Endocrine Abstracts

It has been previously shown that adrenal adenomas are associated with a variety of metabolic disturbances like glucose intolerance and obesity. The aim of this study is to demonstrate the risk of non-alcoholic fatty liver disease development in subjects with adrenal incidentalomas.

Among 302 subjects referred between 2001 and 2008 for the evaluation of incidentally discovered adrenal mass, 150 subjects with appropriate data were included. Computed tomography (CT) was the initial radiological intervention. Initial hormonal evaluation included 1 mg or 2 day 2 mg dexamethasone suppression test, urinary free cortisol (UFC), 0800 a.m. ACTH and DHEAS levels. In subjects with elevated post DST cortisol (>1.8 mcg/dl), elevated UFC (>110 mcg/day), and suppressed ACTH and DHEAS levels, midnight cortisol was evaluated (normal < 7.5 mcg/dl). Urinary catecholamine excretion and aldosterone/renin ratio were also measured. Hepatosteatosis was evaluated with liver ultrasonography and or magnetic resonance imaging. ALT, AST and GGT were also measured.

There were 101 subjects with non-functioning adrenal adenomas, 40 subjects with functioning adrenal adenomas (Cushing or subclinical Cushing syndrome) and nine subjects with myelolipomas. The rate of non-alcoholic liver disease among these groups was 25.7, 22.7 and 11% respectively. After a median follow up duration of 22.5 months in a subgroup generated from study participants (n=35) without non-alcoholic fatty liver disease, we showed that 9% of subjects with non-functioning adenomas but 17% of subjects with sub clinical Cushing syndrome developed non-alcoholic liver disease.

Non-alcoholic liver disease, which is an important manifestation of insulin resistance is significantly associated with adrenal cortical adenomas rather than extra-cortical masses such as myelolipomas. The risk of developing non-alcoholic fatty liver disease is related with cortisol autonomy.