Endocrine Abstracts

Endothelial dysfunction contributes to the cardiovascular complications in Diabetes mellitus and hypertension. The effects of hyperthyroidism on the peripheral vasculature are not fully understood. Decreased central arterial stiffness is a feature of thyrotoxicosis and normalises with treatment (1). The purpose of our study was to establish the effect of thyrotoxicosis and its treatment on surrogate humoral markers of endothelial function; Von Willebrand factor (VWF), Soluble Intercellular adhesion molecule (ICAM-1), L selectin (using R&D kit). 13 hyperthyroid patients (2M and 11F, mean age 47.2 years plus/minus 5.0, BMI 25.7kg/m² plus/minus 1.2, mean FT3, 11.07 pmol/L plus/minus 1.07) were studied at baseline (T) and at six months after treatment with 555MBq of ¹³¹I (E; mean FT3, 5.35 pmol/L plus/minus 0.32). Results are reported as (Mean plus/minus SEM). Compared to T, E was accompanied by a significant decrease in VWF <0.99 plus/minus 0.14 V 2.17 plus/minus 0.39 p<0.01, N= (0.35-1.79IU/mL)>, but not in ICAM-1 <394 plus/minus 37 V 424 plus/minus 38, P<0.58, N= (115-306ng/mL)> or L selectin<1724 plus/minus 303 V 1371 plus/minus 90 p<0.28; N = (660-1250ng/mL)>. It is concluded from these data that thyrotoxicosis results in increased surrogate markers of endothelial dysfunction. Biochemical correction of thyrotoxicosis may precede the complete resolution of humoral markers of endothelial dysfunction. These changes are dissociated from central arterial stiffness (1).

1. Obuobie K., Lazarus JH. (2000) J. Endocrinol., 64 suppl., P320.