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.