Disease relevance of Cyklokapron

• We conclude that until some method can be found to minimize ischemic complications, tranexamic acid is of no benefit in patients with subarachnoid hemorrhage [1].
• Efficacy of unusually high doses of tranexamic acid for the treatment of epistaxis in hereditary hemorrhagic telangiectasia [2].
• We carried out a placebo-controlled, double-blind, randomized study of the hemostatic effect of tranexamic acid mouthwash after oral surgery in 39 patients receiving anticoagulant agents because of the presence of cardiac valvular stenosis, a prosthetic cardiac valve, or a vascular prosthesis [3].
• We studied the effects of tranexamic acid (an antifibrinolytic agent) and cimetidine on acute upper-gastrointestinal-tract bleeding in a double-blind randomized placebo-controlled trial in 775 patients with hematemesis or melena or both [4].
• Deep-vein thrombosis induced by tranexamic acid in idiopathic thrombocytopenic purpura [5].
• Tranexamic acid dose-dependently increased thrombus formation and thrombus weight (minimal effective dose, 100 mg kg(-1 )h(-1) infusion) [6].

High impact information on Cyklokapron

• Before it was sutured, the operative field was irrigated in 19 patients with 10 ml of a 4.8 percent aqueous solution of tranexamic acid (an inhibitor of fibrinolysis) and in 20 patients with a placebo solution [3].
• Cimetidine and tranexamic acid for upper-gastrointestinal-tract bleeding [7].
• In particular, inhibition of plasmin activation and/or activity by tranexamic acid reversed both the accelerated fibrin clearance and the protective effect of PAI-1 deficiency [8].
• Nonreactivated rPAI-1 and tranexamic acid were significantly less potent in reversing the bleeding time prolongation [9].
• Patient 2 was given Factor VIIa concurrent with tranexamic acid in association with the extraction of two primary molars [10].

Chemical compound and disease context of Cyklokapron

• In addition, i.p. injections of tranexamic acid to nude mice treated with cisplatin resulted in a significant inhibition of the ascites formation and prolongation of 50% survival [11].
• Comparative studies of tranexamic acid with epsilon - aminocaproic acid, danazol and combined oral contraceptives, as well as long-term tolerability studies, would help to further define the place of the drug in the treatment of menorrhagia [12].
• Treatments for menorrhagia include tranexamic acid, desmopressin (DDAVP) administered either intranasally or subcutaneously, the oral contraceptive pill, the "Mirena" coil (Schering Oy, Turku, Finland), and endometrial ablation [13].
• Thrombosis was influenced by systemic tranexamic acid, fibrinogen in the aneurysm sac, Gelfoam in both endoleak and aneurysm sac, and by Histoacryl glue in the endoleak [14].
• Beneficial effect of low-molecular-weight heparin against lipopolysaccharide-induced disseminated intravascular coagulation in rats is abolished by coadministration of tranexamic acid [15].

Biological context of Cyklokapron

• Prophylactic tranexamic acid alone appears economical and safe in decreasing blood loss and transfusion requirement after cardiac surgery [16].
• Prior administration of the antifibrinolytic drug tranexamic acid might unmask such an effect, and combination therapy might thereby improve postoperative hemostasis [16].
• SK-mediated platelet aggregation was associated with significantly increased titers of both anti-SK antibodies and SK-neutralizing activity in plasma; it was partially inhibited by aspirin (1 mM) and by aprotinin (500 kallikrein inhibitor units/ml) and completely inhibited by tranexamic acid (1 mM) and by prostaglandin E1 (9 microM) [17].
• Establishment of a human ovarian cancer cell line capable of forming ascites in nude mice and effects of tranexamic acid on cell proliferation and ascites formation [11].
• Rebleeding was predicted by treatment with tranexamic acid (0.4; 0.3-0.7; protective effect); age over 52 (1.9; 1.2-3.0); loss of consciousness at ictus (1.7; 1.1-2.7); or admission to a neurosurgery service (0.6; 0.3-0.9; protective effect) [18].

Anatomical context of Cyklokapron

• The fibrinolytic inhibitor tranexamic acid was given orally to canines before, and for intervals after, pulmonary emboli were released from venous thrombi formed in vivo in femoral veins or the inferior vena cava [19].
• The proliferations of all three cell lines were dose-dependently inhibited by tranexamic acid [11].
• Tranexamic acid partially inhibited gastric juice induced clot lysis but did not exhibit a beneficial effect on coagulation [20].
• Preliminary studies are described, involving immunization with rabbit anti-mouse glomerular basement membrane (GBM) antiserum after pre-immunization with rabbit immunoglobulin G, both with and without treatment with a fibrinolytic inhibitor, Cyklokapron [21].
• Therapeutic action of tranexamic acid in hereditary haemorrhagic telangiectasia (HHT): Regulation of ALK-1/endoglin pathway in endothelial cells [22].

Associations of Cyklokapron with other chemical compounds

• Fibrinolysis inhibitors, including epsilon-aminocaproic acid and tranexamic acid, were effective in treating and preventing bleeding episodes [23].
• Meta-analysis of 60 trials showed tranexamic acid and aprotinin, unlike epsilon-aminocaproic acid (EACA) and desmopressin, to reduce significantly the number of patients requiring allogeneic blood transfusions after cardiac surgery with CPB [24].
• In the presence of tranexamic acid or 6-aminohexanoic acid, lysine analogues that mimic the effects of fibrin, plasmin binding kinetics are changed such that equilibrium is reached slowly following a lag phase after mixing of enzyme and inhibitor [25].
• The prostates of castrated rats, which had been injected daily for 7 days with the anti-PA drugs 6-aminohexanoic acid, tranexamic acid, aprotinin and cortisol, were assayed for PA activity, weight and cell number [26].
• Zymogen-activation kinetics. Modulatory effects of trans-4-(aminomethyl)cyclohexane-1-carboxylic acid and poly-D-lysine on plasminogen activation [27].

Gene context of Cyklokapron

• CONCLUSION: These results show that aprotinin, but not tranexamic acid, modulates the inflammatory response by reducing the IL-8 secretion of blood cells activated by contact with foreign surfaces [28].
• This effect could be inhibited by anti-u-PA antibodies, as well as by tranexamic acid and by aprotinin, indicating that the degrading activity is u-PA mediated and plasmin dependent [29].
• Crystal structures of the recombinant kringle 1 domain of human plasminogen in complexes with the ligands epsilon-aminocaproic acid and trans-4-(aminomethyl)cyclohexane-1-carboxylic Acid [30].
• Quantitative comparison of the cell surface localized tPA, which was eluted by tranexamic acid, with the total cellular tPA showed that cell surface bound tPA could represent up to 10% [31].
• Bleeding episodes due to deficiency of alpha 2-PI in these patients were well controlled by an antifibrinolytic agent, tranexamic acid [32].

Analytical, diagnostic and therapeutic context of Cyklokapron

• At three months there was no statistical difference between the outcomes in the tranexamic acid group and the control group [1].
• Hemostatic effect of tranexamic acid mouthwash in anticoagulant-treated patients undergoing oral surgery [3].
• The impact of tranexamic acid (TA), an antifibrinolytic agent, on blood transfusion in liver resection is unknown [33].
• Tranexamic acid in subarachnoid hemorrhage. A double-blind study [34].
• The entry variables were clinical condition on admission (grades on the Glasgow Coma Scale, Hunt and Hess system), the amount of subarachnoid and intraventricular blood and the presence of hydrocephalus on the admission computed tomogram, and antifibrinolytic treatment with tranexamic acid [35].

References