Aromatization of shikimic acid in the rat and the role of gastrointestinal micro-organisms.
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Fourteen patients with hereditary angioneurotic oedema (Quincke' oedema) treated for an average period of 6 years (ranging from 15 months to 8 years) with tranexamic acid was given an ophthalmological examination in order to reveal any possible toxic damages caused by the treatment. As large doses of tranexamic acid given to animals have been shown to result in retinal degeneration, the examination was focused on checking the retinal function. A complete ophthalmic examination revealed no toxic effects in the eyes of any of the patients. No retinal damages were found that could have been caused by the tranexamic acid. The central corneal thickness was normal.
A case of menstruation-related angioedema is presented. The symptoms observed were cyclically appearing hoarseness due to laryngeal edema without any pain. Symptoms disappeared during intake of contraceptive pills and during pregnancy with recurrence at the onset of menstruation post partum. A therapeutic trial with tranexamic acid was successful. The use of tranexamic acid in secondary and idiopathic angioedema should be considered.
Plasma plasminogen levels were determined by a specific esterolytic assay and a radial immunodiffusion assay, both of which were standardized on a weight basis by using highly purified plasminogen diluted in plasminogen-free plasma. In thirteen normal individuals the functional and antigenic levels were 275 +/- 61 microgram/ml and 285 +/- 61 microgram/ml, respectively (r = 0.95), whereas in 58 plasmas from individuals with hereditary angioedema the levels were 272 +/- 58 microgram/ml and 265 +/- 64 microgram/ml, respectively (r = 0.89). In two patients treated with tranexamic acid either acutely or chronically, both the functional and antigenic plasminogen levels were diminished.
An optimal inhibition of tissue fibrinolysis, studied by a histochemical fibrin slide technique in the rat stomach, was obtained by administration of tranexamic acid in a dose of 60 mg/100 g body weight. A significant fibrinolysis inhibition was found within 5 min, when tranexamic acid in this dose was given either intravenously or intragastrically. A prolonged duration of fibrinolysis inhibition was observed after intragastric administration. After 4 hr no inhibitory effect of tranexamic acid could be recorded, irrespective of the route of administration.
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