycocalyxHumansProteomicsBiomarkersCapillary leakEndotheliumGlyocalcyx

Identifiers

PMID36038904
PMCPMC9421105
OpenAlexW4293531839

What OpenQuestion 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 OpenQuestion graph.