Patients with Glanzmann thrombasthenia (GT) may form isoantibodies which induce refractoriness or inhibition of function of transfused platelets. We monitored the survival and function of transfused platelets by flow cytometry and thrombelastography in a patient with GT. Gating on CD42a+ allowed identification of even a few transfused platelets. Only by gating on these CD41+ CD42a+ cells were we able to demonstrate their capability to bind fibrinogen and PAC-1 upon activation. Platelets were rapidly cleared from the circulation as a result of boosted isoantibodies. The contribution of transfused platelets to clot formation was also demonstrated by thrombelastography by blocking their function with abciximab.