title: Glycoprotein IIb/IIIa inhibitor-induced thrombocytopenia: diagnosis and treatment.
abstract: Thrombocyte glycoprotein IIb/IIIa inhibitors prevent fibrinogen binding and thereby thrombocyte aggregation. The inhibition of thrombocyte activation at the damaged coronary plaque is the target of the new therapeutic strategies in treating acute coronary syndrome. This reduces the ischemic complications associated with the non-STelevation myocardial infarction (NSTEMI) and percutaneous coronary intervention (PCI). Thrombocytopenia is a known complication of glycoprotein (GP) IIb/IIIa inhibitors. Although, in general, GP IIb/IIIa inhibitor-induced thrombocytopenia is a harmless side effect which responds readily to thrombocyte transfusion, it can occasionally be a very serious complication associated with serious bleeding. In addition patients developing thrombocytopenia have unfavorable outcome (e.g., death, myocardial infarction, bypass surgery or additional PCI) in comparison to patients without thrombocytopenia. Advanced age (> 65 years), low BMI and a low initial thrombocyte count (<180,000/microl) are independent risk factors of thrombocytopenia. The risk of bleeding is higher with this form of thrombocytopenia not only due to the low thrombocyte count but also to the impaired function of the remaining thrombocytes. It is important to closely monitor platelet count during GP IIb/IIIa antagonist treatment. Platelet count monitoring two, six, twelve and 24 hour after starting the treatment reveals most cases of acute thrombocytopenia. Side effects can be avoided by the early discontinuation of the GP IIb/IIIa antagonist treatment. This article reviews the diagnosis and treatment of glycoprotein IIb/IIIa inhibitor-induced thrombocytopenia and summarizes the differential diagnosis from heparin-induced thrombocytopenia and laboratory-related pseudothrombocytopenia.
authors.affiliation: Carl-von-Basedow-Klinikum Merseburg, Medizinische Klinik I, Germany. s.said@klinikum-merseburg.de
authors.forename: S M
authors.initials: SM
authors.lastname: Said
authors.forename: J
authors.initials: J
authors.lastname: Hahn
authors.forename: E
authors.initials: E
authors.lastname: Schleyer
authors.forename: M
authors.initials: M
authors.lastname: Müller
authors.forename: G M
authors.initials: GM
authors.lastname: Fiedler
authors.forename: M
authors.initials: M
authors.lastname: Buerke
authors.forename: R
authors.initials: R
authors.lastname: Prondzinsky
mesh_terms: D000208:Acute Disease; D001803:Blood Transfusion / Q000379:methods; D003327:Coronary Disease / Q000188:drug therapy; D003937:Diagnosis, Differential; D016903:Drug Monitoring; D006801:Humans; D010956:Plasmapheresis / Q000379:methods; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects* / Q000627:therapeutic use; D010976:Platelet Count; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D006435:Renal Dialysis / Q000379:methods; D012307:Risk Factors; D013921:Thrombocytopenia / Q000139:chemically induced / Q000175:diagnosis* / Q000628:therapy*; D013997:Time Factors
chemical_list: D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex