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Defective fibrinolytic activity is often a contributory factor in deep venous thrombosis. A family with a high incidence of venous thrombosis in association with such a defect is presented. Of 13 family members who had had thrombosis, 12 showed a defective capacity to release fibrinolytic activity from vessel wall after venous occlusion and/or infusion of DDAVP, a vasopressin derivative. The fibrinolytic activator activity of the vessel wall was normal in all cases. This seems to be the first family in which there is evidence of an inherited abnormal fibrinolytic activity.
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Johansson et al. (1978) studied this question.
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