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Acquired thrombasthenia due to GPIIb/IIIa-specific platelet autoantibodies
H Niessner, KJ Clemetson, S Panzer, C Mueller-Eckhardt, S Santoso and P Bettelheim
An otherwise healthy woman developed a hemorrhagic diathesis with
fluctuating clinical symptoms and laboratory findings, but without
thrombocytopenia, over 8 years. In periods of bad clinical condition, a
platelet defect, characteristic of thrombasthenia, was found. In contrast
to classic thrombasthenia, electrophoresis of the patient's platelet
membranes revealed normal amounts of glycoproteins IIb alpha, IIb beta, and
IIIa in the normal positions. Monoclonal antibodies, specific for GPIIIa
and GPIIb/IIIa, respectively, bound normally to the P1A1-positive platelets
from the patient. Although no antibody and no platelet function inhibitor
were evident in the autologous plasma, an IgG1 antibody that was bound to
the patient's platelets and was directed against GPIIb/IIIa could be
demonstrated. After elution from the patient's platelets, this antibody
immunoprecipitated GPIIb (both subunits), IIIa, and a 200-kilodalton (kd)
band (probably undissociated GPIIb/IIIa complex) from solubilized normal
platelets, but did not react with thrombasthenic platelets. Adding the
eluate from the patient's platelets to normal platelet-rich plasma
immediately caused concentration-dependent inhibition of adenosine
diphosphate (ADP)- induced and collagen-induced aggregation and also strong
inhibition of ADP-stimulated fibrinogen binding. Because it was very
unlikely from the patient's medical history that the antibody was caused by
alloimmunization, the hemorrhagic diathesis must be interpreted as acquired
thrombasthenia due to an anti-GPIIb/IIIa autoantibody.
Volume 68,
Issue 2,
pp. 571-576,
08/01/1986
Copyright © 1986 by The American Society of Hematology
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