Platelet components associated with acute transfusion reactions: the role of platelet-derived soluble CD40 ligand

Cognasse, Fabrice; Payrat, Jean-Marc; Corash, L.; Osselaer, Jean Claude; Garraud, Olivier

doi:10.1182/blood-2008-05-157578

Cited by 50 publications

(63 citation statements)

References 10 publications

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“…De nombreuses études indiquent néanmoins que la majorité des incidents et accidents de nature bactérienne [53,54] mais aussi de nature inflammatoire (RFNH) survient en présence de CP délivrés entre j3 et j5 (et plus encore j7 lorsque ce délai est réglementairement autorisé) en lien direct avec une sécrétion accrue de BRM au-delà de j3, par les plaquettes elles-mêmes, même si ce point n'est pas retrouvé dans l'étude PLADO. L'accroissement de production de BRM par les plaquettes au-delà de 3 jours de conservation est, d'une part, spontanée (physiologique) mais elle peut être majorée par des stress de stockage et de conservation, infligeant des lésions [15,38,[55][56][57]. Le potentiel pro-inflammatoire des plaquettes homologues (allogéniques) transfusées est donc rapidement acquis.…”

Section: âGe Des Pslunclassified

Transfusion et inflammation : hier – aujourd’hui – demain

Garraud

Hamzeh‐Cognasse

Laradi

et al. 2015

Transfusion Clinique et Biologique

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Section: âGe Des Pslunclassified

Transfusion et inflammation : hier – aujourd’hui – demain

Garraud

Hamzeh‐Cognasse

Laradi

et al. 2015

Transfusion Clinique et Biologique

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“…Potential NAFs that accumulate during the routine storage of blood products include lyso-phosphatidylcholines (lysoPCs) [9,36,[38][39][40][41], neutral lipids [34,[38][39][40][41], sCD40L [42][43][44][45], cytokines [37,45,46] and microparticles (MPs) [47,48]. Some NAFs have the ability to prime for PMN respiratory burst [9,34,36,[38][39][40]43].…”

Section: Non-antibody Factors (Nafs)mentioning

confidence: 99%

Evidence behind the pathophysiology of TRALI

Tung

Minchinton

Fraser

et al. 2011

ISBT Science Series

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Transfusion-related acute lung injury (TRALI) is a serious transfusion complication that may lead to significant morbidity and mortality. This has driven a significant research effort focused on understanding why and how TRALI develops. The ultimate goal must be prevention or at least mitigation of the clinical consequences of TRALI.The underlying pathophysiology of TRALI is presently best described by two hypotheses which are not mutually exclusive. These are the antibody mediated TRALI mechanism and the two-event or priming TRALI mechanism. One of the key initial findings in TRALI research was the frequent presence of leucocyte antibodies in associated blood products, providing strong evidence for an antibody driven pathogenesis. In contrast, the two-event mechanism proposed that these transfused antibodies activated neutrophils that had first been primed by the patient's clinical condition.Together, data from haemovigilance programs, clinical reports and experimental findings have led several countries to introduce TRALI risk-reduction strategies. These include either limiting the transfusion of plasma from female donors or, screening female donors for the presence of leucocyte antibodies. Both approaches are justified by adoption of the immune mechanism as the prime driver of the pathogenesis of TRALI. TRALI incidence has gratifyingly been reduced by these measures. Nevertheless, TRALI cases persist and they remain a major concern because of continuing significant morbidity and mortality.While the majority of earlier TRALI research has focused on the role of antibodies in TRALI, evidence for the role of non-antibody factors in TRALI is now growing, based on an increasing number of in vitro, ex vivo and in vivo models. This review aims to present data from such models, which are the foundation for our current understanding of the pathophysiology behind antibody mediated and non-antibody mediated TRALI.

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“…4-8 Of importance, recent data link BRMs to adverse transfusion reactions after human PLT concentrate therapy. 4,7,[9][10][11][12] Register studies suggest that transfusion reactions occur in up to 5% of PLT treatments, 13,14 with a higher incidence in high-risk populations such as pediatric patients. 15 Most of these are likely to resolve relatively quickly, but their occurrence is associated with both adverse outcomes 4,16,17 and longer hospital stays.…”

mentioning

confidence: 98%