Endocrine Abstracts

Adrenal incidentalomas (AIs) are tumours accidentally detected by various imaging methods applied without suspecting adrenal pathology, indicating that most of them are nonfunctional. The most frequent hormonal alteration in AIs is autonomous cortisol secretion (ACS), a condition of altered hypothalamic-pituitary-adrenal axis activity, established on the biochemical parameters of hypercortisolism, without phenotype expression of Cushing’s syndrome. Since mild hypercortisolism is associated with metabolic complications such as abdominal obesity, insulin resistance, hyperglycemia, atherogenic dyslipidemia, and hypertension, which are a cluster of the metabolic syndrome, thenew term ’metabolic autonomous cortisol syndrome’ (MACS) has been suggestedfor this condition. The prevalence of AIs ranges from 3% in 50-year-old patients up to 10% in the elderly. Depending on the applied diagnostic criteria, the prevalence of ACS in patients with AIs is estimated at 5-30%. Given that the overall prevalence of ACS is up to 2%, a significant part of the population may have MACS comorbidities. Postmenopausal aging is accompanied by an unfavorable change in body composition towards an increase in abdominal adiposity. Consequently, this is associated with greater lipolytic activity and inflammation, resulting in the onset or deterioration of cardiometabolic complications. Studies on the influence of regional fat distribution suggest that preservation of gluteo-femoral subcutaneous adipose tissue, independently of the presence of abdominal obesity, could have beneficial effects on insulin sensitivity, and the glucose and lipid metabolism. Regardless of the degree of cortisolemia in postmenopausal women with AIs, tissue specific glucocorticoid sensitivity may influence body composition as well as metabolic parameters determining the individual predisposition for the development of MACS. Chronic mild hypercortisolism is associated with an increased risk of osteoporosis and fragility fractures, but glucocorticoid receptor gene polymorphism may modulate skeletal sensitivity to the glucocorticoid excess.