PROTEIN-A IMMUNOADSORPTION IN CHRONIC REFRACTORY ITP REVERSES INCREASED PLATELET ACTIVATION BUT FAILS TO ACHIEVE SUSTAINED CLINICAL BENEFIT

Adults with chronic relapsing ITP present a difficult therapeutic chal lenge. The ongoing antibody-mediated platelet destruction in this grou p might be expected to be associated with increased expression of plat elet surface membrane activation antigens. We have studied a group of 10 patients with refractory ITP and 35 healthy controls. Using an imme diate, sensitive, unfixed, whole blood, flow cytometric method to dete ct platelet surface P-selectin and GP53, we have detected markedly inc reased platelet activation in the ITP group compared with the controls (P-selectin: patient median 24.5% v control median 2.0%, GP53 median 6.5% v 2.1%, P<0.01 for both). Five patients underwent protein A immun oadsorption therapy. The effect of protein A immunoadsorption on plate let activation before, during and after 18 treatments in these patient s was studied and patients were followed-up to assess clinical outcome . Platelet-associated immunoglobulin measurements were made before and at the end of six treatments. Platelet activation decreased after imm unoadsorption. P-selectin expression fell significantly: pre-and post- treatment median values differed by 15.5%, P<0.01, for GP53 the differ ence was 2.5.%, P=NS, A reduction in both platelet-associated IgG (med ian reduction of 11.8 ng/10(6) platelets, P=0.08) and IgM (7.6 ng/10(6 ) platelets, P=0.06) was recorded.