Literature DB >> 12590950

Markers of platelet activation and platelet-leukocyte interaction in patients with myeloproliferative syndromes.

Torben Villmow1, Bettina Kemkes-Matthes, Axel C Matzdorff.   

Abstract

INTRODUCTION: Changes in platelet count and function contribute to thrombo-hemorrhagic episodes in chronic myeloproliferative syndromes (MPS). We used flow cytometry to study platelet-leukocyte conjugates and markers of platelet activation in patients with MPS.
METHODS: Whole blood from patients with chronic myelogenous leukemia (CML), polycythemia vera (PV), chronic myelofibrosis (MF), and essential thrombocythemia (ET) and from healthy volunteers was prepared for flow cytometry. Platelet microparticles and platelet microaggregates were identified with anti-CD42b and forward scatter, activated platelets with anti-CD62p. Anti-CD42b, anti-CD14, and anti-CD45 were used to study platelet-leukocyte conjugates.
RESULTS: The percentage of CD62p-positive platelets was elevated in all myeloproliferate syndrome subtypes. The median percentage of platelet microparticles was 5.2% in controls and significantly higher in PV (12.0%), MF (11.0%), and ET (11.0%, all p<0.05). There was an increased percentage of platelet-neutrophil conjugates in patients with PV (8.3%) and ET (10.4%) compared to normal controls (6.8%, all p<0.05). Platelet-monocyte conjugates were 8.0% in controls and elevated in PV (15.4%) and ET (15.0%, all p<0.05). Patients with a history of venous or arterial thrombotic events had slightly less platelet-leukocyte conjugates and slightly more microparticles than patients without thrombosis; however, this difference was not statistically significant.
CONCLUSIONS: These findings suggest that platelet-leukocyte conjugate formation occurs in myeloproliferative syndromes and indicates platelet activation. Also, platelet microparticles are elevated and might provide a catalytic surface for thrombin generation. This could explain the clinical observation that patients with myeloproliferative syndromes have an increased risk to experience arterial or venous thrombotic events.

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Year:  2002        PMID: 12590950     DOI: 10.1016/s0049-3848(02)00354-7

Source DB:  PubMed          Journal:  Thromb Res        ISSN: 0049-3848            Impact factor:   3.944


  17 in total

1.  Abnormal P-selectin localization during megakaryocyte development determines thrombosis in the gata1low model of myelofibrosis.

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6.  Neutrophil cytoskeletal rearrangements during capillary sequestration in bacterial pneumonia in rats.

Authors:  Kazuo Yoshida; Ryoichi Kondo; Qin Wang; Claire M Doerschuk
Journal:  Am J Respir Crit Care Med       Date:  2006-06-01       Impact factor: 21.405

7.  Does anti-TNF therapy cause any change in platelet activation in ankylosing spondylitis patients? A comparative study.

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8.  Elevated procoagulant microparticles expressing endothelial and platelet markers in essential thrombocythemia.

Authors:  Marijke C Trappenburg; Muriel van Schilfgaarde; Marina Marchetti; Henri M Spronk; Hugo ten Cate; Anja Leyte; Wim E Terpstra; Anna Falanga
Journal:  Haematologica       Date:  2009-06-08       Impact factor: 9.941

9.  Markers of endothelial and in vivo platelet activation in patients with essential thrombocythemia and polycythemia vera.

Authors:  Marina Karakantza; Nikolaos C Giannakoulas; Panagiotis Zikos; George Sakellaropoulos; Alexandra Kouraklis; Anthi Aktypi; Ioannis C Metallinos; Eleni Theodori; Nicholas C Zoumbos; Alice Maniatis
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10.  Cholesterol efflux in megakaryocyte progenitors suppresses platelet production and thrombocytosis.

Authors:  Andrew J Murphy; Nora Bijl; Laurent Yvan-Charvet; Carrie B Welch; Neha Bhagwat; Adili Reheman; Yiming Wang; James A Shaw; Ross L Levine; Heyu Ni; Alan R Tall; Nan Wang
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