Acute profound thrombocytopenia following C7E3 Fab (abciximab) therapy: Case reports, review of the literature and implications for therapy

Abstract

Platelets play a crucial role in the ischemic complications of percutaneous coronary procedures. The recent availability of C7E3 Fab (Abxiximab or ReoPro™), a chimeric monoclonal antibody Fab fragment directed against the platelet glycoprotein IIb/IIIa receptor, has reduced abrupt closure and other adverse events and lessened the need for revascularization procedures. As the use for this drug has increased, rare cases of severe thrombocytopenia have been revealed. From August 1995 to June 1997, 452 patients at Charleston Area Medical Center who underwent percutaneous coronary revascularization procedures and were treated with abciximab were evaluated for the development of severe thrombocytopenia (i.e., platelet count less than 20,000 within 48 hr of treatment). A review of published reports of severe thrombocytopenia was also reviewed. A review of published reports of abciximab-induced severe thrombocytopenia, as well as our three cases, reveals that: 1) the incidence is less than 0.7%; 2) the nadir platelet count (range 1,000–16,000) was noted within 2–31 hr after abciximab infusion; 3) the platelet count increases to greater than 100,000 within 12 days in all patients; 4) bleeding episodes were treated with platelet transfusion with an improvement in platelet count within 24 hr in all patients in whom they were given; and 5) in the one patient treated with γ globulin alone, no significant rise in platelet count was noted. Acute severe thrombocytopenia can occur after ReoPro™ administration. Its development is not predictable and may occur within 2 hr of administration. Thrombocytopenia, therefore, requires consideration in every patient treated with this drug. It appears prudent to obtain a platelet count 2 hr after initiating ReoPro™. If thrombocytopenia develops, then the drug can be stopped in a timely manner and platelet transfusion can be given. Am. J. Hematol. 61:205–208, 1999. © 1999 Wiley-Liss, Inc.