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Arrest of Growth of Ovarian Tumor by Tranexamic Acid
Birger Åstedt, MD;
Ingemar Glifberg, MD;
Willy Mattsson, MD;
Claes Trope, MD
JAMA. 1977;238(2):154-155.
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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
. . . [Full Text PDF of this Article]
Author Affiliations
From the Departments of Gynecology and Obstetrics (Drs Åstedt and Trope), Radiotherapy (Dr Mattsson), and Pathology (Dr Glifberg), University of Lund, Malmö Allmänna Sjukhus, Sweden.
Footnotes
Reprint requests to Department of Gynecology and Obstetrics, Malmö Allmänna Sjukhus, S-214 01 Malmö, Sweden (Dr Åstedt).
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