@Article{, title={2020 Iraqi Journal of Hematology | Published by Wolters Kluwer ‑ Medknow 41 Heat‑shock protein 70 and pentraxin‑3 inflammatory biomarkers: Implication for thrombosis in polycythemia vera}, author={Farqad Bader Hamdan,}, journal={Iraq Joural of Hematology المجلة العراقية لامراض الدم}, volume={9}, number={1}, pages={41-46}, year={2020}, abstract={BACKGROUND: Chronic inflammation has been suggested to contribute to the pathogenesis ofthrombosis in polycythemia vera (PV) as it triggers in vivo activation of platelets, leukocytes, andendothelial cells, which are all of major importance during thrombus formation.OBJECTIVES: The aims of this study were to evaluate the pathophysiology behind increasedthrombosis in PV in terms of the effect of JAK2V617F gene mutation copies in relation to the intensityof the heat.shock proteins 70 (HSPs70) and long pentraxins.3 (PTX.3).SUBJECTS AND METHODS: Thirty patients with PV, 23 with secondary polycythemia, and thirtyhealthy volunteers were studied. Hemoglobin level, packed‑cell volume, white and red bloodcells count, mean corpuscular volume, and platelet counts were estimated. The enzyme‑linkedimmunosorbent assay was used to estimate the HSP70 and PTX‑3 levels, whereas the real‑timepolymerase chain reaction technique for the assessment of the JAK2 mutation rate was done foronly thirty PV patients.RESULTS: Significantly higher HSP70 and PTX‑3 levels were detected in PV patients. A positiverelationship was demonstrated between the JAK2 mutation rate and each of HSP70 and PTX‑3 andbetween the latter two biomarkers.CONCLUSION: The elevated HSP70 and PTX‑3 concentrations and the clear relationship betweenthem and JAK2 mutation rate can drive the procoagulant activity in blood cells in patients with PV.

} }