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ORIGINAL ARTICLE
Year : 2020  |  Volume : 9  |  Issue : 1  |  Page : 41-46

Heat-shock protein 70 and pentraxin-3 inflammatory biomarkers: Implication for thrombosis 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. Farqad Bader Hamdan
Department of Physiology, College of Medicine, Al-Nahrain University, P.O. Box 70044, Baghdad
Iraq
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijh.ijh_3_20

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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. Objectives: The objectives of this study are 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).


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