Endocrine Abstracts (2008) 16 OC3.8

Plasma endothelin as a biochemical marker of endothelial dysfunction in endocrine diseases with increased cardiovascular risk

Georgi Kirilov

Clinical Center of Endocrinology, Sofia, Bulgaria.

Background: The aim of the present study was to represent our summarized results of plasma endothelin-1 (ET-1) level determined in some endocrine diseases like diabetes, hyper- and hypothyroidism, Cushing’s disease, acromegaly and male hypogonadism in which the existence of endothelial dysfunction and increased cardiovascular risk is proved.

Patients and results: In patients with type 2 diabetes (n=34), plasma ET-1 (0.9±0.17 pmol/l) correlated with the degree of vascular complications and reached the highest level in hemodialysis diabetics (3.4±0.38 pmol/l). ET-1 was significantly elevated in patients with hyperthyroidism (0.78±0.11 pmol/l, n=18) and decreased to normal range after thyrostatic treatment (0.5±0.1 pmol/l). However, in hypothyroid subjects (n=20) ET-1 did not differ from controls (0.49±0.12 vs 0.46±0.2 pmol/l). ET-1 level in patients with Cushing’s disease was 3-fold higher (1.6±0.8 pmol/l, n=13) than in healthy subjects, and decreased significantly after disease remission (0.73±0.53 pmol/l). Hypersomatotropism in acromegaly (n=28) leads to significant elevation of ET-1 (1.24±0.2 pmol/l). After treatment and normalization of IGF-1, ET-1 showed the normal concentration (0.39±0.1 pmol/l). The low testosterone level in male hypogonadism (n=33) caused higher plasma ET-1 (0.95±0.53 pmol/l). Patients with hypergonadotrophic hypogonadism had significantly higher ET-1 in comparison to hypogonadotrophic hypogonadism (1.05±0.57 pmol/l vs 0.89±0.53 pmol/l). In all groups no correlation was observed between the concentrations of ET-1, blood pressure, lipid status and plasma homocystein.

Conclusions: Our results clearly demonstrate that hyperthyroidism, hypercortisolism, hypersomatotropism and hypogonadism lead to activation of endothelin system. Elevated plasma ET-1 levels probably play a role in the pathogenesis of accelerated and early atherosclerosis development in this disorders.

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