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Epsilon-aminocaproic acid

Less severe hemorrhages may be treated successfully with antihbrinolytic amino acids alone or in combination with factor replacement therapy. Tranexamic acid (20-25 mg/kg every 8 to 12 hours) and epsilon aminocaproic acid (50-60 mg/kg every 4—6 hours) maybe administered intravenously or orally. [Pg.995]

Note In fibrinolysis, plasmin, an endopeptidase that is converted from plasminogen by an activator, hydrolyzes fibrin, fibrinogen, factor V, and factor VIII to their inactive products. Hageman factor (factor XII) converts a proactivator to the active activator. Agents such as thrombin, streptokinase, and urokinase therefore enhance the formation of plasmin and hence have fibrin lytic properties. Epsilon-aminocaproic acid inhibits the activator-mediated formation of plasmin and hence may be used as an antidote to streptokinase-urokinase, or in a defibrination syndrome when bleeding from a mucous membrane occurs. [Pg.42]

After purification, the lactam is polymerized by heating at elevated temperatures in an inert atmosphere. During self-condensation, the ring structure of the lactam is opened so that the monomer acts as an epsilon-aminocaproic acid radical. Unlike that of nylon 66, the polymerization of caprolactam is reversible the polymer remains in equilibrium with a small amount of monomer. As with nylon 66, nylon 6 is extruded in thin strands, quenched, and cut into chips for subsequent spinning, or the molten polymer is pumped directly to the spinning equipment. [Pg.456]

Frederiksen MC, Bowsher DJ, Ruo TI, Henthorn TK, Ts ao C-H, Green D, Atkinson AJ Jr. Kinetics of epsilon-aminocaproic acid distribution, elimination, and antifibrinolytic effects in normal subjects. Clin Pharmacol Ther 1984 35 387-93. [Pg.311]

Jordan D, Delphin E, Rose E. Prophylactic epsilon-aminocaproic acid (EACA) administration minimizes blood replacement therapy during cardiac surgery. Anesth Analg 1995 80(4) 827-9. [Pg.116]

Schwartz BS, Williams EC, Coulau MG, Mosher DF. Epsilon-aminocaproic acid in the treatment of patients with acute promyelocytic leukemia and acquired alpha-2-plasmin inhibitor deficiency. Ann Intern Med 1986 105(6) 873-7. [Pg.117]

Wymenga LF, van der Boon WJ. Obstruction of the renal pelvis due to an insoluble blood clot after epsilon-aminocaproic acid therapy resolution with intraureteral streptokinase instillations. J Urol 1998 159(2) 490-2. [Pg.117]

McNicol GP, Fletcher AP, Alkjaersig N, et al. The use of epsilon-aminocaproic acid, a potent inhibitor of fibrinolytic activity, in the management of postoperative hematuria. J Urol 1961 86 829. [Pg.117]

Chakrabarti A, Collett KA. Purpuric rash due to epsilon-aminocaproic acid. BMJ 1980 281(6234) 197-8. [Pg.117]

Brooke CP, Spiers EM, Omura EF. Noninflammatory bullae associated with epsilon-aminocaproic acid infusion. J Am Acad Dermatol 1992 27(5 Pt 2) 880-2. [Pg.117]

Tanaka M, Niizeki H, Miyakawa S. Contact dermatitis from epsilon-aminocaproic acid. Contact Dermatitis 1993 28(2) 124. [Pg.117]

Wysenbeek AJ, Sella A, Vardi M, Yeshurun D. Acute delirious state after epsilon-aminocaproic acid. Lancet 1978 1(8057) 221. [Pg.117]

Seymour BD, Rubinger M. Rhabdomyolysis induced by epsilon-aminocaproic acid. Ann Pharmacother 1997 31(l) 56-8. [Pg.117]

Hocker JR, Saving KL. Fatal aortic thrombosis in a neonate during infusion of epsilon-aminocaproic acid. J Pediatr Surg 1995 30(10) 1490-2. [Pg.117]

Villarreal O. Systemic dermatitis with eosinophilia due to epsilon-aminocaproic acid. Contact Dermatitis 1999 40(2) 114. [Pg.117]

Brodkin HM. Myoglobinuria following epsilon-aminocaproic acid (EACA) therapy. Case report. J Neurosurg 1980 53(5) 690-2. [Pg.117]

Frank MM, Sergent JS, Kane MA, Ailing DW. Epsilon aminocaproic acid therapy of hereditary angioneurotic edema. A double-blind study. N Engl J Med 1972286(15) 808-12. [Pg.117]

Johnstone BR, Syme RR. Myonecrosis complicating epsilon aminocaproic acid treatment of traumatic haematuria. Br J Urol 1987 60(l) 81-2. [Pg.118]

Lane RJ, McLelland NJ, Martin AM, Mastaglia FL. Epsilon aminocaproic acid (EACA) myopathy. Postgrad Med J 1979 55(642) 282-5. [Pg.118]

Winter SS, Chaffee S, Kahler SG, Graham ML. Epsilon-aminocaproic acid-associated myopathy in a child. J Pediatr Hematol Oncol 1995 17(l) 53-5. [Pg.118]

Perazella MA, Biswas P. Acute hyperkalemia associated with intravenous epsilon-aminocaproic acid therapy. Am J Kidney Dis 1999 33(4) 782-5. [Pg.118]

FIGURE 45 The effects of streptokinase or urokinase may be counteracted by epsilon-aminocaproic acid. [Pg.234]

Epsilon-aminocaproic acid inhibits the activator-mediated formation of plasmin and hence may be used as an antidote to streptokinase-nrokinase, or in a defibrination syndrome when bleeding from a mncns membrane occurs (Figure 45). [Pg.652]

Dalmau A, Sabate A, Acosta F, et al. Tranexamic acid reduces red cell transfusion better than epsilon-aminocaproic acid or placebo in liver transplantation. Anesth Anaig 2000 91 29-34. [Pg.1269]


See other pages where Epsilon-aminocaproic acid is mentioned: [Pg.65]    [Pg.1697]    [Pg.261]    [Pg.262]    [Pg.341]    [Pg.1347]    [Pg.337]    [Pg.736]    [Pg.199]    [Pg.200]    [Pg.143]    [Pg.234]    [Pg.234]    [Pg.234]    [Pg.65]    [Pg.1697]   


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The effects of streptokinase or urokinase may be counteracted by epsilon-aminocaproic acid

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