BACKGROUND: Chronic inflammation has been suggested to contribute to the pathogenesis of
thrombosis in polycythemia vera (PV) as it triggers in vivo activation of platelets, leukocytes, and
endothelial cells, which are all of major importance during thrombus formation.
OBJECTIVES: The aims of this study were to evaluate the pathophysiology behind increased
thrombosis in PV in terms of the effect of JAK2V617F gene mutation copies in relation to the intensity
of the heat.shock proteins 70 (HSPs70) and long pentraxins.3 (PTX.3).
SUBJECTS AND METHODS: Thirty patients with PV, 23 with secondary polycythemia, and thirty
healthy volunteers were studied. Hemoglobin level, packed‑cell volume, white and red blood
cells count, mean corpuscular volume, and platelet counts were estimated. The enzyme‑linked
immunosorbent assay was used to estimate the HSP70 and PTX‑3 levels, whereas the real‑time
polymerase chain reaction technique for the assessment of the JAK2 mutation rate was done for
only thirty PV patients.
RESULTS: Significantly higher HSP70 and PTX‑3 levels were detected in PV patients. A positive
relationship was demonstrated between the JAK2 mutation rate and each of HSP70 and PTX‑3 and
between the latter two biomarkers.
CONCLUSION: The elevated HSP70 and PTX‑3 concentrations and the clear relationship between
them and JAK2 mutation rate can drive the procoagulant activity in blood cells in patients with PV.
Keywords:
Heat‑shock proteins 70, inflammation, JAK2, polycythemia vera, PTX‑3
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April 15, 2020
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