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Debendox withdrawn.

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P M Altman. 1984-01-21. Debendox withdrawn.. https://doi.org/10.5694/j.1326-5377.1984.tb103927.x

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[Endoscopic hemostasis in hemorrhagic peptic ulcer. A review and pilot study of local thrombin injection combined with systemic fibrinolysis inhibition (with tranexamic acid)].

Today, most upper GI-haemorrhages can be handled without surgery. We discuss the available endoscopic haemostatic methods. Injection therapy seems to be as effective as laser-, heater probe- and bipolar electrocoagulation, and is often preferred because the equipment is inexpensive. In a pilot study of 37 patients with haemorrhage from peptic ulcer (13 with active bleeding and 24 with stigmata of recent hemorrhage) we injected thrombin in the ulcer base and treated the patients systemically with an antifibrinolytic drug (tranexamic acid) for five days. Endoscopic follow-up revealed stigmata of recent haemorrhage in 23 patients on day 1 and in eight patients on day 5. "Blood in stomach" was seen in eight patients on day 1 and in two patients on day 5. Four patients had clinical signs of rebleeding, but only one of them needed operation (definite hemostasis 97%). There were no obvious side effects of the treatment. Contrary to other endoscopic methods, local injection of thrombin does not damage the normal mucosa. However, the method has not been sufficiently explored as yet, and cannot be recommended without strict control and follow-up measures. Early control endoscopy seems to be a sensitive way of monitoring haemostasis.

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Enhancement of the activation of Glu-plasminogen by urokinase in the simultaneous presence of tranexamic acid or fibrin.

The activation rate of Glu-plasminogen (Glu-plg) by urokinase (UK) was enhanced in the presence of either tranexamic acid or fibrin with an increase in the catalytic rate constant (kcat). The maximum increase in kcat was obtained at 0.5 mM of tranexamic acid and 0.1 microM of fibrin. Km did not change. The addition of fibrin to 1 mM tranexamic acid resulted in a further increase in kcat of the UK activation of Glu-plg. On the other hand, the addition of tranexamic acid to 0.1 microM fibrin further increased kcat of the UK activation of Glu-plg. Thus, stimulatory effects were observed on the activation of Glu-plg by UK in the simultaneous presence of tranexamic acid and fibrin. Fibrin-binding sites on the kringle 5 of Glu-plg may be involved in the further increase in the activation rate of Glu-plg by UK in the presence of both fibrin and tranexamic acid in comparison to that in the presence of tranexamic acid alone. Possibly, the Glu-plg binding with both tranexamic acid and fibrin (at kringle 5) may be most effectively activated by UK. It is also suggested that two molecules of Glu-plg bind to one molecule of fibrin monomer.

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