Platelet transfusion refractoriness in patients with acute myeloid leukemia: The role of anti-platelet antibodies

Introduction/Objective. Platelet transfusion refractoriness represents a common issue in the treatment course of acute myeloid leukemia (AML) patients who require chronic transfusion support. Antibodies to the human platelet antigens could cause immune-mediated transfusion refractoriness. The main goal of this study was to examine the presence and the quantity of antibodies to GP IIb/IIIa, GP Ib/IX and GP Ia/IIa in AML patients refractory to platelet transfusion in comparison to healthy male subjects. Methods. This prospective study involved 22 adult AML patients who demonstrated resistance to platelet transfusion. Antibody titers for the following platelet antigens: GP IIb/IIIa, GP Ib/IX and GP Ia/IIa were measured in these patients before and two hours after platelet transfusion as well as in healthy male controls. Results. The antibodies to platelets antigens taken before the platelet transfusion were significantly increased in all patients compared with healthy untransfused controls (p = 0.001). In all three groups of antibodies, the titers were significantly higher after platelet transfusion (p = 0.001) than before. There was no statistically significant difference between males and females, platelet sources (buffy-coat vs. apheresis-derived) in the examined initial antibody’s levels, as well as in the antibody titers increment after the transfusion. No significant correlation between platelet count increment (absolute numbers) and initial levels of anti-platelet antibodies was found. Conclusion. Platelet transfusion refractoriness in AML patients could be caused by the antibodies to platelet antigens, since their levels are significantly higher in examined patients than in healthy male untransfused controls.