Glanzmann thrombasthenia: A model disease which paved the way to powerful therapeutic agents

Uri Seligsohn*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

Glanzmann thrombasthenia (GT) is an autosomal recessive bleeding disorder characterized by deficient or dysfunctional glycoprotein (GP) IIb/IIIa compexes. The hallmark of the disease is impaired platelet aggregation stemming from defective fibrinogen binding to GPIIb/IIIa. Based on deciphering the abnormality in GT a monoclonal antibody, peptides and peptidominetic agents, all interfering with fibrinogen binding to GPIIb/III complex, have been developed and successfully used to create a transient thrombasthenia - like state in patients with imminent arterial thrombosis. Currently, the main benefit afforded by these agents has been observed in patients undergoing percutaneous coronary interventions who are at high risk of thrombosis but more indications for their use are evolving.

Original languageEnglish
Pages (from-to)216-217
Number of pages2
JournalPathophysiology of Haemostasis and Thrombosis
Volume32
Issue number5-6
DOIs
StatePublished - 2002

Keywords

  • Antiplatelet drugs
  • Glanzmann thrombasthenia
  • Glycoproteins IIb and IIIa

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