The HDL anti-inflammatory function is impaired in the context of low-normal free thyroxine in diabetic and non-diabetic individuals

Abstract

Differences in thyroid function status within the euthyroid range have been proposed to affect the development of (subclinical) atherosclerosis [1], as evidenced by a greater carotid artery intima media thickness and progression of coronary artery calcification in the context of low normal thyroid function, i.e. a higher thyroid stimulating hormone (TSH) or a lower free thyroxine (FT4) thyroid hormone in the euthyroid range [2,3]. Importantly, with respect to high density lipoproteins (HDL) the concept is emerging that abnormalities in function rather than low concentrations of HDL cholesterol per se may give rise to impaired atheroprotective potential of this lipoprotein fraction. In line, a lower FT4 within the euthyroid range associates with a diminished ability of HDL to protect against LDL oxidation in vitro [4].

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