Publication: Activated platelet-derived microparticles in thalassaemia
Issued Date
2007-02-01
Resource Type
ISSN
13652141
00071048
00071048
Other identifier(s)
2-s2.0-33846023689
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Mahidol University
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SCOPUS
Bibliographic Citation
British Journal of Haematology. Vol.136, No.3 (2007), 462-471
Suggested Citation
Kovit Pattanapanyasat, Siriphan Gonwong, Porntip Chaichompoo, Egarit Noulsri, Surada Lerdwana, Kasama Sukapirom, Noppadol Siritanaratkul, Suthat Fucharoen Activated platelet-derived microparticles in thalassaemia. British Journal of Haematology. Vol.136, No.3 (2007), 462-471. doi:10.1111/j.1365-2141.2006.06449.x Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/25004
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Title
Activated platelet-derived microparticles in thalassaemia
Abstract
Thromboembolic complications have been documented in thalassaemia patients. The aggregability of abnormal red blood cells and the high level of membrane-derived microparticles (MPs) stemming from blood cells are thought to be responsible for the associated thrombotic risk. We investigated the number of MPs, their cellular origin and their procoagulant properties in β-thalassaemia. Fresh whole blood was simultaneously stained for annexin V, cellular antigens and the known density beads. The procoagulant properties of these phosphatidylserine (PS)-bearing MPs were also measured by assessing the platelet factor-3-like activity in the blood. Flow cytometric results showed that splenectomised β-thalassaemia/HbE patients had significantly higher levels of PS-bearing MPs than non-splenectomised β-thalassaemia/HbE patients and normal individuals (P < 0·0001). There was a good correlation between PS-bearing MPs and PS-bearing platelets, reflecting the existence of chronic platelet activation in β-thalassaemia/HbE patients (rs = 0·511, P < 0·001). The cellular origin of PS-bearing MPs showed mostly activated-platelet origin with adhesion (CD41a/CD62P/CD36). Moreover, the platelet procoagulant activity was higher in splenectomised β-thalassaemia/HbE patients when compared with non-splenectomised (P < 0·05) and normal individuals (P < 0·01), and the amount correlated with PS-bearing MPs (rs = 0·560, P < 0·001). These findings suggest that MPs originate from activated platelets with a potential to aggravate thrombotic events when the numbers are excessive, as is commonly seen in splenectomised β-thalassaemia/HbE patients. © 2007 The Authors.