Sundqvist S B, Hedner U, Kullenberg H K, Bergentz S E
Br Med J (Clin Res Ed). 1981 Jul 25;283(6286):265-7. doi: 10.1136/bmj.283.6286.265.
Sixty consecutive patients with phlebographically verified deep venous thrombosis of the upper arm were studied for disorders of coagulation and fibrinolysis. No appreciable increase in abnormalities of the factor VIII complex, antithrombin III, or inhibitors of activators of fibrinolysis were found. A decreased fibrinolytic defence mechanism, evident either as a deficient release capacity of fibrinolytic activators from the vein during stasis or as decreased fibrinolytic activity in the vein wall as determined histochemically, was found in 26 out of 53 patients studied (49%). It is concluded that deep venous thrombosis of the upper arm is a multifactorial disease. An impaired fibrinolytic defence mechanism is one of the factors that may be of pathogenetic importance.
对60例经静脉造影证实患有上臂深静脉血栓形成的连续患者进行了凝血和纤维蛋白溶解紊乱的研究。未发现凝血因子VIII复合物、抗凝血酶III或纤维蛋白溶解激活剂抑制剂的异常有明显增加。在53例研究患者中的26例(49%)中发现纤维蛋白溶解防御机制降低,表现为在血流停滞期间静脉中纤维蛋白溶解激活剂的释放能力不足,或通过组织化学测定发现静脉壁中的纤维蛋白溶解活性降低。结论是上臂深静脉血栓形成是一种多因素疾病。纤维蛋白溶解防御机制受损是可能具有发病机制重要性的因素之一。