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dc.rights.licenseopenen_US
hal.structure.identifierCentre Hospitalier Universitaire de Bordeaux [CHU Bordeaux]
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorGUY, Alexandre
hal.structure.identifierCentre Hospitalier Universitaire de Bordeaux [CHU Bordeaux]
dc.contributor.authorHELZY, Khalil
hal.structure.identifierCentre Hospitalier Universitaire de Bordeaux [CHU Bordeaux]
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorMANSIER, Olivier
hal.structure.identifierHôpital Louis Pradel [CHU - HCL]
dc.contributor.authorBORDET, Jean-Claude
hal.structure.identifierService de médecine interne et maladies infectieuses [Bordeaux]
hal.structure.identifierHôpital Haut-Lévêque [CHU Bordeaux]
dc.contributor.authorRIVIERE, Etienne
hal.structure.identifierCentre Hospitalier Universitaire de Bordeaux [CHU Bordeaux]
dc.contributor.authorFIORE, Mathieu
hal.structure.identifierCentre Hospitalier Universitaire de Bordeaux [CHU Bordeaux]
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorJAMES, Chloé
dc.date.accessioned2023-03-10T08:53:59Z
dc.date.available2023-03-10T08:53:59Z
dc.date.issued2023-02
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/172245
dc.description.abstractEnBackground: JAK2V617F and Calreticulin (CALR) mutations are the most frequent molecular causes of Phi-negative myeloproliferative neoplasms (MPN). Patients with CALR mutations are at lower risk of thrombosis than patients with JAK2V617F. We hypothesized that CALR-mutated blood platelets would have platelet function defects that might explain why these patients are at lower risk of thrombosis. Objectives: Our main objective was to explore and compare platelet function depending on the MPN molecular marker. Methods: We analyzed platelet function in 16 patients with MPN with CALR mutations and 17 patients with JAK2V617F mutation and compared them with healthy controls. None of these patients was taking antiplatelet therapy. We performed an extensive analysis of platelet function and measured plasmatic soluble P-selectin and CD40L levels. Results: We observed significant defects in platelet aggregation, surface glycoprotein expression, fibrinogen binding, and granule content in platelets from patients with MPN compared with that in controls. Moreover, soluble CD40L and P-selectin levels were elevated in patients with MPN compared with that in controls, suggesting an in vivo platelet preactivation. Comparison of platelet function between patients with CALR and JAK2V617F MPN revealed only minor differences in platelets from patients with CALR. However, these results need to be interpreted within the context of absence of an inflammatory environment that could impact platelet function during MPN. Conclusions: These results do not support the hypothesis that calreticulin-mutated platelets have platelet function defects that could explain the lower thrombotic risk of patients with CALR.
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subjectArticle clinique
dc.subject.enblood platelets
dc.subject.encalreticulin
dc.subject.enJAK2V617F mutation
dc.subject.enmyeloproliferative neoplasms
dc.subject.enplatelet aggregation
dc.subject.enthrombosis
dc.title.enPlatelet function studies in myeloproliferative neoplasms patients with Calreticulin or JAK2V617F mutation
dc.typeArticle de revueen_US
dc.identifier.doi10.1016/j.rpth.2023.100060en_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologieen_US
bordeaux.journalResearch and Practice in Thrombosis and Haemostasisen_US
bordeaux.page100060en_US
bordeaux.volumeVol. 7en_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires (BMC) - UMR 1034en_US
bordeaux.issueIssue 2en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-04274001
hal.version2
hal.date.transferred2023-11-10T03:37:15Z
hal.exporttrue
workflow.import.sourcepubmed
dc.rights.ccCC BYen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Research%20and%20Practice%20in%20Thrombosis%20and%20Haemostasis&rft.date=2023-02&rft.volume=Vol.%207&rft.issue=Issue%202&rft.spage=100060&rft.epage=100060&rft.au=GUY,%20Alexandre&HELZY,%20Khalil&MANSIER,%20Olivier&BORDET,%20Jean-Claude&RIVIERE,%20Etienne&rft.genre=article


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