Evidence map›Paper›PMID 33774918›Full record

ArticleJournal of thrombosis and haemostasis : JTH2021

Antiprothrombin antibodies induce platelet activation: A possible explanation for anti-FXa therapy failure in patients with antiphospholipid syndrome?

Walid Chayoua, Phillip L R Nicolson, Joost C M Meijers, Caroline Kardeby, Lourdes Garcia-Quintanilla, Katrien M J Devreese, Bas de Laat, Stephen P Watson, Philip G de Groot

Open access · hybridAbstract read
In one paragraph

Article in Journal of thrombosis and haemostasis : JTH, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Lupus anticoagulant and antiprothrombin antibodies: embracing the future.Journal of thrombosis and haemostasis : JTH · 2025
    Review
  9. Review
  10. Article
  11. Review
  12. Platelets and Thrombotic Antiphospholipid Syndrome.Journal of clinical medicine · 2024
    Review
  13. Review
  14. Review
  15. 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

9 authors at 5 institutions in 3 countries.

Walid ChayouaCardiovascular Research Institute Maastricht, Maastricht University Medical Centre, Maastricht, The Netherlands.ORCID 0000-0003-3192-2457
Phillip L R NicolsonInstitute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.ORCID 0000-0002-4843-2975
Joost C M MeijersDepartment of Molecular and Cellular Hemostasis, Sanquin Research, Amsterdam, The Netherlands.
Caroline KardebyInstitute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.ORCID 0000-0002-5025-9454
Lourdes Garcia-QuintanillaInstitute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.
Katrien M J DevreeseCoagulation Laboratory, Department of Laboratory Medicine, Ghent University Hospital, Ghent, Belgium.ORCID 0000-0002-7559-2579
Bas de LaatCardiovascular Research Institute Maastricht, Maastricht University Medical Centre, Maastricht, The Netherlands.
Stephen P WatsonInstitute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.ORCID 0000-0002-7846-7423
Philip G de GrootSynapse Research Institute, Maastricht, The Netherlands.
University of Birmingham · GBMaastricht University Medical Centre · NLGhent University Hospital · BESanquin · NLSynapse (Netherlands) · NL

Funding

British Heart Foundation CH/03/003/15571
6 · The paper itself

Abstract

backgroundArterial and venous thrombosis are both common in antiphospholipid syndrome (APS). Recent studies have shown that anti-factor Xa (FXa) therapy in APS patients leads to a greater number of patients with arterial thrombosis than with warfarin. We hypothesize that this may be due to the lowering of prothrombin levels by warfarin.

objectivesTo investigate whether antiprothrombin antibodies induce platelet aggregation and to identify the platelet receptors involved. A second aim was to investigate the effect of reduced prothrombin levels on antiprothrombin antibody-induced platelet aggregation.

methodsEnzyme-linked immunosorbent assays were performed to measure binding of antiprothrombin antibodies to prothrombin fragment 1+2 and prothrombin. Platelet aggregation assays in washed platelets were performed. FcγRIIA was immunoprecipitated and tyrosine-phosphorylated FcγRIIA was measured by western blot.

resultsThe antiprothrombin antibodies 28F4 and 3B1 had lupus anticoagulant (LAC) activity and caused platelet aggregation in the presence of Ca

conclusionsAntiprothrombin antibodies with LAC activity are able to activate platelets via FcγRIIA. Decreased prothrombin levels resulted in less antiprothrombin antibody-mediated platelet aggregation. This may explain the lower incidence of arterial thrombosis in patients treated with warfarin than with anti-FXa therapy.

Indexed as

Antiphospholipid SyndromeThrombosisHumansImmunoglobulin GLupus Coagulation InhibitorPlatelet ActivationProthrombinImmunoglobulin GLupus Coagulation InhibitorProthrombinantiphospholipid syndromeantiprothrombin antibodiesDOACsthrombosisvitamin K antagonists

Identifiers

PMID33774918
PMCPMC8360052
OpenAlexW3150275124

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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 OpenQuestion graph.