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Delayed haemolytic and serologic transfusion reactions

pathophysiology, treatment and prevention

Siddon, Alexa J.a,b,c; Kenney, Barton C.c; Hendrickson, Jeanne E.a,d; Tormey, Christopher A.a,b

doi: 10.1097/MOH.0000000000000462

Purpose of review The aim of this study was to summarize the basic epidemiology, pathophysiology and management of delayed serologic and delayed haemolytic transfusion reactions (DHTRs), as well as recent developments in our understanding of these adverse events.

Recent findings Several studies have identified risk factors for DHTRs, including high alloantibody evanescence rates among both general patient groups and those with sickle cell disease (SCD). Antibody detection is also hampered by the phenomenon of transfusion record fragmentation. There have also been enhancements in understanding of what may contribute to the more severe, hyperhaemolytic nature of DHTRs in SCD, including data regarding ‘suicidal red blood cell death’ and immune dysregulation amongst transfusion recipients with SCD. With growing recognition and study of hyperhaemolytic DHTRs, there have been improvements in management strategies for this entity, including a multitude of reports on using novel immunosuppressive agents for preventing or treating such reactions.

Summary Delayed serologic and haemolytic reactions remain important and highly relevant transfusion-associated adverse events. Future directions include further unravelling the basic mechanisms, which underlie DHTRs and developing evidence-based approaches for treating these reactions. Implementing practical preventive strategies is also a priority.

aDepartment of Laboratory Medicine, Yale School of Medicine

bPathology & Laboratory Medicine Service, VA Connecticut Healthcare System

cDepartment of Pathology

dDepartment of Pediatrics, Yale School of Medicine, New Haven, Connecticut, USA

Correspondence to Christopher A. Tormey, Department of Laboratory Medicine, Yale School of Medicine, 20 York Street, PS 435B, New Haven, CT 06520, USA. Tel: +1 203 932 5711 x2964; fax: +1 203 937 4746; e-mail:

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