Successful use of recombinant factor VIIa in a patient with acquired Glanzmann thrombasthenia
dc.rights.license | open | en_US |
dc.contributor.author | TUFFIGO, Marie | |
hal.structure.identifier | Biologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases | |
dc.contributor.author | LAZARO, Estibaliz | |
hal.structure.identifier | Biologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases | |
dc.contributor.author | JAMES, C. | |
dc.contributor.author | SUBTIL, C. | |
hal.structure.identifier | Biologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases | |
dc.contributor.author | VIALLARD, Jean-Francois | |
hal.structure.identifier | Biologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases | |
dc.contributor.author | FIORE, Mathieu | |
dc.date.accessioned | 2020-10-27T14:30:35Z | |
dc.date.available | 2020-10-27T14:30:35Z | |
dc.date.issued | 2015-01 | |
dc.identifier.uri | https://oskar-bordeaux.fr/handle/20.500.12278/11514 | |
dc.description.abstractEn | NO ABSTRACT - Immune thrombocytopenic purpura (ITP) is caused by circulating antibodies that react with target antigens on the platelet membrane [1]. In very rare cases, ITP may be associated with acquired Glanzmann thrombasthenia (GT), a severe bleeding disorder [2,3]. While congenital GT is caused by inherited mutations in the genes encoding a IIb or b3 subunits [4], acquired GT results from naturally occurring auto-antibodies directed against the a IIb b 3 complex, inhibiting its function. Patients classically present with thrombocytopenia and defective platelet aggregation in response to all physiological stimuli. ... | |
dc.language.iso | EN | en_US |
dc.subject | Article CLINIQUE | |
dc.title.en | Successful use of recombinant factor VIIa in a patient with acquired Glanzmann thrombasthenia | |
dc.type | Article de revue | en_US |
dc.identifier.doi | 10.1111/hae.12589 | en_US |
dc.subject.hal | Sciences du Vivant [q-bio]/Médecine humaine et pathologie | en_US |
bordeaux.journal | Haemophilia | en_US |
bordeaux.page | 116–118 | en_US |
bordeaux.volume | 1 | en_US |
bordeaux.hal.laboratories | Biologie des maladies cardiovasculaires - U1034 | en_US |
bordeaux.issue | 1 | en_US |
bordeaux.institution | Université de Bordeaux | en_US |
bordeaux.peerReviewed | oui | en_US |
bordeaux.inpress | non | en_US |
hal.identifier | hal-02980612 | |
hal.version | 1 | |
hal.date.transferred | 2020-10-27T14:30:39Z | |
hal.export | true | |
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