科研之友
微信
新浪微博
Facebook
分享链接
摘要
Mechanisms of vascular disorders in beta-thalassemia/HbE patients remain poorly understood. In the present study, we aimed to determine the presence of endothelial dysfunction and its association with altered vascular mediators in this population. Forty-three beta-thalassemia/HbE patients without clinically documented vascular symptoms and 43 age-sex-matched healthy controls were enrolled. Endothelial function was assessed using flow-mediated dilatation (FMD) before and after administration of nitroglycerine (NTG). beta-Thalassemia/HbE patients showed a significant endothelial dysfunction using FMD. The percentage change in the brachial artery diameter before NTG was significantly lower in the thalassemia group compared to the control (5.0 +/- 5.9 vs. 9.0 +/- 4.0%, p < 0.01) while no significant differences after NTG (18.4 +/- 8.3 vs. 17.8 +/- 6.3%, p = 0.71). Plasma nitric oxide metabolites (NO (x) ) and prostaglandin E-2 (PGE(2)) levels were significantly decreased in beta-thalassemia/HbE (117.2 +/- 27.3 vs. 135.8 +/- 11.3 A mu mol/L, p < 0.01) and (701.9 +/- 676.0 vs. 1374.7 +/- 716.5 pg/mL, p < 0.01), respectively, while a significant elevation in soluble thrombomodulin levels in beta-thalassemia/HbE (3587.7 +/- 1310.0 vs. 3093.9 +/- 583.8 pg/mL, p = 0.028). NO (x) and PGE(2) levels were significantly correlated with FMD (r = 0.27, p = 0.025) and (r = 0.35, p = 0.003), respectively. These findings suggest roles for endothelial mediators and a new mechanism underlying endothelial dysfunction in beta-thalassemia/HbE patients.
- 出版日期2017-9
