Chudý Peter, Kotuličová Daniela, Staško Ján, Kubisz Peter
National Center of Hemostasis and Thrombosis, Jessenius Faculty of Medicine, Comenius University, Martin, Slovakia.
Blood Coagul Fibrinolysis. 2011 Sep;22(6):493-8. doi: 10.1097/MBC.0b013e328346f8ca.
Disturbances of coagulation and fibrinolysis in type 2 diabetes mellitus (DM2) contribute to increased rates of macrovascular complications such as myocardial infarction and ischemic stroke. The aim of the study was to investigate the relationship among plasminogen activator inhibitor 1 (PAI-1), thrombin-activable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (t-PA), prothrombin fragments 1+2 (F1+2), glycemic control, hypertension, sex and body mass index (BMI) in DM2 patients with normoalbuminuria and microalbuminuria. Forty-two normoalbuminuric (NAU), 42 microalbuminuric (MAU) patients with DM2 and 42 blood donors as control group were enrolled. TAFI, PAI-1, t-PA and F1+2 were assessed by enzyme-linked immunosorbent assay (ELISA) in all patients. TAFI was significantly increased in the MAU group, PAI-1 and F1+2 were increased in both groups and t-PA was not elevated in either group compared to controls. We found positive correlations in the NAU: TAFI and fibrinogen (r=0.65, P=0.02), PAI-1 and triglycerides (r=0.67, P=0.01), in the MAU: TAFI and F1+2 (r=0.48, P=0.02), TAFI and systolic blood pressure (r=0.53, P=0.01), PAI-1 and BMI (r=0.43, P<0.05). We found decreased fibrinolysis in DM2 patients presented with increased PAI-1 in both NAU and MAU. Hypofibrinolysis in MAU is further accented by the elevation of TAFI. TAFI-mediated inhibition of fibrinolysis in DM2 is regulated independently from PAI-1. Patient[Combining Acute Accent]s sex does not affect diabetes-related changes in hemostasis and fibrinolysis.
2型糖尿病（DM2）患者的凝血和纤维蛋白溶解紊乱会导致心肌梗死和缺血性中风等大血管并发症的发生率增加。本研究的目的是调查2型糖尿病伴正常白蛋白尿和微量白蛋白尿患者中纤溶酶原激活物抑制剂1（PAI-1）、凝血酶激活的纤维蛋白溶解抑制剂（TAFI）、组织纤溶酶原激活物（t-PA）、凝血酶原片段1+2（F1+2）、血糖控制、高血压、性别和体重指数（BMI）之间的关系。纳入42例2型糖尿病正常白蛋白尿（NAU）患者、42例2型糖尿病微量白蛋白尿（MAU）患者和42例献血者作为对照组。所有患者均通过酶联免疫吸附测定（ELISA）评估TAFI、PAI-1、t-PA和F1+2。与对照组相比，MAU组TAFI显著升高，两组PAI-1和F1+2均升高，两组t-PA均未升高。我们发现NAU组中存在正相关：TAFI与纤维蛋白原（r=0.65，P=0.02）、PAI-1与甘油三酯（r=0.67，P=0.01）；MAU组中：TAFI与F1+2（r=0.48，P=0.02）、TAFI与收缩压（r=0.53，P=0.01）、PAI-1与BMI（r=0.43，P<0.05）。我们发现，在NAU和MAU中，PAI-1升高的2型糖尿病患者纤维蛋白溶解减少。MAU中的低纤维蛋白溶解因TAFI升高而进一步加重。DM2中TAFI介导的纤维蛋白溶解抑制独立于PAI-1进行调节。患者的性别不影响糖尿病相关的止血和纤维蛋白溶解变化。
