Summary
A young patient developed chronic idiopathic thrombocytopenic purpura. Prednisone
therapy normalized platelet number, but bleeding symptoms did not disappear. Platelet
function was severely impaired, since platelet aggregation, ATP release and adhesion
to collagen and subendothelial matrix were significantly reduced. Plasma and purified
immunoglobulins of the patient reproduced the functional defects in normal platelets.
Immunoblotting revealed that patient’s plasma contained an antibody reacting with
a component of platelets with the same electrophoretic mobility of glycoproteins IIIa
of normal platelets. Moreover, patient’s plasma inhibited the binding of an anti-GPIIb/IIIa
monoclonal antibody to platelet surface. Additional immunosuppressive therapy with
prednisone and azathioprine normalized platelet function and induced the disappearance
of bleeding symptoms.
