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Intrinsically impaired platelet production in some patients with persistent or chronic immune thrombocytopenia

dc.rights.licenseopenen_US
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorRIVIÈRE, Étienne
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorVIALLARD, Jean-François
dc.contributor.authorGUY, Alexandre
dc.contributor.authorKILANI, Badr
dc.contributor.authorVIEIRA-DIAS, Juliana
dc.contributor.authorPONS, Anne C.
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorCOUFFINHAL, Thierry
dc.contributor.authorPELLEGRIN, Jean-Luc
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorJAMES, Chloé
dc.date.accessioned2020-10-27T12:25:42Z
dc.date.available2020-10-27T12:25:42Z
dc.date.issued2015-08
dc.identifier.issn0007-1048en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/11493
dc.description.abstractEnPersistent or chronic immune thrombocytopenias (P/C-ITP) are acquired blood disorders lasting more than 3 months or 1 year, respectively. The pathogenesis of these disorders is thought to be immunological. We hypothesized that some patients with P/C-ITP might have an intrinsic megakaryopoiesis defect. We identified a group of P/C-ITP patients with acquired isolated mild thrombocytopenia (30-100 × 10(9) /l), undetectable anti-platelet antibodies, negative autoimmune investigations and no need for treatment. We examined in vitro megakaryocyte differentiation and compared these patients' results with those of acute-ITP patients and healthy controls. No difference in proliferation, ploidy or expression of surface markers was found. In contrast, P/C-ITP patients had significantly fewer proplatelet-forming megakaryocytes. This novel observation demonstrated that some patients diagnosed with P/C-ITP have an intrinsic megakaryopoiesis defect independent of the bone-marrow environment. Further investigations are needed to dissect mechanisms underlying this impaired proplatelet formation in these patients.
dc.language.isoENen_US
dc.subjectArticle CLINIQUE
dc.title.enIntrinsically impaired platelet production in some patients with persistent or chronic immune thrombocytopenia
dc.title.alternativeBr J Haematol.en_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1111/bjh.13444en_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologieen_US
bordeaux.journalBritish Journal of Haematologyen_US
bordeaux.page408–415en_US
bordeaux.volume170en_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires - U1034en_US
bordeaux.issue3en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-02980037
hal.version1
hal.date.transferred2020-10-27T12:25:46Z
hal.exporttrue
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