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dc.rights.licenseopenen_US
dc.contributor.authorFIORE, Mathieu
dc.contributor.authorD'OIRON, Roseline
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorPILLOIS, Xavier
dc.contributor.authorALESSI, Marie-Christine
dc.date.accessioned2020-11-17T08:41:47Z
dc.date.available2020-11-17T08:41:47Z
dc.date.issued2018-04
dc.identifier.issn1365-2141en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/14048
dc.description.abstractEnGlanzmann thrombasthenia (GT) is caused by inherited defects of the αIIb β3 platelet glycoprotein. This bleeding disorder can be treated with platelet transfusion therapy, but some patients will be immunized and begin to form anti-human leucocyte antigen (HLA) and/or anti-αIIb β3 antibodies. These antibodies can bind and interfere with the function of the transfused platelets, rendering treatment ineffective. However, platelet transfusion refractoriness attributable to HLA antibodies may be managed by the selection of compatible donors, although they are not always readily available, particularly in an emergency. Thus, anti-αIIb β3 antibodies represent one of the most severe complications in GT. Both genetic and environmental factors may contribute to the risk of anti-αIIb β3 development, but the underlying pathogenic mechanisms are still unknown. This review will summarize the current knowledge of the risk factors for development of anti-αIIb β3 antibodies in patients with GT and discuss how these findings may influence the clinical management of patients.
dc.language.isoENen_US
dc.subjectArticle RECHERCHE
dc.subject.enAutoantibodies
dc.subject.enGlanzmann thrombasthenia
dc.subject.enHumans
dc.subject.enimmunization
dc.subject.enImmunization
dc.subject.enplatelet antibody
dc.subject.enPlatelet Glycoprotein GPIIb-IIIa Complex
dc.subject.enPlatelet Transfusion
dc.subject.enrFVIIa
dc.subject.enRisk Factors
dc.subject.enThrombasthenia
dc.subject.enTransfusion Reaction
dc.subject.enαIIbβ3
dc.title.enAnti-αIIb β3 immunization in Glanzmann thrombasthenia: review of literature and treatment recommendations
dc.typeArticle de revueen_US
dc.identifier.doi10.1111/bjh.15087en_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologieen_US
dc.identifier.pubmed29611179en_US
bordeaux.journalBritish Journal of Haematologyen_US
bordeaux.page173–182en_US
bordeaux.volume181en_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires - U1034en_US
bordeaux.issue2en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.exportfalse
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=British%20Journal%20of%20Haematology&rft.date=2018-04&rft.volume=181&rft.issue=2&rft.spage=173%E2%80%93182&rft.epage=173%E2%80%93182&rft.eissn=1365-2141&rft.issn=1365-2141&rft.au=FIORE,%20Mathieu&D'OIRON,%20Roseline&PILLOIS,%20Xavier&ALESSI,%20Marie-Christine&rft.genre=article


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