Sibal L, Aldibbiat A, Agarwal S C, Mitchell G, Oates C, Razvi S, Weaver J U, Shaw J A, Home P D
ICM-Diabetes, Newcastle University, Framlington Place, Newcastle upon Tyne NE2 4HH, UK.
Diabetologia. 2009 Aug;52(8):1464-73. doi: 10.1007/s00125-009-1401-0. Epub 2009 May 30.
AIMS/HYPOTHESIS: Type 1 diabetes is associated with premature arterial disease. Bone-marrow derived, circulating endothelial progenitor cells (EPCs) are believed to contribute to endothelial repair. The hypothesis tested was that circulating EPCs are reduced in young people with type 1 diabetes without vascular injury and that this is associated with impaired endothelial function and increased carotid intima-media thickness (CIMT).
We compared 74 people with type 1 diabetes with 80 healthy controls. CD34, CD133, vascular endothelial (VE) growth factor receptor-2 (VEGFR-2) and VE-cadherin antibodies were used to quantify EPCs and progenitor cell subtypes using flow-cytometry. Ultrasound assessment of endothelial function by brachial artery flow-mediated dilatation (FMD) and CIMT was made. Circulating endothelial markers, inflammatory markers and plasma plasminogen activator inhibitor-1 (PAI-1) levels were measured.
CD34+VE-cadherin+, CD133+VE-cadherin+ and CD133+VEGFR-2+ EPC counts were significantly lower in people with diabetes (46-69%; p = 0.004-0.043). In people with type 1 diabetes, FMD was reduced by 45% (p < 0.001) and CIMT increased by 25% (p < 0.001), these being correlated (r = -0.25, p = 0.033). There was a significant relationship between FMD and CD34+VE-cadherin+ (r = 0.39, p = 0.001), CD133+VEGFR-2+ (r = 0.25, p = 0.037) and CD34+ (r = 0.34, p = 0.003) counts. Circulating high-sensitivity C-reactive protein, PAI-1, interleukin-6 and E-selectin were significantly higher in the diabetes group (p < 0.001 to p = 0.049), the last two of these correlating with FMD (r = -0.27, p = 0.028 and r = -0.24, p = 0.048, respectively).
CONCLUSIONS/INTERPRETATION: These findings suggest that abnormalities of endothelial function in addition to pro-inflammatory and pro-thrombotic states are already common in people with type 1 diabetes before development of clinically evident arterial damage. Low EPC counts confirm risk of macrovascular complications and may account for impaired endothelial function and predict future cardiovascular events.
目的/假设:1型糖尿病与动脉疾病过早发生相关。骨髓来源的循环内皮祖细胞(EPCs)被认为有助于内皮修复。本研究检验的假设是,无血管损伤的1型糖尿病青年患者循环EPCs数量减少,且这与内皮功能受损和颈动脉内膜中层厚度(CIMT)增加有关。
我们将74例1型糖尿病患者与80例健康对照者进行比较。使用CD34、CD133、血管内皮(VE)生长因子受体-2(VEGFR-2)和VE-钙黏蛋白抗体,通过流式细胞术对EPCs和祖细胞亚型进行定量分析。通过肱动脉血流介导的血管舒张功能(FMD)和CIMT的超声评估来评估内皮功能。检测循环内皮标志物、炎症标志物和血浆纤溶酶原激活物抑制剂-1(PAI-1)水平。
糖尿病患者中CD34⁺VE-钙黏蛋白⁺、CD133⁺VE-钙黏蛋白⁺和CD133⁺VEGFR-2⁺ EPC计数显著降低(46%-69%;p = 0.004-0.043)。在1型糖尿病患者中,FMD降低了45%(p < 0.001),CIMT增加了25%(p < 0.001),二者具有相关性(r = -0.25,p = 0.033)。FMD与CD34⁺VE-钙黏蛋白⁺(r = 0.39,p = 0.001)、CD133⁺VEGFR-2⁺(r = 0.25,p = 0.037)和CD34⁺(r = 0.34,p = 0.003)计数之间存在显著相关性。糖尿病组循环高敏C反应蛋白、PAI-1、白细胞介素-6和E-选择素显著升高(p < 0.001至p = 0.049),其中后两者与FMD相关(分别为r = -0.27,p = 0.028和r = -0.24,p = 0.048)。
结论/解读:这些发现表明,在临床上明显的动脉损伤发生之前,1型糖尿病患者除了存在促炎和促血栓状态外,内皮功能异常已经很常见。EPC计数低证实了大血管并发症的风险,可能是内皮功能受损的原因,并可预测未来心血管事件。