Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Aminocaproic acid
General information
During normal fibrinolysis, inactive circulating plasminogen binds to fibrin through an active site that binds lysine. The bound plasminogen is then converted to plasmin by activators (such as tissue plasminogen activator, t-PA) and converted to plasmin, which breaks down the fibrin. Aminocaproic acid (ε-aminocaproic acid, EACA, 6-aminohexanoic acid, Amicar) and tranexamic acid (Cyklokapron) are structural analogues of lysine, which bind irreversibly to the lysine-binding sites on plasminogen, inhibiting binding to fibrin and thus the whole process of fibrinolysis [ , ]. These agents inhibit the natural degradation of fibrin and so stabilize clots.
Aminocaproic acid was the first such agent to be used widely, but it has largely been superseded in clinical practice by tranexamic acid, which is about 10 times more potent. Para-aminomethylbenzoic acid (PAMBA) is similar to aminocaproic acid, but is about three times more active in inhibiting plasminogen activators [ ]. However, it is no longer used despite the fact that it is well tolerated.
Uses
Antifibrinolytic agents are of benefit in the treatment of primary menorrhagia [ ], recurrent epistaxis [ ], oral bleeding in patients with congenital and acquired coagulation disorders [ , ], hemorrhage associated with thrombolytic therapy, and to reduce blood loss associated with surgery (especially cardiac surgery, joint replacement, and orthotopic liver transplantation) [ ]. Antifibrinolytic therapy can be of value in other conditions as well [ ]. It is effective in the bleeding diathesis that can accompany acute promyelocytic leukemia [ , ], but it does not improve outcome after subarachnoid hemorrhage [ ].
General adverse effects and reactions
Some adverse effects are associated with all antifibrinolytic agents, reflecting their effect on clot stability. Dissolution of extravascular blood clots may be resistant to physiological fibrinolysis. These drugs should not to be used to treat hematuria due to blood loss from the upper urinary tract, as this can provoke painful clot retention and even renal insufficiency associated with bilateral ureteric obstruction [ ].
Well-controlled studies on aminocaproic acid in a limited number of patients showed no serious adverse effects. Minor unwanted effects have been reported in 10–20% of patients and include headache, nasal congestion, conjunctival suffusion, nausea, vomiting, diarrhea, and transient hypotension [ ]. Skin rashes have also been associated with aminocaproic acid, including maculopapular and morbilliform eruptions. Rarer dermatological reactions reported include purpuric rashes [ ], bullous eruptions [ ], and contact dermatitis with positive patch tests [ ]. Treatment with a high dose (the maximum daily dose is 36 g/day) can result in an osmotic diuresis [ ].
Miscellaneous adverse reactions attributed by the authors of single case reports have included a psychotic reaction [ ], convulsions after intravenous administration of aminocaproic acid in a 60-year-old man treated for bleeding esophageal varices [ ], and renal insufficiency due to glomerular capillary thrombosis [ ].
Aminocaproic acid used during cardiopulmonary bypass reduced mediastinal blood losses by about one-third, while transfusion requirements were unchanged [ ]. In one series of over 950 patients, not a single thromboembolic complication could be ascribed to aminocaproic acid. However, a few cases of muscle necrosis and rhabdomyolysis with renal insufficiency have been reported with aminocaproic acid [ , ].
You're Reading a Preview
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here