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Arkadiusz Jawień, Piort Jurkowski, Marek Ciecierski, Maria Kotschy, Andrzej Swiatkiewicz
Med Sci Monit 2002; 8(4): CR263-268
BACKGROUND: Thrombophilia is caused mainly by disturbances of hemostasisinvolving excessive coagulation system activation, reduction of anticoagulation system (antithrombinIII, protein C, protein S, RAPC) or fibrinolytic activity. MATERIAL/METHODS: In 34 young patients (aged2 incidents) the activity of antithrombin III, proteinC, S, platelet count, adhesion and aggregation, APTT, stipven-kephalin, prothrombin time and INR wereinvestigated. Fibrinogen, factor XIII, ELT, FDP, Ag t-PA levels, antigen concentration and PAI-1 activitywere determined. Patients with idiopathic DVT, after elimination of most important thromboembolism riskfactors, were qualified for the study. DVT was confirmed in all patients by phlebography, plethysmographyand ultrasonography. Results were compared with a group of 54 healthy controls. RESULTS: In almost 50%of patients with recurrent DVT (15/34) decrease of at least one plasma coagulation inhibitor (AT III,PC, PS) level was observed. In the patient group (with AT III and/or PC and/or PS decrease) statisticallysignificant reduction of kaolin-kephalin time in comparison with controls was observed (α<0. 01). Analysis of fibrinolysis system demonstrated significant factor XIII level decrease (to 58.3&percnt;), fibrinogen level increase, ELT prolongation, and fibrinogen and fibrin degradation product increase in comparison with controls. The patients demonstrated 3-fold higher t-PA antigen level (13.1 ng/ml, α<0. 0001) and over 3-fold higher PAI-1 activity (26.7 AU/ml, α<0. 001) than healthy controls.
Conclusions: Reduced antithrombin III, protein C, protein S activity and excessive activation of the coagulation system with secondary fibrinolytic activity increase were found in patients with recurrent DVT.