ANTIPLATELET ANTIBODY DETECTION IN ALLOIMMUNIZED PATIENTS WITH ACUTE-LEUKEMIA

One hundred and ten previously untransfused patients with newly diagno sed acute leukaemia received 1407 transfusions of pooled random donor platelet concentrates (PRDP) over a 3 year period. Patients were monit ored for development of anti-HLA and/or platelet-specific antibody by lymphocy totoxicity (LCT), flow cytometry (FCIgG and FCIgM) and by sol id phase red cell adherence (Capture-P) assays. Response to platelet t ransfusion and clinical factors associated with non-immune causes of p latelet destruction were examined. Fifty-seven percent of the transfus ion episodes were excluded from evaluation because of coexistent facto rs potentially mediating non-immune platelet destruction (n = 741) or incomplete data (n = 56). In the remaining 610 episodes, a poor post-t ransfusion corrected count increment (CCI) was observed in 23% of tran sfusion episodes and a good, or appropriate, CCI in 77% of transfusion s. Time to antibody formation was variable 137 +/- 171 days (range 9-3 11), as was the extent of donor exposure (59 +/- 43 donor exposures fo r subjects developing antibody). Patients who failed to develop detect able antibody had a mean of 94 +/- 65 donor exposures. In 463 (76%) of the 610 evaluable transfusions, antibody tests were negative and 91% of these transfusions resulted in a 24 h CCI of > 4.5 x 10(9)/L. In co ntrast, of the 147 transfusions associated with a positive antibody te st, only 32% gave a 24 h CCI > 4.5 x 10(9)/L. The different techniques showed good specificity (96-98%), but varied in sensitivity (32-69%). FCIgG was the most accurate technique for predicting immune refractor iness with FCIgG > Capture-P > LCT > FCIgM. Combining two or more test s yielded only marginal improvement in sensitivity. Copyright (C) 1996 Elsevier Science Ltd.