Evidence map›Paper›PMID 23929305›Full record

ReviewSeminars in thrombosis and hemostasis2013

Glanzmann thrombasthenia: state of the art and future directions.

Alan T Nurden, Xavier Pillois, David A Wilcox

Abstract readReview
In one paragraph

Review in Seminars in thrombosis and hemostasis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Efficacy and safety of recombinant activated factor VII in Glanzmann thrombasthenia: A systematic literature review.Haemophilia : the official journal of the World Federation of Hemophilia · 2025
    Pooled it
  2. Trial
  3. Observational
  4. Article
  5. European Management of Glanzmann's Thrombasthenia: A Survey of Current Clinical Practice.Haemophilia : the official journal of the World Federation of Hemophilia · 2025
    Article
  6. Observational
  7. Article
  8. One day at a time: Life with Glanzmann thrombasthenia - Qualitative results from the GT 360 study.Haemophilia : the official journal of the World Federation of Hemophilia · 2024
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. DMAG, a novel countermeasure for the treatment of thrombocytopenia.Molecular medicine (Cambridge, Mass.) · 2021
    Article
  16. Gene Therapy for Inherited Bleeding Disorders.Seminars in thrombosis and hemostasis · 2021
    Review
  17. Review
  18. Review
  19. Review
  20. Heterogeneity of Integrin αInternational journal of molecular sciences · 2020
    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

3 authors at 3 institutions in 2 countries.

Alan T NurdenPlateforme Technologique et d'Innovation Biomédicale, Hôpital Xavier Arnozan, Pessac, France. nurdenat@gmail.com
Xavier Pillois
David A Wilcox
Hôpital Xavier Arnozan · FRPlateforme Technologique d'Innovation Biomédicale · FRVersiti Blood Center of Wisconsin · US

Funding

Therapeutic-Expression of a Platelet-Specific IntegrinR01HL068138 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI WILCOX, DAVID ALLEN · 2002 to 2010
$2.4M
NHLBI NIH HHS HL-68138NHLBI NIH HHS R01 HL068138
6 · The paper itself

Abstract

Glanzmann thrombasthenia (GT) is the principal inherited disease of platelets and the most commonly encountered disorder of an integrin. GT is characterized by spontaneous mucocutaneous bleeding and an exaggerated response to trauma caused by platelets that fail to aggregate when stimulated by physiologic agonists. GT is caused by quantitative or qualitative deficiencies of αIIbβ3, an integrin coded by the ITGA2B and ITGB3 genes and which by binding fibrinogen and other adhesive proteins joins platelets together in the aggregate. Widespread genotyping has revealed that mutations spread across both genes, yet the reason for the extensive variation in both the severity and intensity of bleeding between affected individuals remains poorly understood. Furthermore, although genetic defects of ITGB3 affect other tissues with β3 present as αvβ3 (the vitronectin receptor), the bleeding phenotype continues to dominate. Here, we look in detail at mutations that affect (i) the β-propeller region of the αIIb head domain and (ii) the membrane proximal disulfide-rich epidermal growth factor (EGF) domains of β3 and which often result in spontaneous integrin activation. We also examine deep vein thrombosis as an unexpected complication of GT and look at curative procedures for the diseases, including allogeneic stem cell transfer and the potential for gene therapy.

Indexed as

MutationBlood PlateletsGenetic TherapyHemorrhageHumansPlatelet Glycoprotein GPIIb-IIIa ComplexStem Cell TransplantationThrombastheniaTransplantation, AutologousPlatelet Glycoprotein GPIIb-IIIa Complex

Identifiers

PMID23929305
PMCPMC4011384
OpenAlexW2004082240

What OpenQuestion holds

Textmetadata
LicenceTDM
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.