Coagulation and fibrinolysis in chronic venous insufficiency

Background: Varicose veins (VV) are common, but only some patients will develop chronic venous insufficiency (CVI) with skin changes or venous ulcer: The pathophysiology of venous ulcer development is complex, and mail involve abnormalities in coagulation, fibrinolysis and proinflammatory cytokines. The purpose of this study was to correlate plasma markers within these systems and skin pathology. Method: A group of twenty consecutive patients with active or recent venous ulcer were matched for sex and age with further three groups of individuals i.e. controls and patients with VV with and without skin changes respectively. Blood samples were analysed for hemoglobin (HB), total platelet count (TPC), C-reactive protein (CRP), activated partial thromboplastin time (APTT), prothrombin complex (PT), fibrinogen, interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF alpha), D-dimer; tissue plasminogen activator (t-PA), plasminogen activator inhibitor I(PAI-1), prothrombin fragments I and 2 (F1 +2), and thrombin antithrombin III complex (TAT). Results and conclusion: There was an increase of systemic levels of PAI-1 activity and tPA with progressive skin pathology in patients with CVI, and in the group with active ulcer there was an elevation of F 1 +2. Those findings could reflect a defect fibrinolysis, a thrombotic potential or a damaged endothelium.