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Year : 2018  |  Volume : 7  |  Issue : 1  |  Page : 8-13

Role of endothelial dysfunction in relation to prothrombogenesis in polycythemia vera

1 Department of Physiology, College of Medicine, Al-Nahrain University, Baghdad, Iraq
2 Department of Medicine, College of Medicine, Al-Nahrain University, Baghdad, Iraq

Correspondence Address:
Dr. Waseem F Al-Tameemi
PO Box 70044, College of Medicine, Al Nahrain University, Kadhmiyia, Baghdad
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijh.ijh_32_17

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Background: The morbidity and mortality in polycythemia vera (PV) are closely associated with cardiovascular diseases burden and clonal evolution. These complications were primarily attributed to abnormal rheology consequent to the raised hematocrit, leukocytosis, and thrombocytosis, and in vivo activation of leukocytes, thrombocytes, and endothelial cells. It has been established that damage of endothelium determines the release in circulation of specific markers including thrombomodulin (TM), selectins, and von Willbrand factor (vWF) which are released and favor the formation of cellular aggregates. Objectives: The objective of this study is to evaluate the pathophysiological role of endothelial dysfunction (ED) in relation to increased risk of thrombosis in PV patients. Patients and Methods: In a case–control study, 53 patients enrolled in this study from Al-Imamain Al-Khadimiyan Medical City, and the National Center for Hematology Diseases and Researches. They comprised of thirty patients with PV with mean age of − 54.87 ± 13.44 years-and another twenty-three patients with secondary polycythemia, whose mean age was 40.13 ± 12.21 years. Another thirty aged- and sex-matched, non-smokers healthy volunteers comprised 16 males and 14 females were also studied, their mean age was = 52.1 ± 11.16 years. JAK2 mutation was assessed for PV group while Serum erythropoietin (Epo), vWF and TM were determined for all patient and control group. Results: TM was significantly different among the three studied groups (P < 0.001) as well as vWF was significantly higher (P < 0.001) in patients with PV as compared to the patients with secondary polycythemia and controls. Epo level was significantly lower (P = 0.004) in the newly diagnosed patients with PV when compared to those with a history of thrombosis or longstanding disease. There is positive correlation between JAK2 and TM (r = 0.431, P = 0.017), while negative correlation with vWF (r = −0.565, P = 0.001) in PV patients. Conclusion: ED is one of mechanisms that contribute in prothrombogenesis in PV patient.

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