Tranexamic acid: Difference between revisions
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In [[medicine]], [[tranexamic acid]] a hemostatic agent approved for hemorrhaging in [[hemophilia]], and, orally, for heavy mestrual bleeding, with unapproved uses in [[cyanide]] poisioning, hereditary [[angioedema]], [[hyperfibrinolysis]] induced hemorrhage, postsurgical [[hemorrhage]] and prevention of hemorrhage from cardiovascular instability after [[coronary artery bypass graft]]. It is an "inhibitor of plasminogen activation, and at much higher concentrations, a noncompetitive inhibitor of plasmin, i.e., actions similar to aminocaproic acid." It is similar to, but more potent than [[aminocaproic acid]].<ref name="urlDailyMed: tranexamic acid">{{cite web |url=http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=7849 |title=cyklokapron (tranexamic acid) injection, solution |author=Anonymous |authorlink= |coauthors= |date= |format= |work= |publisher=U.S. National Library of Medicine |pages= |language= |archiveurl= |archivedate= |quote= |accessdate=2009-02-19}}</ref> It is also used to treat acquired [[angioedema]] due to deficiency of [[complement C1 inhibitor protein]]. | |||
== Role in trauma medicine == | == Role in trauma medicine == | ||
The large multicenter CRASH-2 trial, in 2010, has shown striking mortality reductions after [[trauma (physical)|trauma]] and [[elective surgery]] after administration of tranexamic acid. <ref>{{citation | The large multicenter CRASH-2 trial, in 2010, has shown striking mortality reductions after [[trauma (physical)|trauma]] and [[elective surgery]] after administration of tranexamic acid. <ref>{{citation | ||
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| author = CRASH-2 trial collaborators* | | author = CRASH-2 trial collaborators* | ||
| date = June 15, 2010 | | date = June 15, 2010 | ||
| doi= 10.1016/S0140-6736(10)60835-5 | | doi= 10.1016/S0140-6736(10)60835-5}}</ref> This was reflected in the new European guidelines.<ref>{{citation | ||
|journal = Crit Care. | |journal = Crit Care. | ||
| date= 2010| volume = 14 |issue = 2 | page = R52 | | date= 2010| volume = 14 |issue = 2 | page = R52 | ||
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| url = http://www.medscape.com/viewarticle/722751}}</ref> | | url = http://www.medscape.com/viewarticle/722751}}</ref> | ||
== Mechanism of Action == | == Mechanism of Action == | ||
At low concentration, | Work in the CRASH trial is prompting reexamination of the broader clinical implications of antifibrinolysis. <ref>{{citation | ||
| title = Antifibrinolytic therapy: new data and new concepts | |||
| author = Levy, JH | |||
| journal = Lancet | year = 2010 | |||
| url = http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2810%2960939-7/fulltext}}</ref> | |||
At low concentration, tranexamic acid, which binds to the kringle domain of plasminogen, is a competetive inhibitor of plasminogen activation into [[plasmin]] (fibrinolysin), an [[enzyme]] that degrades [[fibrin]] clots, fibrinogen, and procoagulant plasma proteins such as [[factor V]] and [[factor VIII]]. At higher concentrations it is a noncompetetive inhibitor of plasmin. It binds to the strong and weak receptor sites of plasminogen with affnities about 10 times greater than [[aminocaproic acid]]. | |||
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<references/> | <references/> | ||
[[Category:Suggestion Bot Tag]] | |||
Latest revision as of 06:01, 30 October 2024
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| Uses: | antifibrinolytic | ||||||
| Properties: | fibrinogen inhibitor | ||||||
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In medicine, tranexamic acid a hemostatic agent approved for hemorrhaging in hemophilia, and, orally, for heavy mestrual bleeding, with unapproved uses in cyanide poisioning, hereditary angioedema, hyperfibrinolysis induced hemorrhage, postsurgical hemorrhage and prevention of hemorrhage from cardiovascular instability after coronary artery bypass graft. It is an "inhibitor of plasminogen activation, and at much higher concentrations, a noncompetitive inhibitor of plasmin, i.e., actions similar to aminocaproic acid." It is similar to, but more potent than aminocaproic acid.[1] It is also used to treat acquired angioedema due to deficiency of complement C1 inhibitor protein.
Role in trauma medicine
The large multicenter CRASH-2 trial, in 2010, has shown striking mortality reductions after trauma and elective surgery after administration of tranexamic acid. [2] This was reflected in the new European guidelines.[3]
Mechanism of Action
Work in the CRASH trial is prompting reexamination of the broader clinical implications of antifibrinolysis. [4]
At low concentration, tranexamic acid, which binds to the kringle domain of plasminogen, is a competetive inhibitor of plasminogen activation into plasmin (fibrinolysin), an enzyme that degrades fibrin clots, fibrinogen, and procoagulant plasma proteins such as factor V and factor VIII. At higher concentrations it is a noncompetetive inhibitor of plasmin. It binds to the strong and weak receptor sites of plasminogen with affnities about 10 times greater than aminocaproic acid.
References
- ↑ Anonymous. cyklokapron (tranexamic acid) injection, solution. U.S. National Library of Medicine. Retrieved on 2009-02-19.
- ↑ CRASH-2 trial collaborators* (June 15, 2010), "Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial", Lancet, DOI:10.1016/S0140-6736(10)60835-5
- ↑ Rolf Rossaint; Bertil Bouillon; Vladimir Cerny; Timothy J Coats; Jacques Duranteau; Enrique Fernández-Mondéjar; Beverley J Hunt; Radko Komadina; Giuseppe Nardi; Edmund Neugebauer; Yves Ozier; Louis Riddez; Arthur Schultz; Philip F Stahel; Jean-Louis Vincent; Donat R Spahn (2010), "Management of Bleeding Following Major Trauma: An Updated European Guideline", Crit Care. 14 (2): R52
- ↑ Levy, JH (2010), "Antifibrinolytic therapy: new data and new concepts", Lancet