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| __NOTOC__
| | #REDIRECT [[Aminocaproic acid#Drug Interactions]] |
| {{Aminocaproic acid}}
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| {{CMG}}; {{AE}} {{SS}}
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| ==Drug Interactions==
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| Prolongation of the template bleeding time has been reported during continuous intravenous infusion of AMICAR at dosages exceeding 24 g/day. Platelet function studies in these patients have not demonstrated any significant platelet dysfunction. However, in vitro studies have shown that at high concentrations (7.4 mMol/L or 0.97 mg/mL and greater) aminocaproic acid inhibits ADP and collagen-induced platelet aggregation, the release of ATP and serotonin, and the binding of fibrinogen to the platelets in a concentration-response manner. Following a 10 g bolus of AMICAR, transient peak plasma concentrations of 4.6 mMol/L or 0.60 mg/mL have been obtained. The concentration of AMICAR necessary to maintain inhibition of fibrinolysis is 0.99 mMol/L or 0.13 mg/mL. Administration of a 5 g bolus followed by 1 to 1.25 g/hr should achieve and sustain plasma levels of 0.13 mg/mL. Thus, concentrations which have been obtained in vivo clinically in patients with normal renal function are considerably lower than the in vitro concentrations found to induce abnormalities in platelet function tests. However, higher plasma concentrations of AMICAR may occur in patients with severe renal failure.<ref>{{Cite web | last = | first = | title = DailyMed: Search | url = http://dailymed.nlm.nih.gov/dailymed/search.cfm?startswith=Aminocaproic+acid&x=-1148&y=-229 | publisher = | date = | accessdate = 31 January 2014 }}</ref>
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| ==References==
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| {{Reflist|2}}
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| [[Category:Antifibrinolytics]]
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| [[Category:Cardiovascular Drugs]]
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| [[Category:Amino acids]]
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| [[Category:Antifibrinolytics]]
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| [[Category:Hematology]]
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| [[ja:Ε-アミノカプロン酸]]
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| [[pl:Kwas ε-aminokapronowy]]
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