Akademik Veri Yönetim Sistemi
WORLD JOURNAL OF SURGERY, cilt.24, sa.12, ss.1584-1588, 2000 (SCI-Expanded, Scopus)
Behcet disease (BD) is an inflammatory illness that may attack several systems. Vascular involvement with thrombosis is one of the basic characteristics of this disease. The etiology of thrombosis tendency in ED has not been understood well. In this study, the role of primary coagulation parameters in patients with ED who have thromboembolic events was evaluated. In addition, the relation between the clinical activity of the disease and these parameters was compared. A total of 96 patients,vith a diagnosis of ED were studied at Ankara University, Medical School, Department of General Surgery and Behcet Center. ED patients were separated into two groups with respect to vascular involvement. Group A contained 22 patients dth vascular attacks, and group B contained 74 patients without vascular attacks. In addition, 25 healthy persons comprised the control group (group C). The coagulation parameters assessed included protein C, protein S, antithrombin III activity, fibrinogen level, prothrombin time (PT), and partial thromboplastin time (PTT). There were no differences among the three groups with respect to protein C, protein S, fibrinogen, PT, and PTT values (p > 0.05). The antithrombin III value vias found to be high in ED patients compared to those in the control group (p = 0.011). There was no difference regarding the antithrombin III value between ED patients with or without vascular attacks (p = 0.954). There was no correlation between the activity of disease and coagulation parameters (p > 0.05), but a positive correlation mas seen between the duration of illness and vascular involvement. Fifty percent of patients who had had ED more than 8 years had vascular involvement (p = 0.002). We could not determine a specific pathology in relation to coagulation parameters that could explain the etiology of thrombosis in patients with ED. The elevated antithrombin III levels in patients with ED (compared to controls) may be due to a compensatory defense mechanism against increased procoagulant activity. There was a correlation between the duration of illness and vascular involvement.