Intrinsically impaired platelet production in some patients with persistent or chronic immune thrombocytopenia. (14th April 2015)

• Record Type: Journal Article
• Authors: Rivière, Étienne; Viallard, Jean‐François; Guy, Alexandre; Kilani, Badr; Vieira‐Dias, Juliana; Pons, Anne C.; Couffinhal, Thierry; Pellegrin, Jean‐Luc; James, Chloé
• Is Part Of: British journal of haematology. Volume 170:Number 3(2015:Aug.)
• Page Start: 408
• Page End: 415
• Publication Date: 2015-04-14
• Subjects: Hematology -- Periodicals; Blood -- Diseases -- Periodicals; 616.15
• DOI: 10.1111/bjh.13444
• Languages: English
• ISSNs: 0007-1048

Abstract

<abstract abstract-type="main" id="bjh13444-abs-0001"> <title>Summary</title> <p>Persistent 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 × 10⁹/l), undetectable anti‐platelet antibodies, negative autoimmune investigations and no need for treatment. We examined <italic>in vitro</italic> 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.</p> </abstract>