Severe Pulmonary Hypersensitivity Associated With Passive Transfusion of a Neutrophil-Specific Antibody

Yomtovían, Roslyn; Press, Cynthia; Engman, H.; Kline, William E.; Clay, Mary; Hammerschmidt, Dale E.; McCullough, Jeffrey

doi:10.1016/s0140-6736(84)90124-7

Cited by 161 publications

(108 citation statements)

References 22 publications

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“…As in other causes of acute alveolar capillary leak, the pulmonary exudate in TRALI has high albumin content. Peripheral blood neutropenia has been reported but neutrophilia is more common [13,14]. As noted in our patient, is occasionally observed and is believed to be due to the sequestration of leukocytes in pulmonary circulation.…”

Section: Discussionsupporting

confidence: 59%

Transfusion-Related Acute Lung Injury (TRALI) Following Urological Surgery-Alarming Reaction: A Case Report

Bhat¹,

Kaul²,

Karoli³

2014

J Blood Disord Transfus

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Section: Discussionsupporting

confidence: 59%

Transfusion-Related Acute Lung Injury (TRALI) Following Urological Surgery-Alarming Reaction: A Case Report

Bhat¹,

Kaul²,

Karoli³

2014

J Blood Disord Transfus

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“…Serological work up of TRALI patients identified antibodies to a HNA in a number of cases (Yomtovian et al, 1984;Nordhagen et al, 1986;Bux et al, 1996;Leach et al, 1998); a description of HNA antigens and their implication in TRALI has been published previously (Bux, 2005).…”

Section: Antibodies To Human Neutrophil Antigensmentioning

confidence: 99%

The pathogenesis of transfusion‐related acute lung injury (TRALI)

2007

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SummaryIn recent years, transfusion-related acute lung injury (TRALI) has developed from an almost unknown transfusion reaction to the most common cause of transfusion-related major morbidities and fatalities. A clinical definition of TRALI was established in 2004, based on acute respiratory distress, noncardiogenic lung oedema temporal association with transfusion and hypoxaemia. Histological findings reveal lung oedema, capillary leucostasis and neutrophil extravasation. However, the pathogenesis of TRALI remains controversial. Leucocyte antibodies, present in fresh frozen plasma and platelet concentrates from multiparous donors, and neutrophil priming agents released in stored cellular blood components have been considered to be causative. As neutrophils and endothelial cells are pivotal in the pathogenesis of TRALI, a threshold model was established to try to unify the various reported findings on pathogenesis. This model comprises the priming of neutrophils and/or endothelium by the patient's co-morbidity, neutrophil and/or endothelial cell activation by the transfused blood component, and the severity of the TRALI reaction.

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“…[5][6][7][8] The pathophysiology of TRALI has not been elucidated despite numerous studies. [9][10][11][12][13][14] The first mechanism proposed was the infusion of donor antibodies directed against the HLA class I or granulocyte-specific antigens on the recipient's leukocytes with animal models composed of an in vivo murine model and an isolated, perfused rabbit lung that provided physiologic relevance. [9][10][11][12]14 In addition, the neutrophil (PMN) was proposed to be the effector cell, identical to other forms of ALI and the acute respiratory distress syndrome (ARDS).…”

Section: Introductionmentioning

confidence: 99%

“…[9][10][11][12][13][14] The first mechanism proposed was the infusion of donor antibodies directed against the HLA class I or granulocyte-specific antigens on the recipient's leukocytes with animal models composed of an in vivo murine model and an isolated, perfused rabbit lung that provided physiologic relevance. [9][10][11][12]14 In addition, the neutrophil (PMN) was proposed to be the effector cell, identical to other forms of ALI and the acute respiratory distress syndrome (ARDS). [9][10][11][12]14 However, look-back studies of donors with specific antibodies directed against HLA or granulocyte antigens demonstrated that the infusion of donor antibodies into a recipient that expressed the cognate antigen resulted in TRALI in a minority of these patients, implying that the clinical condition of the recipient may be important for the development of TRALI.…”

Section: Introductionmentioning

confidence: 99%

Plasma from stored packed red blood cells and MHC class I antibodies causes acute lung injury in a 2-event in vivo rat model

Kelher

Masuno

Moore

et al. 2009

Blood

140

276

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Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion death. We hypothesize that TRALI requires 2 events: (1) the clinical condition of the patient and (2) the infusion of antibodies against MHC class I antigens or the plasma from stored blood. A 2-event rat model was developed with saline (NS) or endotoxin (LPS) as the first event and the infusion of plasma from packed red blood cells (PRBCs) or antibodies (OX18 and OX27) against MHC class I antigens as the second event. ALI was determined by Evans blue dye leak from the plasma to the bronchoalveolar lavage fluid (BALF), protein and CINC-1 concentrations in the BALF, and the lung histology. NS-treated rats did not evidence ALI with any second events, and LPS did not cause ALI. LPS-treated animals demonstrated ALI in response to plasma from stored PRBCs, both prestorage leukoreduced and unmodified, and to OX18 and OX27, all in a concentration-dependent fashion. ALI was neutrophil (PMN) dependent, and OX18/OX27 localized to the PMN surface in vivo and primed the oxidase of rat PMNs. We conclude that TRALI is the result of 2 events with the second events consisting of the plasma from stored blood and antibodies that prime PMNs. IntroductionTransfusion-related acute lung injury (TRALI) is the leading cause of transfusion mortality in the United States. 1,2 TRALI is the acute onset of noncardiogenic pulmonary edema as documented by chest radiograph and profound hypoxemia, in accordance with the definition of acute lung injury (ALI), that occurs within 6 hours of transfusion. 3,4 TRALI may occur with or without conditions that predispose the patient to ALI, and may be the worsening of pulmonary function in patients with preexisting ALI. 3,4 All blood products have been implicated in TRALI, but components that contain large amounts of plasma are mainly responsible. 5,6 The current incidence of TRALI has been estimated as 1/7900 to 1/1330 in the United Kingdom and the United States with lesser incidences in Europe. [5][6][7][8] Current mortality rates vary from 5% to 35% with the lesser mortality rates predominating. [5][6][7][8] The pathophysiology of TRALI has not been elucidated despite numerous studies. [9][10][11][12][13][14] The first mechanism proposed was the infusion of donor antibodies directed against the HLA class I or granulocyte-specific antigens on the recipient's leukocytes with animal models composed of an in vivo murine model and an isolated, perfused rabbit lung that provided physiologic relevance. [9][10][11][12]14 In addition, the neutrophil (PMN) was proposed to be the effector cell, identical to other forms of ALI and the acute respiratory distress syndrome (ARDS). [9][10][11][12]14 However, look-back studies of donors with specific antibodies directed against HLA or granulocyte antigens demonstrated that the infusion of donor antibodies into a recipient that expressed the cognate antigen resulted in TRALI in a minority of these patients, implying that the clinical condition of the recipient may be important for the d...

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Severe Pulmonary Hypersensitivity Associated With Passive Transfusion of a Neutrophil-Specific Antibody

Cited by 161 publications

References 22 publications

Transfusion-Related Acute Lung Injury (TRALI) Following Urological Surgery-Alarming Reaction: A Case Report

Transfusion-Related Acute Lung Injury (TRALI) Following Urological Surgery-Alarming Reaction: A Case Report

The pathogenesis of transfusion‐related acute lung injury (TRALI)

Plasma from stored packed red blood cells and MHC class I antibodies causes acute lung injury in a 2-event in vivo rat model

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