Abstract:
BACKGROUND: Polycythemia vera (PV) is a chronic myeloproliferative stem cell disease usually
combined with JAK2 mutation. Active JAK2 mutation directly promote platelets and granulocytes
activation and indirectly initiate endothelial activation. Such interactions can provoke endothelial
injury with subsequent release of procoagulant factors. The aim of this study was to understand
of this study is to understand the pathophysiology of increased thrombosis in PV in terms of the
effect of JAK2V617F gene mutation in relation to the intensity of the neutrophil CD11b and platelet
CD62P.
SUBJECTS AND METHODS: A group of 53 patients was examined comprised 30 PV patients
and 23 with secondary polycythemia. In parallel, 30 aged‑ and sex‑matched, nonsmokers healthy
volunteers served as a control group. Hemoglobin level, packed cell volume, white and red blood
cells count, mean corpuscular volume, and platelet count were estimated for all the 83 participants.
Flow cytometry for the detection of neutrophil CD11b and platelet CD62P were done for all the
participants; whereas quantitative polymerase chain reaction technique for the assessment of JAK2
mutation rate was done for the 30 PV patients only.
RESULTS: We were able to detect significantly higher neutrophil CD11b and platelet CD62P
expressions in PV patients. Within PV, JAK2 mutation rate was significantly higher in those with a
history of thrombosis. A positive relationship was demonstrated between the JAK2 mutation rate
and each of CD11b and CD62P.
CONCLUSION: There is an overexpression of neutrophil CD11b and platelets CD62P in patients
with PV which can be considered as a marker of procoagulant activity in blood cells. Active JAK2
mutation directly promote platelets and granulocytes activation and indirectly initiate endothelial
activation and in turn endothelium into a proadhesive and procoagulant surface.
Keywords:
CD11b, CD62P, flow cytometry, JAK2, polycythemia vera
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17-10-2019
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