Impairment of endothelium-dependent arterial dilation in Hashimoto's thyroiditis patients with euthyroidism

Recent studies have shown that immune responses contribute to atherosclerosis, and endothelial dysfunction is an important early event in atherogenesis. The aim of this study was to investigate the alteration of endothelial function in Hashimoto's thyroiditis (HT) patients with euthyroidism.

Study subjects included 28 female HT patients with euthyroidism, 23 female HT patients with hypothyroidism, and 22 healthy women. High-resolution ultrasound was used to measure brachial artery diameter at rest, after reactive hyperaemia and after sublingual glyceryltrinitrate (GTN).

Flow-mediated arterial dilation in HT patients with euthyroidism was significantly lower (3.88%) than in controls (4.98%, P = 0.000) and higher than in HT patients with hypothyroidism (3.26%, P < 0.001). Flow-mediated arterial dilation among HT patients with hypothyroidism was significantly lower than that in controls (P = 0.000). GTN-induced arterial dilation, baseline vessel size, and baseline blood flow were not significantly different among the three groups (P > 0.05). On multiple regression analysis, anti-thyroid peroxidase antibody (TPO-Ab), TSH, free T3, low density lipoprotein cholesterol (LDL-C) and lipoprotein (a) [Lp(a)] were found to be significant factors associated with endothelium-dependent arterial dilation.

Endothelial dysfunction exists in HT patients with euthyroidism. Autoimmune reactivity and an elevated Lp(a) level might be responsible for the endothelial dysfunction.