ABH antibodies causing platelet transfusion refractoriness

Abstract

Two alloimmunized patients with multispecific anti-HLA and high-titered ABH antibodies showed transfusion failures after ABH-mismatched HLA-identical platelet transfusions, whereas ABH-matched HLA-identical platelets showed sufficient increments. The anti-A and -B could be demonstrated on platelets by immunofluorescence tests using FITC-labeled goat anti-human IgG. These platelet antibodies could be absorbed with red cells and platelets of the appropriate ABH type. In contrast to previous reports about the influence of ABH antibodies on platelet survival, not only a proportion of the platelet population were destroyed after infusion, but almost all ABH-incompatible platelets were destroyed.

Determinants of ABH expression on human blood platelets

“…Transfusion of ABH-incompatible platelets, even in the presence of HLA matching, can be associated with a decrease in the posttransfusion corrected count increment, [8][9][10][11]17 increased platelet utilization, 12,44 incompatible platelet crossmatches, 11,14 HLA alloimmunization, 12,13,44 and ABH-specific refractoriness. [8][9][10][11]16,18,23,24 The impact of ABH incompatibility is determined by patient and donor factors, including the type of ABH mismatch and recipient isohemagglutinin titers. 8,9,[16][17][18] Overall, clinical ABH incompatibility is most commonly observed with group A platelets transfused to group O patients, due to increased antigenicity of the A antigen and higher mean anti-A titers.…”

“…[8][9][10][11]16,18,23,24 The impact of ABH incompatibility is determined by patient and donor factors, including the type of ABH mismatch and recipient isohemagglutinin titers. 8,9,[16][17][18] Overall, clinical ABH incompatibility is most commonly observed with group A platelets transfused to group O patients, due to increased antigenicity of the A antigen and higher mean anti-A titers. 8,9,12,16,17 Repeated transfusions of ABH-incompatible platelets can further exacerbate these effects through immune stimulation, leading to increased isohemagglutinin titers and HLA alloimmunization.…”

“…8,9,[16][17][18] Overall, clinical ABH incompatibility is most commonly observed with group A platelets transfused to group O patients, due to increased antigenicity of the A antigen and higher mean anti-A titers. 8,9,12,16,17 Repeated transfusions of ABH-incompatible platelets can further exacerbate these effects through immune stimulation, leading to increased isohemagglutinin titers and HLA alloimmunization. 12,17 Despite these findings, few studies have examined what factors regulate ABH on donor platelets.…”

“…Risk factors in the recipient can include a group O phenotype and unusually high levels of anti-A and anti-B isohemagglutinins. 8,9,12,[16][17][18] Donor and/or platelet factors are less well described but may include storage time, [19][20][21] and Lewis and ABO subtypes. 2,4,5,8,[22][23][24] In addition, an ABH-high expresser (ABH-HXP) platelet phenotype has been identified that is specifically linked to transfusion failures.…”

Prevention and Management of Platelet Transfusion Refractoriness

“…The subsequently formed immune complexes were bound by the platelet Fc and complement receptors followed by removal by the reticulo–endothelial system slightly impairing platelet transfusion outcome [44]. Impaired platelet recovery and even febrile transfusion reactions were reported after ABO–antigen–incompatible platelet transfusion [45]. In these patients, IgG antibody titres were above 64.…”