We studied activation of hemostatic reactions together with mechanisms of systemic inflammation and genetic factors responsible for thrombogenic risk in 65 patients suffering exacerbation of chronic obstructive pulmonary disease with 2 or 3 positive criteria proposed by N.Anthonisen at al. (1987). The levels of indicators of systemic inflammation, such as C-reactive protein and tumour necrosis factor-alpha, increased concurrently with those of homocysteine, endothelin-1, Willebrand factor plasminogen activator inhibitor type 1, and thrombin-antithrombin complex (marker of thrombinemia). The prevalence of pathological alleles ofprotein genes involved in the hemostasis system and folate cycle remained as in the control group. A relationship between plasma levels of thrombin-antithrombin complex and Willebrand factor and the activity of indicators of systemic inflammation was documented. Treatment of exacerbation resulted in the decrease in the levels of the thrombin- antithrombin complex, inhibitor of the extrinsic pathway of coagulation, and plasminogen activator inhibitor type 1. The treatment failed to normalize parameters of thrombinemia and blood fibrinolytic potential.
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