Almér L A, Pandolfi M
Diabetes. 1976;25(2 SUPPL):807-10.
The spontaneous fibrinolytic activity of the blood is abnormally low significantly more often in persons with diabetes mellitus than in nondiabetic controls. The fibrinolytic response stimulated by venous occlusion is poor six times more frequently in diabetics than in controls, and the fibrinolytic activity of the endothelial cells is abnoramlly low in one-fourth of the diabetics tested. These changes are not related to the duration of diabetes. However, if patients with long-standing diabetes (greater than 10 years) are separated into those with retinopathy and those without, it is found that those who remain free from opthalmoscopically visible retinopathy have an almost normal fibrinolytic response on stimulation, while the others have a significantly lower response. This difference seems to be caused by a faulty plasminogen activator release mechanism. Compared with the other diabetics, those with retinopathy also have a significantly increased level of fibrinogen and of alpha2-macroglobulin, a protein that acts as an inhibitor of fibrinolysis. These findings imply a poor defense mechanism against fibrin deposits in the vessel walls in diabetes, which might contribute to the development of diabetic microangiopathy.
与非糖尿病对照组相比，糖尿病患者血液的自发纤溶活性显著降低的情况更为常见。静脉阻塞刺激引起的纤溶反应，糖尿病患者比对照组差6倍，且在四分之一的受测糖尿病患者中，内皮细胞的纤溶活性异常低。这些变化与糖尿病病程无关。然而，如果将病程较长（超过10年）的糖尿病患者分为有视网膜病变和无视网膜病变两组，就会发现眼底镜检查未见视网膜病变的患者在受到刺激时纤溶反应几乎正常，而其他患者的反应则明显较低。这种差异似乎是由纤溶酶原激活物释放机制缺陷引起的。与其他糖尿病患者相比，有视网膜病变的患者纤维蛋白原和α2-巨球蛋白水平也显著升高，α2-巨球蛋白是一种作为纤溶抑制剂的蛋白质。这些发现表明糖尿病患者对血管壁纤维蛋白沉积的防御机制较差，这可能有助于糖尿病微血管病变的发展。
