Background : Thrombotic complications are among the most common causes of morbidity and mortality in myeloproliferative neoplasms, including polycythemia vera (PV). 95% PV patients share JAK2V617F mutation, that is associated with increased thrombotic risk. The role of platelet and leukocyte activation, accounting for coagulation activation in PV, is well established, while data on hemostatic abnormalities in PV, and their relationship with JAK2V617F burden is contradictory. Aims : To evaluate the hemostatic parameters in PV patients, predisposing high thrombosis risk, and their relation with JAK2V617F allele burden. Methods : The study included 27 PV patients. JAK2V617F mutation presence and allele burden were determined using allele specific polymerase-chain reaction. Coagulation assays (factors V, VIII, von Willebrand, antithrombin, protein C activities, fibrinogen concentration, von Willebrand factor antigen and free protein S level) were performed by standard techniques. The control group consisted of 68 healthy persons. STATISTICA 6.0 was used. Median and 95% confidence interval (CI) were calculated. Mann-Whitney and Spearman rank tests were applied, the differences considered statistically significant with p<0,05. Results : All but 3 PV patients in the study were JAK2V617F-positive, and 1 had mutation in JAK2-gene 12 exon. The age median constituted 55,5 years (95%CI 27,5-70,8). JAK2V617F allele burden data was available in 15 PV patients with median 15,6% (95%CI 4,5-34,0). The results of hemostatic parameters and JAK2V617F allele burden correlations are shown in Tables 1 and 2 respectively. Conclusions : The coagulation factor VIII increase and natural anticoagulants PC and PS decrease alongside with high fibrinogen in PV patients confirm the hypercoagulability, while VWF:Ag increase suggests the endothelium damage and dysfunction that can further enhance prothrombotic state in PV. The correlation analysis revealed a direct relationship between JAK2V617F allele burden and such procoagulants as FVIII and VWF (both activity and, especially, antigen) that contributes to the higher incidence of thrombosis depending on JAK2V617F burden. (Table Presented) .