AMICAR is generally well tolerated. The following adverse experiences have been reported: 

General: Edema, headache, malaise. 

Hypersensitivity Reactions: Allergic and anaphylactoid reactions, anaphylaxis. 

Local Reactions: Injection site reactions, pain and necrosis. 

Cardiovascular: Bradycardia, hypotension, perpheral ischemia, thrombosis. 

Gastrointestinal: Abdominal pain, diarrhea, nausea, vomiting. 

Hematologic: Agranulocytosis, coagulation disorder, leukopenia, thrombocytopenia. 

Musculoskeletal: CPK increased, muscle weakness, myalgia, myopathy (see WARNINGS), myositis, rhabdomyolysis. 

Neurologic: Confusion, convulsions, delirium, dizziness, hallucinations, intracranial hypertension, stroke, syncope. 

Respiratory: Dyspnea, nasal congestion, pulmonary embolism. 

Skin: Pruritus, rash. 

Special Senses: Tinnitus, vision decreased, watery eyes. 

Urogenital: BUN increased, renal failure. There have been some reports of dry ejaculation during the period of AMICAR treatment. These have been reported to date only in hemophilia patients who received the drug after undergoing dental surgical procedures. However, this symptom resolved in all patients within 24-48 hours of completion of therapy. 

Laboratory Tests 

The use of AMICAR 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 lysis of a clot of blood or plasma; and (b) more specific tests for the study of various phases of fibrinolytic mechanisms. These latter tests include both semiquantitative and quantitative techniques for the determination of profibrinolysin, fibrinolysin, and antifibrinolysin. 

Drug Laboratory Test Interactions 

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) EACA 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. 

Bookmark this page: