Cyklokapron 500 mg
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Tranexamic acid produces an antifibrinolytic effect by competitively inhibiting the activation of plasminogen to plasmin. It is also a weak noncompetitive inhibitor of plasmin. These properties make possible its clinical use as an antifibrinolytic in the treatment of both general and local fibrinolytic hemorrhages. It has an action mechanism similar to, but about 10 times more potent in vitro than that of epsilon aminocaproic acid (EACA).
Absorption from the human gastrointestinal tract is not complete (40%).
Tranexamic acid binds considerably more strongly than EACA to both the strong and weak sites in the plasminogen molecule in a ratio corresponding to the difference in potency between the compounds. The pharmacological significance of the binding to these different sites has not yet been evaluated.
Tranexamic acid does not bind to serum albumin. The plasma protein binding seems to be fully accounted for by its binding to plasminogen and appears to be negligible at therapeutic plasma levels of 5 to 10 mg/L.
Possible routes of biotransformation are acetylation or deamination followed by oxidation or reduction. After oral administration approximately 50% of the parent compound, 2% of the deaminated dicarboxylic acid, and 0.5% of the acetylated product are excreted.
Tranexamic acid is eliminated by glomerular filtration, excretion being about 30% at 1 hour, 55% at 3 hours and 90% at 24 hours after i.v. administration of 10 mg/kg body weight. After oral administration of 10 to 15 mg/kg body weight excretion was 1% at 1 hour, 7% at 3 hours and 39% at 24 hours.
I.V. administration of 10 mg/kg body weight gave plasma concentrations of 18.3 µg, 9.6 µg and 5 µg/mL 1, 3 and 5 hours after the injection.
When administered 36 to 48 hours before surgery in 4 doses of 10 to 20 mg/kg body weight an antifibrinolytically active concentration (10 µg/mL) of tranexamic acid remained up to 17 hours in the tissues investigated, and up to 7 to 8 hours in the serum.
Tranexamic acid crosses the placenta. After an i.v. injection of 10 mg/kg the concentration can rise to about 30 µg/mL of fetal serum.
Tranexamic acid also passes over into the breast milk during lactation in concentrations 1/100 of the corresponding serum levels.
After both oral and i.v. administration tranexamic acid passes into the semen and inhibits its fibrinolytic activity, but without affecting the motility of the spermatozoa.
The ability of tranexamic acid to cross the blood-brain barrier has been demonstrated when administered to patients with ruptured intracranial aneurysms.
Tranexamic acid diffuses rapidly to the joint fluid and to the synovial membrane. In the joint fluid, the same concentration was obtained as in the serum. The biological half-life in the joint fluid was about 3 hours.
Three hours after a single oral dose of 25 mg/kg body weight the peak serum level was 15.4 g/L and the aqueous humour level was 1.6 g/L.
Hereditary angioneurotic edema. Increased local fibrinolysis when the diagnosis is indicative of hyperfibrinolysis, as with conization of the cervix, dental extraction in patients with coagulopathies (in conjunction with antihemophilic factor), epistaxis, hyphema, and menorrhagia (hypermenorrhea).
Clinically important interactions have not been observed with tranexamic acid tablets. Because of the absence of interaction studies, simultaneous treatment with anticoagulants must take place under the strict supervision of a physician experienced in this field.
Tranexamic acid is secreted in the mother's milk at a concentration only a hundredth of the corresponding serum levels. The investigators are of the opinion that tranexamic acid can be given during lactation without risk to the child.
Clinical experience with tranexamic acid in menorrhagic children under 15 years of age is not available.
Each white, film-coated, capsule-shaped tablet, with CY engraved in arcs, contains: tranexamic acid 500 mg. Tartrazine-free. Bottles of 100.
Store at room temperature between 15 and 30°C.
Each ampul contains: tranexamic acid BP 100 mg/mL. Ampuls of 5 and 10 mL. Packages of 10.
Patients with a history or risk of thrombosis should not be given tranexamic acid, unless at the same time it is possible to give treatment with anticoagulants. The preparation should not be given to patients with acquired disturbances of color vision. If disturbances of color vision arise during the course of treatment the administration of the preparation should be discontinued.
Patients with active thromboembolic disease, such as deep vein thrombosis, pulmonary embolism and cerebral thrombosis.
Patients with subarachnoid haemorrhage: the limited clinical experience shows that a reduced risk for re-bleeding is offset by an increase in the rate of cerebral ischaemia.
Hypersensitivity to tranexamic acid or any of the ingredients.
The safety of tranexamic acid during pregnancy has not yet been established. No harmful effects have been reported.
A woman with fibrinolytic bleeding in the fourth month of pregnancy was treated with tranexamic acid for a total of 64 days. The total dose was 256 g. The delivery occurred spontaneously in the 30th week of pregnancy and was normal in all other respects. The infant was healthy.
In a case of threatened placental abruption that was prevented by giving tranexamic acid, the patient had already lost 2 children in connection with placental abruption. In the 26th week of her third pregnancy bleeding occurred, indicating abruption. Pathological proteolysis with predominant activation of the fibrinolytic system was established. Between the 26th and 33rd week of pregnancy about 250 g of tranexamic acid were given, both i.v. and orally. The bleeding was arrested and a healthy child was delivered by Caesarean section.
Tranexamic acid crosses over to the fetus. After an i.v. injection of 10 mg/kg the concentration can reach a level of about 30 µg/mL fetal serum. Fibrinolytic activity is very high in neonates. It is not known for certain whether a reduction of this activity during the first hours of life is harmful. Kullander and Nilsson who have wide experience with tranexamic acid in connection with childbirth have observed no negative effect on the infants.
Tranexamic acid therapy is not indicated in hematuria caused by diseases of the renal parenchyma. Intravascular precipitation of fibrin frequently occurs in these conditions and may aggravate the disease. In addition, in cases of massive renal hemorrhage of any cause, antifibrinolytic therapy carries the risk of clot retention in the renal pelvis.
Gastrointestinal symptoms (nausea, vomiting, diarrhea) occur but disappear when the dose is reduced. Isolated cases of dizziness or reduced blood pressure have been reported. Allergic skin reactions have been reported less commonly.
To be observed by reason of experimental findings in animals: in the dog, retinal changes have been observed after long-term administration of large doses of tranexamic acid and in the cat, after i.v. injection of 250 mg/kg body weight/day for 14 days. Such changes have not been obtained in the rat, where the maximum tolerated dose has been administered. No retinal changes have been reported or observed at ophthalmic checkups of patients treated with tranexamic acid for several weeks or months.
Post-market Surveillance: Rare cases of adverse events have been reported with the use of tranexamic acid; thromboembolic events, impaired colour vision or other visual disturbances and dizziness. Hypotension may occur after fast injection.
There is no known case of overdosage of tranexamic acid in humans. Symptoms may be nausea, diarrhoea, dizziness, headache, vomiting orthostatic symptoms and hypotension.
Initiate vomiting, institution of gastric lavage, charcoal therapy, and symptomatic treatment. Maintain adequate diuresis.
It has been seen that 37 g of tranexamic acid caused mild intoxication in a 17-year-old after gastric lavage.
Dosage should be calculated according to body weight at 25 mg/kg, 2 to 3 times a day.
Patients with Impaired Renal Function: In patients with serum creatine concentrations of 120 to 250 μmol/L, 15 mg orally or 10 mg i.v. tranexamic acid/kg body weight twice daily. At serum creatine levels of 250 to 500 μmol/L the dosage should be 15 mg orally or 10 mg i.v./kg body weight at 24 hourly intervals, and at serum creatine levels of 500 μmol/L or more, the same dose should be given at intervals of 48 hours between doses.