Detection of Splenic Anti‐Platelet Antibody Synthesis in Idiopathic Autoimmune Thrombocytopenic Purpura (ATP)

Abstract

S ummary . A significant decline in the serum anti‐platelet antibody titre, as measured by the platelet factor 3 (PF‐3) immuno‐injury technique, followed splenectomy in seven out of eight patients with autoimmune thrombocytopenic purpura (ATP). Anti‐platelet antibody could be eluted from the splenic extracts of 11 of 13 patients with ATP. The anti‐platelet antibody detected could be adsorbed with washed human platelets and could be removed with rabbit anti‐human IgG (RAHIgG). Extracts of spleens from six ‘control’ patients (five with hereditary spherocytosis and one with Milroy's disease) had no detectable anti‐platelet antibody. Minced spleen from nine patients with ATP and five ‘controls’ were cultured for 17 hr in a medium containing 14 C amino acids. Washed platelets adsorbed at least five times more Ladioactivity from globulin fractions of cultured ATP spleens than did ‘control’ spleens. In contrast, washed granulocytes failed to adsorb significant radioactivity. Supernatants obtained from these splenic incubates were also tested for anti‐platelet antibody (PF‐3 test). Anti‐platelet antibody was detectable in all seven ATP patients tested and was absent in the three control subjects tested. The anti‐platelet antibody could be adsorbed with washed human platelets but not with washed human granulocytes or red blood cells. These data suggest that the spleen might be a significant site for anti‐platelet antibody synthesis in ATP.