IGG FROM PATIENTS WITH ANTIPHOSPHOLIPID SYNDROME BINDS TO PLATELETS WITHOUT INDUCTION OF PLATELET ACTIVATION

The clinical manifestations of the antiphospholipid syndrome (APLS) in clude arterial and venous thrombosis, thrombocytopenia and fetal loss, but the pathogenic mechanisms remain unclear. It has been hypothesize d that platelet activation by autoantibody may be a pathogenic mechani sm. We studied IgG binding, microparticle (mp) formation and P-selecti n expression by Bow cytometry in normal platelets after incubation in serum from 11 patients with antiphospholipid antibodies and that from 10 normal healthy subjects. Levels of platelet-associated IgG were sig nificantly higher after incubation in patient sera (mean 17.2, range 2 .0-75.0%) compared with normal sera (mean 2.0, range 1.2-3.7%, P<0.05) . Incubation of normal platelets in serum led to increased micropartic le formation (P<0.01) and P-selectin expression (P<0.05), compared wit h unstimulated platelets, There was no significant difference, however , between microparticle formation nor P-Selectin expression induced by patient serum (mp 3.0 (1.6-5.0)%; P-selectin 8.0 (4.0-16.6)%) versus normal serum (mp 3.2 (2.1-4.5)%; P-selectin 10.1 (4.0-15.6); median (r ange)). Pre-activation of platelets with subthreshold ADP concentratio ns or thrombin receptor activator peptide resulted in a small increase in microparticle formation, but there was still no significant differ ence between the effects of patient and control sera. Despite the pres ence of platelet membrane binding IgG in serum from 5/11 patients with antiphospholipid antibodies, there was no evidence for associated enh anced platelet-activating ability. This study supports antiplatelet re activity in anti phospholipid syndrome, but not a direct platelet-acti vating role for platelet-directed autoantibodies.