Evaluation of endothelial function in subclinical thyroid dysfunction

We read with interest the article on the evaluation of endothelial function in subclinical hypothyroidism (SH) and subclinical hyperthyroidism (SHr) by Cikim et al. (1). As the authors state, SH may have adverse effects on endothelial function independent from other well-known atherosclerotic risk factors such as dyslipidemia. Indeed, the association of SH with changes in serum lipoprotein profile and the effect of Levothyroxine replacement therapy on these changes are still open questions (2–4). We also agree with the authors that endothelial dysfunction, a condition characterized by decreased nitric oxide availability, plays a pivotal role in the pathogenesis of coronary artery disease (5). However, the authors state that endothelial impairment has not been clearly demonstrated in mild thyroid dysfunction. We had previously demonstrated a reversible alteration of endothelium dependent vasodilatation and reduced nitric oxide availability in SH patients (6). The study population included 14 SH patients and 28 euthyroid controls, matched to the patient group for sex, age and body mass index and divided, according to the lipid profile, into a normocholesterolemic (n 14) and a slightly hypercholesterolemic group (n 14, matched to SH patients). Our results indicated that the endothelial impairment of SH patients cannot be accounted for exclusively by the concomitant mild hypercholesterolemia since endothelium dependent vasodilation was significantly reduced in comparison to both the control groups. Therefore, besides serum lipid alterations, we suggested a direct effect of thyroid hormone reduction in endothelial dysfunction development of SH patients