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Autoantibodies against platelet glycoproteins in autoimmune
thrombocytopenic purpura: their clinical significance and response to
treatment
P Berchtold and M Wenger
Department of Medicine, University of Bern, Inselspital, Switzerland.
Autoantibodies against platelet glycoproteins (GP) have been demonstrated
in patients with autoimmune thrombocytopenic purpura (ATP). However, their
clinical and pathogenetic significance as well as their response to
immunosuppressive treatment is unknown. Using an immunobead assay capable
of measuring autoantibodies against GPIIb-IIIa and GPIb-IX, we studied 58
adult patients with active ATP (platelet count < 150 x 10(9)/L) and 26
patients with ATP in remission (platelet count > 150 x 10(9)/L and
without any therapy at time of investigation). Platelet-associated
autoantibodies were detected in 39 of 53 patients with active ATP (73.6%)
and in 2 of 26 patients in remission (7.7%). Circulating plasma
autoantibodies were noted in 17 of 58 patients in the group with active
disease (29.3%) and in none of the patients in remission. Twelve patients
with active ATP and autoantibodies against GPIIb-IIIa were studied
prospectively during treatment with corticosteroids. Of eight patients
whose platelet count normalized during treatment, platelet-associated and
plasma antibodies decreased significantly in two or became undetectable in
six. In contrast, of four patients whose platelet counts were unchanged or
increased moderately, we noted no significant change in antibodies.
Moreover, autoantibodies reappeared in two responding patients at the time
of relapse. The effect of high-dose intravenous immunoglobulin was studied
in six active ATP patients with antiglycoprotein autoantibodies and
refractoriness to prednisone. In one patient who developed a sustained
remission after IvIgG, platelet-associated and plasma antibodies to
GPIIb-IIIa decreased and became undetectable. In contrast, two patients who
had only a transient rise of the platelet count after IvIgG showed no
significant change in autoantibody. In three unresponsive patients,
autoantibodies were without change in two and decreased transiently in one
patient. We conclude that in ATP the presence of autoantibodies to
GPIIb-IIIa and GPIb-IX is related to the activity of the disease.
Corticosteroids may inhibit autoantibody formation in some ATP patients,
whereas during the early response to IvIgG, autoantibody production may not
be affected.
Volume 81,
Issue 5,
pp. 1246-1250,
03/01/1993
Copyright © 1993 by The American Society of Hematology
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