Yener Serkan, Comlekci Abdurrahman, Akinci Baris, Demir Tevfik, Yuksel Faize, Ozcan Mehmet Ali, Bayraktar Firat, Yesil Sena
Division of Endocrinology and Metabolism, Department of Internal Medicine, Dokuz Eylul University School of Medicine, Izmir, Turkey.
Med Princ Pract. 2009;18(4):266-71. doi: 10.1159/000215722. Epub 2009 Jun 2.
To evaluate subclinical inflammation and fibrinolysis in low-risk type 2 diabetic subjects and to assess the efficacy of metformin and rosiglitazone in this group.
Sixty-one normotensive, normoalbuminuric type 2 diabetic subjects without diabetes-related complications were included in a 4-week standardization period with glimepiride. After the standardization period, 21 subjects were excluded and the remaining 40 were randomly divided into two groups matched for age, gender, body mass index and disease duration. The first group (n = 20) received metformin (1,700 mg/day), the second group (n = 20) rosiglitazone (4 mg/day) for 12 weeks. Patients with low-density lipoprotein-cholesterol higher than 130 mg/dl at the beginning of the randomization period were treated with simvastatin (maximum dose 20 mg/day). Twenty-three healthy controls were also recruited. Cytokine measurements were performed with ELISA kits.
Baseline plasma plasminogen activator inhibitor-1 (PAI-1) level of type 2 diabetic subjects was significantly elevated (p = 0.038), but baseline levels of soluble CD40 ligand (sCD40L) and thrombin-activatable fibrinolysis inhibitor-1 (TAFI) antigen did not differ from healthy controls. Twelve weeks of metformin or rosiglitazone therapy did not cause significant changes in sCD40L, PAI-1 and TAFI antigen levels. In simvastatin-treated subjects (n = 9) significant reductions of PAI-1 were achieved (p = 0.028), while sCD40L and TAFI-Ag did not differ from baseline values.
Our results showed that nonobese diabetic patients at low cardiovascular risk had similar levels of subclinical markers of inflammation and fibrinolysis as matched healthy controls. Neither metformin nor rosiglitazone caused marked changes in sCD40L, PAI-1 and TAFI antigen levels. A subset of patients who received simvastatin showed a modest decrease in PAI-1 level and could contribute to beneficial vasculoprotective effect of the drug in type 2 diabetics.
评估低风险2型糖尿病患者的亚临床炎症和纤维蛋白溶解情况，并评估二甲双胍和罗格列酮对该组患者的疗效。
61例血压正常、尿白蛋白正常且无糖尿病相关并发症的2型糖尿病患者进入为期4周的格列美脲标准化治疗期。标准化治疗期结束后，排除21例受试者，其余40例根据年龄、性别、体重指数和病程随机分为两组。第一组（n = 20）接受二甲双胍（1700毫克/天）治疗，第二组（n = 20）接受罗格列酮（4毫克/天）治疗，为期12周。随机分组期开始时低密度脂蛋白胆固醇高于130毫克/分升的患者用辛伐他汀治疗（最大剂量20毫克/天）。还招募了23名健康对照者。使用酶联免疫吸附测定试剂盒进行细胞因子检测。
2型糖尿病患者的基线血浆纤溶酶原激活物抑制剂-1（PAI-1）水平显著升高（p = 0.038），但可溶性CD40配体（sCD40L）和凝血酶激活的纤维蛋白溶解抑制剂-1（TAFI）抗原的基线水平与健康对照者无差异。二甲双胍或罗格列酮治疗12周未导致sCD40L、PAI-1和TAFI抗原水平发生显著变化。在接受辛伐他汀治疗的受试者（n = 9）中，PAI-1显著降低（p = 0.028），而sCD40L和TAFI-Ag与基线值无差异。
我们的结果表明，心血管风险较低的非肥胖糖尿病患者的亚临床炎症和纤维蛋白溶解标志物水平与匹配的健康对照者相似。二甲双胍和罗格列酮均未引起sCD40L、PAI-1和TAFI抗原水平的明显变化。一部分接受辛伐他汀治疗的患者PAI-1水平适度降低，这可能有助于该药物对2型糖尿病患者产生有益的血管保护作用。
