Global InformationHyperfibrinolysis information
The fibrinolysis system is responsible for removing blood clots. Hyperfibrinolysis describes a situation with markedly enhanced fibrinolytic activity, resulting in increased, sometimes catastrophic bleeding. Hyperfibrinolysis can be caused by acquired or congenital reasons. Among the congenital conditions for hyperfibrinolysis, deficiency of alpha-2-antiplasmin[1] (alpha-2-plasmin inhibitor) or plasminogen activator inhibitor type 1 (PAI-1)[2] are very rare. The affected individuals show a hemophilia-like bleeding phenotype. Acquired hyperfibrinolysis is found in liver disease,[3] in patients with severe trauma,[4] during major surgical procedures,[5] and other conditions.[6] 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, hyperfibrinolysis is associated with poor outcome.[7] Moreover, hyperfibrinolysis may be associated with blood brain barrier impairment, a plasmin-dependent effect due to an increased generation of bradykinin.[8]
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 hyperfibrinolysis 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.
- ^ Carpenter SL, Mathew P (2008). "Alpha-2-antiplasmin and its deficiency: fibrinolysis out of balance". Haemophilia. 14 (6): 1250–4. doi:10.1111/j.1365-2516.2008.01766.x. PMID 19141165.
- ^ Takahashi Y, Tanaka T, Minowa H, Ookubo Y, Sugimoto M, Nakajima M, Miyauchi Y, Yoshioka A (July 1996). "Hereditary partial deficiency of plasminogen activator inhibitor-1 associated with a lifelong bleeding tendency". International Journal of Hematology. 64 (1): 61–8. doi:10.1016/0925-5710(96)00460-4. PMID 8757969.
- ^ Görlinger K (August 2006). "[Coagulation management during liver transplantation]". Hamostaseologie (in German). 26 (3 Suppl 1): S64–76. doi:10.1055/s-0037-1617084. PMID 16953295.
- ^ Levrat A, Gros A, Rugeri L, Inaba K, Floccard B, Negrier C, David JS (2008). "Evaluation of rotation thrombelastography for the diagnosis of hyperfibrinolysis in trauma patients". Br J Anaesth. 100 (6): 792–7. doi:10.1093/bja/aen083. PMID 18440953.
- ^ Vanek T, Jares M, Snircova J, Maly M (December 2007). "Fibrinolysis in coronary artery surgery: detection by thromboelastography". Interactive Cardiovascular and Thoracic Surgery. 6 (6): 700–4. doi:10.1510/icvts.2007.161463. PMID 17709365.
- ^ Chapin JC, Hajjar KA (January 2015). "Fibrinolysis and the control of blood coagulation". Blood Reviews. 29 (1): 17–24. doi:10.1016/j.blre.2014.09.003. PMC 4314363. PMID 25294122.
- ^ Schöchl H (2008). "Hyperfibrinolysis:a prognostic marker of poor survival following major trauma?". Haemostaseologie. 28: A57.
- ^ Marcos-Contreras, Oscar A.; Lizarrondo, Sara Martinez de; Bardou, Isabelle; Orset, Cyrille; Pruvost, Mathilde; Anfray, Antoine; Frigout, Yvann; Hommet, Yannick; Lebouvier, Laurent (2016-01-01). "Hyperfibrinolysis increases blood brain barrier permeability by a plasmin and bradykinin-dependent mechanism". Blood. 128 (20): blood–2016-03-705384. doi:10.1182/blood-2016-03-705384. ISSN 0006-4971. PMID 27531677.