Is there an association between non-functioning adrenal adenoma and endothelial dysfunction?
OBJECTIVE
Subtle changes in hypothalamic- pituitary-adrenal (HPA) axis of subjects with nonfunctioning adrenal adenoma may be associated with endothelial alterations. We sought to investigate endothelial function, visceral adiposity and osteoprotegerin (OPG) and interleukin- 18 (IL-18) levels in subjects with non-functioning adrenal adenomas.


METHODS
The adenoma group included 40 subjects without clinical and subclinical findings of hypercortisolism or other adrenal gland disorders. Twenty-two body mass index-matched controls were also enroled. The patients and control subjects underwent hormonal evaluation and assessment of anthropometric and metabolic parameters. Endothelial function was assessed with flowmediated dilatation (FMD) of the brachial artery and intima media thickness (IMT) of common carotid arteries. Visceral adipose tissue area was measured by computed tomography. Plasma OPG and serum IL-18 levels were also measured.


RESULTS
When compared with healthy controls, the adenoma group had elevated systolic blood pressure, post-dexamethasone suppression test cortisol and reduced DHEAS. Visceral adipose tissue area and IMT of common carotid arteries were comparable. In the adenoma group, FMD of the brachial artery was significantly impaired and IL-18 level was significantly elevated. Visceral adipose tissue area was independently related with FMD. Homeostasis model assessment (HOMA) was the independent factor associated with visceral adipose tissue area. Cortisol, DHEAS and visceral adipose tissue area were independently associated with HOMA.


CONCLUSIONS
We achieved evidence that could be attributable to endothelial alterations in subjects with non-functioning adrenal adenomas. Impaired FMD appeared to be a consequence of subtle changes in HPA axis in terms of elevated cortisol and reduced DHEAS as these conditions were known to disturb endothelial-dependent vasodilatation.
Division of Endocrinology and Metabolism, School of Medicine, Dokuz Eylul University, Inciralti, 35340, Izmir, Turkey. serkan.yener@deu.edu.tr
S
S
Yener
M
M
Baris
M
M
Secil
B
B
Akinci
A
A
Comlekci
S
S
Yesil
D000236:Adenoma / Q000473:pathology / Q000503:physiopathology*; D050154:Adiposity / Q000502:physiology; D000310:Adrenal Gland Neoplasms / Q000473:pathology / Q000503:physiopathology*; D018246:Adrenocortical Adenoma / Q000473:pathology / Q000503:physiopathology*; D000328:Adult; D002318:Cardiovascular Diseases / Q000503:physiopathology; D004727:Endothelium / Q000502:physiology* / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology / Q000503:physiopathology; D020382:Interleukin-18 / Q000097:blood; D050152:Intra-Abdominal Fat / Q000502:physiology; D008297:Male; D008875:Middle Aged; D053244:Osteoprotegerin / Q000097:blood; D010913:Pituitary-Adrenal System / Q000502:physiology / Q000503:physiopathology
D020382:Interleukin-18; D053244:Osteoprotegerin; D006854:Hydrocortisone