Abstract
Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion related morbidity and mortality. Immunemediated TRALI is caused by leucocyte and neutrophil antibodies in the transfused blood products that react with white blood cell antigens of the recipient, hereby inducing endothelial damage and lung injury. About two thirds of TRALI cases are thought to be immunemediated. Both Human Leucocyte Antibodies (HLA Class I and II) and Human Neutrophil Antibodies (HNA) are involved in TRALI. Most antibodies result from allo-exposure of the blood donor, with multiparous donors having the highest incidence of antibodies. Detection of anti-leucocyte and anti-neutrophil antibodies is complex and many uncertainties still exist regarding the interpretation of the test results.
In this review we discuss the evidence and effectiveness of measurements to prevent immune-mediated TRALI from a bloodbank and bedside perspective. From a bloodbank perspective various preventive measures have been implicated. In some countries bloodbanks have successfully implemented donor selection strategies, ranging from testing of allo-exposed donors for leucocyte antibodies to the exclusion of all females from donating high plasma volume products. Another strategy involves dilution of antibodies present by pooling of plasma donations of multiple donors.
From a bedside view, the most important measure to prevent TRALI is to limit patients’ exposure to allogenic bloodproducts. Furthermore recognition and awareness of the syndrome need to be heightened among clinicians.
Keywords: Transfusion related lung injury, HLA and HNA antibody, prevention, transfusion related morbidity, endothelial damage, allo-exposure, high plasma volume products, plasma donations, fresh frozen plasma, platelet transfusion
Current Pharmaceutical Design
Title:Prevention of Immune-mediated Transfusion-related Acute Lung Injury; from Bloodbank to Patient
Volume: 18 Issue: 22
Author(s): Marcella C.A. Muller, Leendert Porcelijn and Alexander P.J. Vlaar
Affiliation:
Keywords: Transfusion related lung injury, HLA and HNA antibody, prevention, transfusion related morbidity, endothelial damage, allo-exposure, high plasma volume products, plasma donations, fresh frozen plasma, platelet transfusion
Abstract: Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion related morbidity and mortality. Immunemediated TRALI is caused by leucocyte and neutrophil antibodies in the transfused blood products that react with white blood cell antigens of the recipient, hereby inducing endothelial damage and lung injury. About two thirds of TRALI cases are thought to be immunemediated. Both Human Leucocyte Antibodies (HLA Class I and II) and Human Neutrophil Antibodies (HNA) are involved in TRALI. Most antibodies result from allo-exposure of the blood donor, with multiparous donors having the highest incidence of antibodies. Detection of anti-leucocyte and anti-neutrophil antibodies is complex and many uncertainties still exist regarding the interpretation of the test results.
In this review we discuss the evidence and effectiveness of measurements to prevent immune-mediated TRALI from a bloodbank and bedside perspective. From a bloodbank perspective various preventive measures have been implicated. In some countries bloodbanks have successfully implemented donor selection strategies, ranging from testing of allo-exposed donors for leucocyte antibodies to the exclusion of all females from donating high plasma volume products. Another strategy involves dilution of antibodies present by pooling of plasma donations of multiple donors.
From a bedside view, the most important measure to prevent TRALI is to limit patients’ exposure to allogenic bloodproducts. Furthermore recognition and awareness of the syndrome need to be heightened among clinicians.
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Cite this article as:
C.A. Muller Marcella, Porcelijn Leendert and P.J. Vlaar Alexander, Prevention of Immune-mediated Transfusion-related Acute Lung Injury; from Bloodbank to Patient, Current Pharmaceutical Design 2012; 18 (22) . https://dx.doi.org/10.2174/1381612811209023241
DOI https://dx.doi.org/10.2174/1381612811209023241 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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