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.
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http://dx.doi.org/10.3233/CH-221678 | DOI Listing |
Aliment Pharmacol Ther
January 2025
Division of Gastroenterology and Hepatology, Department of Medicine, University of Pennsylvania, Philadelphia, USA.
Background And Aims: We assessed clinical, procoagulant and genetic risk factors and clinical outcomes in dabigatran-treated patients with non-tumoural acute and acute-on-chronic portal vein thrombosis (PVT).
Methods: Patients with a new diagnosis of non-tumoural acute and acute-on-chronic PVT between January 2021 and January 2024 (aged ≥ 18 years) in those without/with cirrhosis (Child-Pugh (CP)-A/B/C ≤ 10) were started on dabigatran and followed and compared with those on vitamin K antagonist (VKA) and untreated individuals.
Results: Dabigatran was prescribed in 119 patients with PVT type 1 (61, 51.
Hamostaseologie
December 2024
Klinik für Innere Medizin II, Abteilung Hämatologie und Internistische Onkologie, Universitätsklinikum Jena, Jena, Germany.
Background: The risk of thrombosis and bleeding in myelofibrosis (MF) has been historically underappreciated. We sought to investigate potential molecular and clinical risk factors for venous (VTE) and arterial (ATE) thrombotic events as well as bleeding episodes.
Methods: Data from 246 consecutive MF patients were analyzed.
Hemasphere
December 2024
Department of Hematology, Oncology, Hemostaseology and Stem Cell Transplantation, Medical Faculty RWTH Aachen University Aachen Germany.
Myelofibrosis (MF) is a clonal myeloid neoplasm characterized by bone marrow fibrosis, splenomegaly, and disease-associated symptoms, as well as increased mortality, due to thrombosis, severe bleeding, infections, or progression to acute leukemia. Currently, the management of MF patients is tailored according to risk scores, with higher-risk (intermediate-2 and high-risk) patients being assessed for allogeneic stem cell transplantation, which remains the only potentially curative treatment option. On the other hand, lower risk (low- and intermediate-1 risk) patients who are symptomatic may be treated with JAK inhibitors or other drugs.
View Article and Find Full Text PDFSaudi Med J
December 2024
From the Department of Preventive Medicine (Alsharif, Alharazi), Directorate of Health Affairs; from the Hematology Department (Mansory, Badawi), Faculty of Medicine, King Abdulaziz University; and from the Hematology Research Unit (Mansory, Badawi), King Fahd Medical Research Center, King Abdulaziz University, and from the Blood Transfusion Services Unit (Badawi), King Abdulaziz University Hospital, Jeddah, Kingdom of Saudi Arabia.
Objectives: To systematically review evidence on the prevalence of the JAK2V617F (JAK2) mutation and polycythemia vera (PV) among all blood donors, focusing on those with elevated hematocrit. Although blood donors are generally healthy, considering a preclinical stage of myeloproliferative neoplasm, especially in those with polycythemia, is crucial. Evidence on managing these donors is limited.
View Article and Find Full Text PDFThromb Res
January 2025
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark; Department of Neurology, Zealand University Hospital, Roskilde, Denmark.
Background: The JAK2V617F mutation is a driver of Philadelphia chromosome-negative myeloproliferative neoplasms (MPN) and is also implicated in cardiovascular diseases. Thrombosis in MPN involves JAK2V617F-associated platelet activation and endothelial dysfunction, all potentially influenced by chronic inflammation. Whether the mutation affects thromboinflammatory markers similarly in non-MPN patients remains unclear.
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