Depleted nitric oxide and prostaglandin E2 levels are correlated with endothelial dysfunction in β-thalassemia/HbE patients

Abstract

Mechanisms of vascular disorders in β-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 β-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). β-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 E2 (PGE2) levels were significantly decreased in β-thalassemia/HbE (117.2±27.3 vs. 135.8±11.3µmol/L, p<0.01) and (701.9±676.0 vs. 1374.7±716.5pg/mL, p<0.01), respectively, while a significant elevation in soluble thrombomodulin levels in β-thalassemia/HbE (3587.7±1310.0 vs. 3093.9±583.8pg/mL, p=0.028). NO x and PGE2 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 β-thalassemia/HbE patients.