MALIGNANT ovarian tumors possess coagulative properties resulting in formation of fibrin, which serves as a matrix for proliferating vessels. Such neoplasms also possess fibrinolytic properties, which are of importance for the removal of residual fibrin.1 Fibrinolysis, ie, conversion of plasminogen into plasmin, is initiated by certain activators. In tissue culture of human ovarian tumors, a stable fibrinolytic activator, which has been shown to be similar to that in urine (ie, urokinase), is released.2
Hypothetically, interference with the coagulative and fibrinolytic properties of the tumor could have an antineoplastic effect. Heparin sodium inhibits fibrin formation and has been used as an adjuvant in tumor therapy.3,4 We recently observed regression of ascites in patients receiving the fibrinolytic inhibitor, tranexamic acid. We thought that inhibition of the tumor activator would prevent removal of fibrin formed despite anticoagulant therapy and would thereby more effectively interfere with, and have a static effect
Åstedt B, Glifberg I, Mattsson W, Trope C. Arrest of Growth of Ovarian Tumor by Tranexamic Acid. JAMA. 1977;238(2):154–155. doi:10.1001/jama.1977.03280020058026
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