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Article type: Research Article
Authors: Aswad, Mohamed Hussama; b; * | Kissova, Jarmilaa; b | Ovesna, Petrac | Říhová, Luciea; b | Penka, Miroslava; b
Affiliations: [a] Department of Clinical Hematology, Faculty of Medicine, University Hospital Brno, Brno, Czech Republic | [b] Faculty of Medicine, Masaryk University, Brno, Czech Republic | [c] Institute of Biostatistics and Analyses, Faculty of Medicine, Masaryk University, Brno, Czech Republic
Correspondence: [*] Corresponding author: Mohamed Hussam Aswad, MD, Department of Clinical Hematology, University Hospital Brno, Jihlavska 20, Brno 625 00, Czech Republic. Tel.: +420608597958; E-mail: aswad.mohamedhussam@fnbrno.cz.
Abstract: The clinical course of essential thrombocythemia (ET) is complicated with thrombosis which significantly impacts patients’ mortality. Studies have identified JAK2V617F mutation as an independent risk factor for thrombosis. Circulating extracellular vesicles (EVs) were evaluated in several studies regarding myeloproliferative neoplasms and thrombosis as potential biomarkers. The present study investigates the relationship between JAK2V617F mutation and EVs levels in 119 ET patients. Our analyses revealed that JAK2V617F-positive patients are at a significantly increased risk of thrombosis within five years before the ET diagnosis (hazard ratio [95% CI]: 11.9 [1.7–83.7], P = 0.013), and that JAK2V617F mutation is an independent risk factor for thrombosis at ET diagnosis or during the follow-up (hazard ratio [95% CI]: 3.56 [1.47–8.62], P = 0.005). ET patients have higher levels of platelet-EVs, erythrocyte-EVs and procoagulant activity of EVs than the healthy population. Absolute and relative counts of platelet-EVs are increased in the presence of JAK2V617F mutation (P = 0.018, P = 0.024, respectively). In conclusion, our results support the role of JAK2V617F mutation in the pathogenesis of thrombosis in essential thrombocythemia through enhancing platelet activation.
Keywords: Essential thrombocythemia, thrombosis, risk factor, JAK2V617F mutation, extracellular vesicles
DOI: 10.3233/CH-221678
Journal: Clinical Hemorheology and Microcirculation, vol. 84, no. 4, pp. 359-368, 2023
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