The Impact of Mean Platelet Volume (MPV) and JAK-2 Mutation on Thrombosis in Chronic Myeloproliferative Diseases

Abstract

Thrombosis and bleeding are the main complications of chronic myeloproliferative diseases. Mean platelet volume (MPV) is an important indicator of the platelet activation. The aim of the present study was to assess the interrelationships between MPV, JAK-2 gene mutation and thromboembolic events in patients with ET and PV. Patients with ET (n = 60) and PV (n = 46) were compared to the secondary erythrocytosis group (n = 19); and a control group of age and sex matched healthy volunteers (n = 52). Besides demographic, clinical and laboratory data; thrombotic and hemorrhagic events were recorded for each patient. Platelet counts, MPV and JAK2 mutations were studied; and their relation with thromboembolic events were investigated using SPSS program for statistical analysis. There was no significant difference between groups regarding age ( = 0.188). Mean platelet count was significantly higher in ET group than other groups ( < 0.0001). Mean platelet count in PV group was significantly higher than control ( < 0.0001) and secondary erythrocytosis groups ( < 0.0001). In the ET group, MPV values were significantly lower than the control group and PV group. In the ET group, those with thromboembolia had lower platelet counts. There was no relation between MPV and thromboembolic event rate in PV, ET and secondary erithrocytosis groups; while no event was recorded in the control group. There was no relation between thromboembolic event rate and JAK 2 mutation. The association of JAK-2 mutation and high MPV especially in ET and PV groups does not contribute to the thromboembolic events.

Correlation of clinical signs and symptoms of Behçet’s disease with mean platelet volume (MPV) and red cell distribution width (RDW)

“…Important alterations in volume parameters of thrombocytes may have prophylactic and diagnostic importance in thrombotic events and prothrombotic tendency. In addition, increments in the platelet volume causes ischemia and infarction [ 14 ].…”

Increased mean platelet volume (MPV) is an independent predictor of inferior survival in patients with primary and secondary myelofibrosis

“…We identified six previous studies [21,22,[29][30][31][32] assessing role of MPV in Ph-MPN patients (PMF patients comprised a minority of analyzed populations in two works [21,22] and were not included in other studies). These studies investigated relationship between MPV, JAK2 mutational status and history of thrombosis with inconsistent findings among studies.…”

Clinical Aspects of Janus Kinase (JAK) Inhibitors in the Cardiovascular System in Patients with Rheumatoid Arthritis

“…This makes the IFN and STAT/JAK pathway the potential target to treat atherosclerosis. A few animal studies confirmed therapeutic potentials of IFN blockade resulting in inhibition of atherosclerotic plaque progression, stabilization of lipid- and macrophage-rich advanced plaques in ApoE knockout mice, and reduction of atherosclerosis in the graft vessels and the aorta in mice heart transplantation models [ 88 , 89 , 90 ]. Unfortunately, the inhibition of IFN blockade in atherosclerosis has not been tested in humans yet and studies on IFN inhibition in other indications (Crohn diseases and SLE) have been terminated prematurely due to lack of efficacy [ 87 ].…”

“…So, the inhibition of this pathway may exert anti-platelet activity [ 88 ]. The opposite conclusions come from the study of Ayer et al, who investigated the role of mutation of JAK2 in the development of thrombosis in chronic myeloproliferative diseases, finding no relationship between thromboembolic events and JAK2 mutation [ 89 ]. Recently, the role of tissue factor (TF) and its regulatory mechanism attracted attention of many researchers.…”