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The fibrinolytic system during short-term treatment with tenoxicam
1Department of Rheumatology, Aalborg Sygehus Nord, Denmark.
Abstract:
The effect of 20 mg tenoxicam once daily for 7 days on various components of the fibrinolytic system was studied in 10 healthy volunteers. Plasma plasminogen, antithrombin 3, and prekallikrein decreased significantly while plasma plasminogen activator inhibitor increased significantly. The medication did not affect fibrin plate lysis area or the plasma level of plasminogen activator, alpha-2-antiplasmin, alpha-2-macroglobulin, C1 inactivator or Factor XII. It is suggested that these changes may be caused by interference with hepatic enzyme systems. The reduction in plasma prekallikrein may indicate that tenoxicam exerts its anti-inflammatory effect by more than one mechanism.
Insights
Tenoxicam (20 mg daily for 7 days) significantly altered fibrinolytic system components in healthy volunteers. Key changes included decreased plasma plasminogen, antithrombin 3, and prekallikrein, with increased plasminogen activator inhibitor.
Area of Science:
- Pharmacology
- Hemostasis
- Biochemistry
Background:
- The fibrinolytic system is crucial for regulating blood clot breakdown.
- Non-steroidal anti-inflammatory drugs (NSAIDs) can influence coagulation and fibrinolysis.
- Understanding tenoxicam's impact on fibrinolysis is important for its clinical application.
Purpose of the Study:
- To investigate the effects of a 7-day course of 20 mg tenoxicam on key components of the human fibrinolytic system.
- To determine if tenoxicam influences plasma levels of specific coagulation factors and inhibitors.
Main Methods:
- Ten healthy volunteers received 20 mg tenoxicam once daily for 7 days.
- Plasma levels of plasminogen, antithrombin 3, prekallikrein, plasminogen activator inhibitor, plasminogen activator, alpha-2-antiplasmin, alpha-2-macroglobulin, C1 inactivator, and Factor XII were measured.
- Fibrin plate lysis area was also assessed.
Main Results:
- Significant decreases were observed in plasma plasminogen, antithrombin 3, and prekallikrein levels.
- A significant increase in plasma plasminogen activator inhibitor was noted.
- No significant changes were found in fibrin plate lysis area or levels of plasminogen activator, alpha-2-antiplasmin, alpha-2-macroglobulin, C1 inactivator, or Factor XII.
Conclusions:
- Tenoxicam administration alters specific components of the fibrinolytic system.
- Observed changes suggest potential interference with hepatic enzyme systems.
- The reduction in plasma prekallikrein may imply that tenoxicam's anti-inflammatory effects involve multiple mechanisms.