Discussion:
Platelets play a major role in the formation and propagation of a thrombus, which is the key mechanism in developing Acute coronary syndromes(1). GP IIB/IIIA receptors are found on the surface of platelets and play a crucial role in the aggregating platelets by binding to fibrinogen and Von Willebrand factors(2).
Eptifibatide is an antiplatelet medication which reversibly binds and inhibits glycoprotein IIb/IIIa receptor on the surface of platelets (1), which means that it will prevent the binding of fibrinogen and Von Willebrand factors to GP IIb/IIIA receptors, thus inhibiting platelet aggregation and decreasing risk of thrombosis and thrombus propagation (3).
Eptifibatide had been approved by FDA based on three large, randomized trials, the PURSUIT, ESPIRIT, and IMPACT-II trials (5-7), the PURSUIT trial showed benefits in the settings of acute coronary syndrome (unstable angina and Non-ST elevation MI), while both ESPIRIT, and IMPACT-II approved eptifibatide for patients undergoing percutaneous coronary intervention only (PCI).
Profound thrombocytopenia is a rare side effect of GP IIB/IIIA in general. It has been reported with large molecule GPIIB/IIIA inhibitors such as Abciximab (8), but its incidence is quite rare with smaller molecules, specifically with Eptifibatide, with a risk of thrombocytopenia around (0.1 to –1%) (3,10). The data and evidence that are available suggest that Eptifibatide induced thrombocytopenia noticed to be profound within 24 hours of administration of the medication (9).
One of the suggested mechanisms for Eptifibatide induced thrombocytopenia is formation of antibodies against a group of epitopes, called ligand-induced binding sites (LIBSs), which are normally hidden, but binding of the GP IIb/IIIa to the receptors will expose these (LIBs) and allows the antibodies to bind to them (LIBs) which facilitates the clearance of platelets by the reticuloendothelial system (4)
Other causes of thrombocytopenia needs to be excluded like, Heparin induced thrombocytopenia (HIT) , (HIT)-type 1 is less likely in our case, as it usually develops in the first 2 days of heparin administration and usually is mild, with platelets usually staying within the normal range, and type II which usually develops 5-10 days if no previous heparin exposure, and even within hours if there is a history of heparin exposure (12) . It is usually diagnosed with platelet-factor 4 immunoassays. In our case, the platelet-factor 4 immunoassay for HIT was negative and the drop was acute immediately after starting eptifibatide and improved after stopping it, which makes HIT unlikely.
Eptifibatide induced thrombocytopenia was reported in multiple case reports (4,9-11) which was treated by withholding the eptifibatide, with significant improvement of platelet count, as in our patient.
In summary, we have presented here a case of eptifibatide induced thrombocytopenia in a patient with acute coronary syndrome who underwent PCI. While eptifibatide is a rare cause of thrombocytopenia, it is a serious side effect that warrants careful and close follow up of platelet counts if it happens.