A1,
A2,
B,
C1,
C2,
D,
E,
F,
G-H,
I-K,
L,
M,
N,
O,
P1,
P2,
Q-R,
S,
T,
U-V,
W-Z
Amicar Side Effects, and Drug Interactions - Aminocaproic Acid
Amicar Side Effects, and Drug Interactions - Aminocaproic Acid
SIDE EFFECTS
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 INTERACTIONS
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.
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