Related Experiment Videos
Inhibition of the fibrinolytic system in Behçet's disease?
Insights
Behçet
Area of Science:
- Hematology
- Immunology
Background:
- Behçet's disease is characterized by a suppressed fibrinolytic system, often attributed to increased inhibitory potential.
- Investigating the fibrinolytic system in Behçet's disease is crucial for understanding its pathogenesis.
Observation:
- A venous occlusion test revealed significantly reduced fibrinolytic system activatability in 5 male patients with severe chronic Behçet's disease.
- Standard assays for known inhibitors like antithrombin III, alpha2-macroglobulin, and alpha2-antiplasmin showed normal levels.
Findings:
- The suppression of fibrinolysis in Behçet's disease was not explained by alterations in common inhibitory factors.
- Elevated alpha1-antitrypsin and fibrinogen were observed in some patients, suggesting an acute phase reaction.
Implications:
- The findings suggest that a decrease in the production or release of vessel wall activators may contribute to fibrinolysis suppression in Behçet's disease.
- Further research is needed to identify potential novel inhibitors or confirm the role of reduced activator release in the disease's pathophysiology.
Abstract:
Suppression of the fibrinolytic system is a well-known phenomenon in patients with Behçet's disease. It is generally explained by an increase in the inhibitory potential. In order to prove this theory, the fibrinolytic system was investigated in 5 male patients with severe chronic Behçet's disease. By the venous occlusion test, a marked suppression of the activatability of the system could be demonstrated (euglobulin lysis time, various fibrin plate assays). Results of analysis of the known inhibitors could not explain the phenomenon: antithrombin III, alpha2-macroglobulin, fast-reacting alpha2-antiplasmin, C1 inactivator, and the plasmin-antiplasmin complex were normal. The only change was an elevation of alpha1-antitrypsin and fibrinogen in 4 patients possibly due to an acute phase reaction. In addition to the possibility of a hitherto unidentified inhibitor, therefore, a decrease in production or in release of vessel wall activators must also be considered in the pathogenesis of this disorder.