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[The mechanisms of intravascular blood coagulation in patients with systemic scleroderma]
Hemostasis was investigated in 2 groups of patients with systemic scleroderma (SSD) with minimal (12 patients) and moderate (9 patients) activity of the process. It has been shown that in SSD, the triggering factor of intravascular blood coagulation is the release of Willebrand's factor, an activator of platelets, from the impaired endothelium. Hyperaggregation and labilization of platelets characterizes the course of SSD irrespective of the disease activity. The main changes in coagulation hemostasis are related to the dramatically accelerated triggered thrombin formation and deficiency of the antithrombin potential. The status of fibrinolysis confirming the thrombogenic situation is marked by a number of features: depression of contact lysis is maximally pronounced in chronic SSD with minimal activity, accumulation of the soluble complexes of fibrin monomer only correlates with the disease activity, and no significant rise of the level of fibrin/fibrinogen degradation products has been discovered.
Hemostasis was investigated in 2 groups of patients with systemic scleroderma (SSD) with minimal (12 patients) and moderate (9 patients) activity of the process. It has been shown that in SSD, the triggering factor of intravascular blood coagulation is the release of Willebrand's factor, an activator of platelets, from the impaired endothelium. Hyperaggregation and labilization of platelets characterizes the course of SSD irrespective of the disease activity. The main changes in coagulation hemostasis are related to the dramatically accelerated triggered thrombin formation and deficiency of the antithrombin potential. The status of fibrinolysis confirming the thrombogenic situation is marked by a number of features: depression of contact lysis is maximally pronounced in chronic SSD with minimal activity, accumulation of the soluble complexes of fibrin monomer only correlates with the disease activity, and no significant rise of the level of fibrin/fibrinogen degradation products has been discovered.