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Protein A immunoadsorption in chronic refractory ITP reverses increased platelet activation but fails to achieve sustained clinical benefit
Author(s) -
Mary R. Cahill,
Marion G. Macey,
Jamie Cavenagh,
Adrian C. Newland
Publication year - 1998
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1998.00568.x
Subject(s) - immunoadsorption , platelet , medicine , platelet activation , refractory (planetary science) , p selectin , gastroenterology , antibody , immunology , biology , astrobiology
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/10 6 platelets, P = 0.08) and IgM (7.6 ng/10 6 platelets, P = 0.06) was recorded.