Platelet transfusion refractoriness in patients with acute myeloid leukemia – the role of antiplatelet antibodies

Abstract

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 human platelet antigens could cause immune-mediated transfusion refractoriness. The main goal of this study was to examine the presence and 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 platelet 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 levels, as well as in the antibody titer increments after the transfusion. No significant correlation between platelet count increment (absolute numbers) and initial levels of antiplatelet 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 the examined patients than in healthy male untransfused controls.

Keywords: platelet transfusion refractoriness; acute myeloid leukemia; human platelet antigens; AML; HPA