• platelet activation;
  • ITP;
  • protein A immunoadsorption;
  • P-selectin;
  • platelet-associated immunoglobulin

Adults with chronic relapsing ITP present a difficult therapeutic challenge. The ongoing antibody- mediated platelet destruction in this group might be expected to be associated with increased expression of platelet surface membrane activation antigens.

We have studied a group of 10 patients with refractory ITP and 35 healthy controls. Using an immediate, sensitive, unfixed, whole blood, flow cytometric method to detect platelet surface P-selectin and GP53, we have detected markedly increased 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 immunoadsorption therapy. The effect of protein A immunoadsorption on platelet activation before, during and after 18 treatments in these patients 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 immunoadsorption. P-selectin expression fell significantly; pre- and post-treatment median values differed by 15.5%, P < 0.01, for GP53 the difference was 2.5.%, P = NS. A reduction in both platelet-associated IgG (median reduction of 11.8 ng/106 platelets, P = 0.08) and IgM (7.6 ng/106 platelets, P = 0.06) was recorded.