Faculty Collaboration Database

Thrombocytopenia resulting from sensitivity to GPIIb-IIIa inhibitors. Semin Thromb Hemost 2004 Oct;30(5):569-77

Date

10/22/2004

Pubmed ID

15497099

DOI

10.1055/s-2004-835677

Scopus ID

2-s2.0-7044269109 (requires institutional sign-in at Scopus site)   31 Citations

Abstract

Agents that inhibit the binding of fibrinogen to its platelet receptor (glycoprotein [GP] IIb-IIIa, alpha(IIb)/beta3 integrin) constitute a promising new group of antithrombotic drugs. Acute thrombocytopenia, often occurring within a few hours of starting treatment, is a recognized side effect of this family of compounds. Although most affected patients recover uneventfully, severe bleeding and fatal outcomes have been described. Both nonimmune and immune mechanisms have been implicated in the pathogenesis of this complication, but accumulating evidence suggests that drug-dependent antibodies are responsible for platelet destruction in many (and perhaps most) affected individuals. These antibodies are unique in that they can be present in persons not previously exposed to a GPIIb-IIIa inhibitor, allowing for the possibility that thrombocytopenia can occur within hours of starting treatment. Additional studies are needed to more fully define the characteristics of these antibodies and to identify risk factors that predispose patients to this complication.

Author List

Aster RH, Curtis BR, Bougie DW

Author

Brian Curtis PhD Director in the Platelet & Neutrophil Immunology Laboratory department at BloodCenter of Wisconsin

MESH terms used to index this publication - Major topics in bold

Antibodies, Monoclonal
Diagnosis, Differential
Humans
Immunoglobulin Fab Fragments
Immunoglobulin G
Ligands
Models, Chemical
Peptides
Platelet Aggregation Inhibitors
Platelet Glycoprotein GPIIb-IIIa Complex
Risk Factors
Thrombocytopenia
Tyrosine