Atopic predisposition of recipients in allergic transfusion reactions to apheresis platelets

Authors

  • William J. Savage,

    Corresponding author
    1. From the Department of Pathology and the Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.
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  • Aaron A.R. Tobian,

    1. From the Department of Pathology and the Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.
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  • Jessica H. Savage,

    1. From the Department of Pathology and the Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.
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  • Robert G. Hamilton,

    1. From the Department of Pathology and the Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.
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  • Paul M. Ness

    1. From the Department of Pathology and the Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.
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  • This study was supported in part from internal funds provided by the Johns Hopkins DACI Reference Laboratory. WS acknowledges funding support from 5K12HL087169. JS acknowledges support from T32AI007056-31.

William Savage, MD, Carnegie 667, 600 N. Wolfe Street, Baltimore, MD 21287; e-mail: wsavage1@jhmi.edu.

Abstract

BACKGROUND: The biologic mechanisms of allergic transfusion reactions (ATRs) are largely unknown. We sought to compare the atopic predisposition of platelet (PLT) recipients who experienced an ATR to nonreactive control recipients.

STUDY DESIGN AND METHODS: We identified 37 consecutive apheresis PLT recipients who experienced an ATR and 26 matched controls. Total immunoglobulin (Ig)E and aero- and food allergen–specific IgE were quantified in plasma by a blood test for allergies (ImmunoCAP: Phadiatop and Fx5). IgE testing of apheresis PLT supernatants was also performed.

RESULTS: Pruritus and urticaria were manifest in 91.9 and 83.8% of all ATRs, with more severe respiratory symptoms and angioedema occurring in less than 15% of cases. No subject had anaphylaxis. Sex, age, and primary diagnosis were balanced between the two groups. Total and aeroallergen-specific IgE was higher among subjects experiencing an ATR in comparison to control subjects (median total IgE, 55.5 kU/L vs. 8.3 kU/L, p = 0.002; and median aeroallergen-specific IgE, 0.57 kUa/L vs. 0.36 kUa/L, p = 0.046). IgE antibody levels in apheresis products associated with ATRs were similar to control products (p > 0.1 for all IgE tests).

CONCLUSION: Recipient atopic predisposition, as defined by IgE sensitization, is a risk factor associated with ATRs.

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