"The U.S. Food and Drug Administration today approved Tretten, Coagulation Factor XIII A-Subunit (Recombinant), the first recombinant product for use in the routine prevention of bleeding in adults and children who have a rare clotting disorder, k"...
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In patients with upper urinary tract bleeding, AMICAR (aminocaproic acid) administration has been known to cause intrarenal obstruction in the form of glomerular capillary thrombosis or clots in the renal pelvis and ureters. For this reason, AMICAR (aminocaproic acid) should not be used in hematuria of upper urinary tract origin, unless the possible benefits outweigh the risk.
Subendocardial hemorrhages have been observed in dogs given intravenous infusions of 0.2 times the maximum human therapeutic dose of AMICAR (aminocaproic acid) and in monkeys given 8 times the maximum human therapeutic dose of AMICAR (aminocaproic acid) .
Fatty degeneration of the myocardium has been reported in dogs given intravenous doses of AMICAR (aminocaproic acid) at 0.8 to 3.3 times the maximum human therapeutic dose and in monkeys given intravenous doses of AMICAR (aminocaproic acid) at 6 times the maximum human therapeutic dose.
Rarely, skeletal muscle weakness with necrosis of muscle fibers has been reported following prolonged administration. Clinical presentation may range from mild myalgias with weakness and fatigue to a severe proximal myopathy with rhabdomyolysis, myoglobinuria, and acute renal failure. Muscle enzymes, especially creatine phosphokinase (CPK) are elevated. CPK levels should be monitored in patients on long-term therapy. AMICAR (aminocaproic acid) administration should be stopped if a rise in CPK is noted. Resolution follows discontinuation of AMICAR (aminocaproic acid) ; however, the syndrome may recur if AMICAR (aminocaproic acid) is restarted.
The possibility of cardiac muscle damage should also be considered when skeletal myopathy occurs. One case of cardiac and hepatic lesions observed in man has been reported. The patient received 2 g of aminocaproic acid every 6 hours for a total dose of 26 g. Death was due to continued cerebrovascular hemorrhage. Necrotic changes in the heart and liver were noted at autopsy.
AMICAR (aminocaproic acid) inhibits both the action of plasminogen activators and to a lesser degree, plasmin activity. The drug should NOT be administered without a definite diagnosis and/or laboratory finding indicative of hyperfibrinolysis (hyperplasminemia).1
Inhibition of fibrinolysis by aminocaproic acid may theoretically result in clotting or thrombosis. However, there is no definite evidence that administration of aminocaproic acid has been responsible for the few reported cases of intravascular clotting which followed this treatment. Rather, it appears that such intravascular clotting was most likely due to the patient's preexisting clinical condition, e.g., the presence of DIC. It has been postulated that extravascular clots formed in vivo may not undergo spontaneous Iysis as do normal clots.
Reports have appeared in the literature of an increased incidence of certain neurological deficits such as hydrocephalus, cerebral ischemia, or cerebral vasospasm associated with the use of antifibrinolytic agents in the treatment of subarachnoid hemorrhage (SAH). All of these events have also been described as part of the natural course of SAH, or as a consequence of diagnostic procedures such as angiography. Drug relatedness remains unclear.
Aminocaproic acid should not be administered with Factor IX Complex concentrates or Anti-Inhibitor Coagulant concentrates, as the risk of thrombosis may be increased.
The use of AMICAR (aminocaproic acid) should be accompanied by tests designed to determine the amount of fibrinolysis present. There are presently available: (a) general tests such as those for the determination of the Iysis of a clot of blood or plasma; and (b) more specific tests for the study of various phases of the fibrinolytic mechanisms. These latter tests include both semiquantitative and quantitative techniques for the determination of profibrinolysin, fibrinolysin, and antifibrinolysin.
Carcinogenesis, Mutagenesis, Impairment of Fertility
Long-term studies in animals to evaluate the carcinogenic potential of AMICAR (aminocaproic acid) and studies to evaluate its mutagenic potential have not been conducted. Dietary administration of an equivalent of the maximum human therapeutic dose of AMICAR (aminocaproic acid) to rats of both sexes impaired fertility as evidenced by decreased implantations, litter sizes and number of pups born.
Pregnancy Category C
Animal reproduction studies have not been conducted with AMICAR (aminocaproic acid) . It is also not known whether AMICAR (aminocaproic acid) can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity. AMICAR (aminocaproic acid) should be given to a pregnant woman only if clearly needed.
It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when AMICAR (aminocaproic acid) is administered to a nursing woman.
Safety and effectiveness in pediatric patients have not been established.
1 Stefanini M, Dameshek W: The Hemorrhagic Disorders, Ed. 2, New York, Grune and Stratton; 1962:510-514.
Last reviewed on RxList: 3/11/2009
This monograph has been modified to include the generic and brand name in many instances.
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