Possible involvement of heparin‐binding protein in transfusion‐related acute lung injury

Yasui, Kazuta; Furuta, Rie; Matsuyama, Nobuki; Fukumori, Yasuo; Kimura, Takafumi; Tani, Yoshihiko; Shibata, Hirotoshi; Hirayama, Fumiya

doi:10.1111/j.1537-2995.2007.01632.x-i2

Cited by 8 publications

(2 citation statements)

References 46 publications

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“…However, the mechanism of leukocyte activation after their accumulation in the lung should be carefully investigated thereafter. A recent finding by Yasui et al has revealed the possible involvement of heparin-binding protein as one of the primary effector molecules of antibody-mediated TRALI [59].…”

Section: Pathogenesis Of Tralimentioning

confidence: 99%

Fight against TRALI

Okazaki

2009

ISBT Science Series

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Transfusion‐related acute lung injury (TRALI) is a life‐threatening adverse reaction to transfusion. It is characterized by non‐cardiogenic pulmonary edema that develops during or within 6 h after transfusion. Transfusion of blood products or massive transfusion has long been known as a rare cause of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Because the main causes of ALI/ARDS are sepsis and/or pneumonia, little attention has been paid to transfusion as a cause of lung injury. Owing to indifference to and underrecognition of this complication, ALI after transfusion may be attributed to other causes. Moreover, physicians tend to attribute the cause of respiratory failure to more common complications of transfusion such as allergic reaction and circulatory overload. Even if an appropriate diagnosis of non‐cardiogenic pulmonary edema is made, transfusion may not be identified as its cause. Although anti‐leukocyte antibodies have been proved to be one of the main causes of TRALI, the precise mechanism of this syndrome is poorly understood. Anti‐HLA and ‐HNA antibodies in labile blood products are reported to cause TRALI, and animal models of TRALI show that these antibodies induce lung injury under certain experimental conditions. We have recently showed that anti‐CD36 antibody caused TRALI in two patients. This finding suggests that as‐yet‐unknown antibodies other than anti‐HLA or ‐HNA antibodies might cause TRALI. According to current haemovigilance reports and previous look‐back studies, the incidence of TRALI is not very high. This finding supports the concept of the two‐hit theory of ALI, where certain patients’ clinical conditions are prerequisite in addition to transfusion for developing TRALI. A recent study in the ICU of a tertiary care medical centre has revealed a high incidence of suspected TRALI cases. This study revealed that female plasma, number of pregnancies in donors, number of donor units positive for anti‐granulocyte antibodies and anti‐HLA class II antibodies and concentration of lysophophatidylcholine in donor products are associated with developing TRALI. Our recent prospective study has revealed the predominance of male Fresh frozen plasma (FFP) FFP in post‐transfusion respiratory function when comparing male only FFP and mixed FFP in surgical patients. The incidence of TRALI in the UK was successfully reduced by using preferentially male plasma. Although TRALI has a relatively better prognosis than ALI with other causes, TRALI has still been the leading cause of transfusion‐related death in the United States in recent years. The prevention of TRALI caused by plasma products has been successful, but TRALI caused by apheresis platelets is still problematic. A recent study has suggested that the prevalence of anti‐HLA antibodies in female donors increases with the number of pregnancies. Thus, screening for anti‐HLA antibodies has emerged as an effective measure to prevent TRALI caused by apheresis platelets. At present, no single measure can thoroughly eliminate TRALI;...

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Section: Pathogenesis Of Tralimentioning

confidence: 99%

Fight against TRALI

Okazaki

2009

ISBT Science Series

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“…Leukocyte antibodies (e.g. anti-HNA-3a or anti-HLA-A2) stiffen neutrophils or even agglutinate them so that they cannot pass through the narrow lung capillaries and are trapped in the lung where the neutrophils become pro-adhesive (increased CD11b expression) (42), secrete proinflammatory mediators azurocidin, and heparin-binding protein) which can injure the endothelium (40,42,43). In a mouse TRALI model using a monoclonal HLA class I antibody, the occurrence of TRALI was dependent on neutrophils and their Fcγ receptors as well as on platelets and on housing of the mice in a nonpathogen-free barrier room (39,44).…”

Section: Pathophysiology Of Immune Tralimentioning

confidence: 99%

TRALI – new challenges for histocompatibility and immunogenetics in transfusion medicine

2011

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Antibodies against human leukocyte antigens (HLAs) have long been associated with transfusion-related acute lung injury (TRALI). In contrast to febrile transfusion reactions and refractoriness to platelet transfusions in immunized patients, the causative antibodies in TRALI are present in the transfused blood component, i.e. they are formed by the blood donor and not by the recipient. Consequently, blood components with high plasma volume are particularly associated with TRALI. In addition to antibodies against HLAs, antibodies directed against human neutrophil antigens (HNAs) present in the plasma of predominantly multiparous female blood donors can induce severe TRALI reactions. Especially, antibodies to HLA class II and HNA-3a antigens can induce severe or even fatal ALI in critically ill patients. Over the last decade, the clinical importance of TRALI as major cause for severe transfusion-related morbidities has led to the establishment of new guidelines aimed at preventing this condition, including routine testing for HLA and -HNA antibodies for plasma donors with a history of allogeneic sensitization. This, in turn, poses new challenges for close collaboration between blood transfusion centers and histocompatibility and immunogenetics laboratories, for sensitive and specific detection of the relevant antibodies.

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Heparin‐binding protein as a biomarker of post‐injury sepsis in trauma patients

Halldorsdottir

Eriksson

Persson

et al. 2018

Acta Anaesthesiol Scand

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In trauma patients, HBP levels are related to severity of injury and organ dysfunction. Heparin-binding protein was weakly associated with sepsis and only at the later stage of the observation period of 1 week. Moreover, HBP showed poor discriminatory properties as an early biomarker of post-injury sepsis. Trauma-induced inflammation during the post-injury phase may blunt the sepsis-predictive performance of HBP.

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Possible involvement of heparin‐binding protein in transfusion‐related acute lung injury

Cited by 8 publications

References 46 publications

Fight against TRALI

Fight against TRALI

TRALI – new challenges for histocompatibility and immunogenetics in transfusion medicine

Heparin‐binding protein as a biomarker of post‐injury sepsis in trauma patients

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