Antiplatelet antibody detection in alloimmunized patients with acute leukaemia

Abstract One hundred and ten previously untransfused patients with newly diagnosed acute leukaemia received 1407 transfusions of pooled random donor platelet concentrates (PRDP) over a 3 year period. Patients were monitored for development of anti-HLA and/or platelet-specific antibody by lymphocytotoxicity (LCT), flow cytometry (FCIgG and FCIgM) and by solid phase red cell adherence (Capture-P) assays. Response to platelet transfusion and clinical factors associated with non-immune causes of platelet destruction were examined. Fifty-seven percent of the transfusion episodes were excluded from evaluation because of coexistent factors potentially mediating non-immune platelet destruction ( n = 741) or incomplete data ( n = 56). In the remaining 610 episodes, a poor post-transfusion corrected count increment (CCI) was observed in 23% of transfusion episodes and a good, or appropriate, CCI in 77% of transfusions. Time to antibody formation was variable 137 ± 171 days (range 9–311), as was the extent of donor exposure (59 ± 43 donor exposures for subjects developing antibody). Patients who failed to develop detectable 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 × 10 9 /L. In contrast, of the 147 transfusions associated with a positive antibody test, only 32% gave a 24 h CCI > 4.5 × 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 refractoriness with FCIgG > Capture-P > LCT > FCIgM. Combining two or more tests yielded only marginal improvement in sensitivity.