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 the 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 a 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 the mechanisms that contribute in prothrombogenesis in PV patient.
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February 2018
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