Asymmetric Dimethylarginine (Adma): A Novel Marker of Endothelial Dysfunction in Hyperthyroidism

Disturbance of thyroid function, mainly hyperthyroidism has long been associated with cardiovascular complications. Clinical studies suggested that dysfunction of endothelial L-arginine-nitric oxide pathway is related in the development of Endothelial Dysfunction (ED) and to further vascular events. Asymmetric Dimethylarginine (ADMA), an endogenous competitive inhibitor of Nitric Oxide (NO) synthase, inhibits NO production by competing with L-arginine and its concentration was strongly predictive of premature cardiovascular disease. Symmetric Dimethylarginine (SDMA), another endogenous arginine analogue, is unable to inhibit NO synthase. The aim of this study was to examine the plasma levels of ADMA, SDMA, L-arginine and NO metabolites in hyperthyroid females and healthy volunteers. In this study sixty females (40 patients with primary hyperthyroidism and 20 normal healthy control) were included and subjected to determination of levels of serum fT3, fT4 and TSH by ELISA technique, plasma ADMA, SDMA and arginine by HPLC method, whereas serum NO metabolites levels were measured by colorimetric method. Our results showed that there were a significant increased ADMA and arginine levels and decreased NO metabolites levels in hyperthyroid patients than control subjects. In conclusion, ADMA was elevated in hyperthyroid patients. Elevation of ADMA was associated with decreased NO production, which could be related to endothelial dysfunction and its cardiovascular alterations. ADMA may be a novel risk factor for endothelial dysfunction in hyperthyroidism. Further studies should be doing to measure and assess the endothelial function itself in these patients.