The fibrinolysis system is responsible for removing blood clots.<unk>  describes a situation with markedly enhanced fibrinolytic activity, resulting in increased, sometimes catastrophic bleeding.<unk>  can be caused by acquired or congenital reasons. Among the congenital conditions for<unk> , deficiency of alpha-2-antiplasmin (alpha-2-plasmin inhibitor) or plasminogen activator inhibitor type 1 (PAI-1) are very rare. The affected individuals show a hemophilia-like bleeding phenotype. Acquired<unk>  is found in liver disease, in patients with severe trauma, during major surgical procedures, and other conditions. A special situation with temporarily enhanced fibrinolysis is thrombolytic therapy with drugs which activate plasminogen, e.g. for use in acute ischemic events or in patients with stroke. In patients with severe trauma,<unk>  is associated with poor outcome. Moreover,<unk>  may be associated with blood brain barrier impairment, a plasmin-dependent effect due to an increased generation of bradykinin. Bleeding is caused by the generation of fibrinogen degradation products which interfere with regular fibrin polymerization and inhibit platelet aggregation. Moreover, plasmin which is formed in excess in<unk>  can proteolytically activate or inactivate many plasmatic or cellular proteins involved in hemostasis. Especially the degradation of fibrinogen, an essential protein for platelet aggregation and clot stability, may be a major cause for clinical bleeding.
Hyperfibrinolysis
Procoagulant platelets
Warfarin resistance
Venom-induced consumption coagulopathy
Primary fibrinogenolysis
Thrombocythemia
Vitamin K reaction
Intravascular hemolysis