In platelets, GPIIb and GPIIIa are joined together
as a dimer (referred to as GPIIb/IIIa). Once activated, GPIIb/IIIa binds to
one end of fibrinogen (and/or von Willebrand factor), while another
platelet, with its own GPIIb/IIIa, can bind to the other extremity of the
fibrinogen, thus leading to a large aggregation of bound platelets
(so-called white blood clot). In patients with Glanzmann thrombasthenia,
GPIIb/IIIa is defective and platelets cannot aggregate; no blood clot is
formed and bleeding does not stop.