Summary
Abciximab is an anti-GPIIb-IIIa drug widely used to prevent thrombotic complications
during percutaneous coronary intervention. We now report on the immunologic origin
of thrombocytopenia developing between 7 and 12 days after the onset of abciximab
infusion. Antibodies directed against abciximabcoated platelets were located in 5
patients with delayed thrombocytopenia, just as they were present in a patient whose
platelet count fell within a few hours after receiving the drug. Abciximab-dependent
IgG antibody was revealed in serum using control platelets in the monoclonal antibody
immobilization of platelet antigens assay (MAIPA) performed with SZ22, a MoAb to GPIIb.
The presence of IgG antibodies specific for platelets sensitized with abciximab was
confirmed by flow cytometry. They were not located in 13 patients receiving abciximab
but whose platelet counts remained stable. For three patients, antibodies were transient
and their presence related to the extent of the thrombocytopenia. Surprisingly, antibodycontaining
plasma from three patients induced abciximabdependent activation and aggregation of
normal platelets, a finding confirmed by electron microscopy. Immunogold labeling
revealed that abciximab was associated with platelets in the aggregate, suggesting
that its inhibitory effect was overcome by the platelet stimulation. In summary, these
results show that abciximab-dependent thrombocytopenia can be delayed and potentially
prothrombotic.
Keywords
Abciximab - percutaneous coronary intervention - delayed thrombocytopenia - thrombotic
risk