Zumbach M, Hofmann M, Borcea V, Luther T, Kotzsch M, Müller M, Hergesell O, Andrassy K, Ritz E, Ziegler R, Wahl P, Nawroth P P
Department of Medicine I, University of Heidelberg, Germany.
Exp Clin Endocrinol Diabetes. 1997;105(4):206-12. doi: 10.1055/s-0029-1211753.
Patients with late diabetic complications have increased levels of parameters indicating activation of coagulation (Takakashi et al., 1989; Ceriello, 1993; Murakami et al., 1993; Kario et al., 1995; Shimizu et al., 1995; Yokoyama et al., 1996), endothelial cell damage (Jensen, 1989; Iwashima et al., 1990; Sernau et al., 1995; Gabath et al., 1996). TF is believed to activate the coagulation mechanism in patients with late complications of diabetes. We studied the TF antigen plasma levels in 72 patients with diabetes mellitus (36 type I, 36 type II) with respect to its relevance as a marker of microvascular diabetic complications. TF levels did not correlate with macrovascular disease, diabetes type or age. Sixty patients with decreased renal function not due to diabetes were studied for evaluation of the contribution of renal failure to TF antigen plasma levels. We did not find a significant correlation of TF with s-creatinine in non diabetic patients (r = 0.27, p > 0.05). However, TF levels were elevated in diabetic patients with microvascular disease. Patients with retinopathy had higher TF levels than without (0.30 ng/ml vs 0.11 ng/ml, p < 0.007). When patients were divided into subgroups according to the urine albumin concentration, TF antigen of patients without albuminuria (0.019 ng/ml, n = 25) did not differ from patients with microalbuminuria (0.095 ng/ml, n = 19 p > 0.05). However, TF levels were significantly higher in patients with macroalbuminuria (n = 28; 0.215 ng/ml, p < 0.005). Thus activation of coagulation in patients with microvascular complications of diabetes may be triggered by tissue factor.
患有晚期糖尿病并发症的患者，其凝血激活相关参数水平升高（高木等人，1989年；切列洛，1993年；村上等人，1993年；卡里奥等人，1995年；清水等人，1995年；横山等人，1996年），同时存在内皮细胞损伤（詹森，1989年；岩岛等人，1990年；塞尔瑙等人，1995年；加巴斯等人，1996年）。组织因子被认为可激活糖尿病晚期并发症患者的凝血机制。我们研究了72例糖尿病患者（36例I型，36例II型）的组织因子抗原血浆水平，以探讨其作为微血管糖尿病并发症标志物的相关性。组织因子水平与大血管疾病、糖尿病类型或年龄无关。研究了60例非糖尿病所致肾功能减退患者，以评估肾衰竭对组织因子抗原血浆水平的影响。我们发现非糖尿病患者的组织因子与血清肌酐无显著相关性（r = 0.27，p > 0.05）。然而，患有微血管疾病的糖尿病患者组织因子水平升高。患有视网膜病变的患者组织因子水平高于无视网膜病变者（0.30纳克/毫升对0.11纳克/毫升，p < 0.007）。当根据尿白蛋白浓度将患者分为亚组时，无蛋白尿患者（0.019纳克/毫升，n = 25）的组织因子抗原与微量白蛋白尿患者（0.095纳克/毫升，n = 19，p > 0.05）无差异。然而，大量白蛋白尿患者（n = 28；0.215纳克/毫升，p < 0.005）的组织因子水平显著更高。因此，糖尿病微血管并发症患者的凝血激活可能由组织因子触发。
