Abstract

Red blood cell (RBC) alloimmunization is a significant clinical complication of transfusion-dependent patients; it is related to delays in obtaining matched blood as well as potentially life-threatening delayed hemolytic transfusion reactions (DHTRs), autoantibody formation, and hyperhemolysis syndrome.1 Because of its critical significance, the phenomenon of RBC alloimmunization has been investigated in a variety of settings. With a better understanding of the factors that predispose to RBC alloimmunization, it is possible to devise strategies for blood transfusions that reduce the risk of alloimmunization and adverse reactions to transfusion. Clinical and biological factors such as disease state, human leukocyte antigen (HLA) polymorphisms, underlying inflammation, immunogenicity of the antigens and patient age are independent variables involved in RBC alloimmunization.2 In addition, stored leukocyte-reduced RBCs have been reported to produce higher rates of immunogenicity than fresh blood in murine models.3 These findings led to speculate that the transfusion of older RBCs might create a cytokine burst that predisposes a human recipient to RBC alloimmunization and thus raised the interest of some groups to perform studies in humans. Some recent studies have suggested that RBC storage length is associated with adverse patient outcomes ranging from death to pneumonia to increased length of hospital and intensive care unit stays.4,5 RBC alloimmunization was chosen as an outcome in these studies because it can be both medically and logistically problematic.6,7 By identifying associations, it may be possible to support or not support changing

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