Endocrine Abstracts

An increased cardiovascular risk has been described in patients (pts) with adrenal incidentaloma (AI), similarly to pts with overt Cushing’s syndrome (CS). Some echocardiographic abnormalities and alterations in adipokine secretion involved in insulin resistance, inflammation and atherosclerosis have been reported in pts with CS. In this study the possible correlation between echocardiographic parameters and adipokine levels in pts with AI was evaluated.

Subjects and methods: Morphological and functional echocardiographic characteristics and plasma IL-6, TNF-α, MCP-1 and resistin levels (ELISA methods) were studied in 7 pts (60.0±2.5 yrs, BMI 31.1±2.1) with AI and subclinical Cushing’s syndrome (SCS) and in 17 pts (58.8±2.3 yrs, BMI 29.5±1.2) with non functioning masses. All adrenal masses were identified as cortical adenoma. In all pts plasma ACTH, serum cortisol and urinary free cortisol (UFC) were measured.

Results: In pts with SCS the interventricular (IV) septum thickness was significantly greater than in pts with non functioning masses (13.2±0.1 vs 10.7±0.03 mm, P<0.05) and in 8 obese normotensive subjects (10.5±0.5 mm, P<0.001). Plasma IL-6, TNF-α, MCP-1, and resistin levels were higher in pts than in 20 normal subjects (60.3±2.5 vs 5.5±0.6 pg/ml, 27.2±1.3 vs 22.1±1.4 pg/ml, 164.3±17.0 vs 104.3±19.4 pg/ml, 12.9±2.4 vs 5.1±0.2 ng/ml, respectively, P<0.05). The other echocardiographic parameters and adipokine values were not different in pts with SCS and with non functioning AI. In all patients, UFC excretion positively correlated with left ventricular (LV) diameter end-systole (r=0.549, P=0.01) and with LV mass (r=0.479, P<0.05). Significant correlations were found between early wave diastolic filling velocity and IL-6 and TNF-α levels (r=−0.633, P=0.01 and r=−0.547, P<0.05, respectively), and between late wave diastolic filling velocity and TNF-α levels (r=−0.520, P<0.05), in all pts.

Conclusions: In AI a long-lasting exposure to an even slight cortisol excess and inflammatory stimuli might be responsible for a gradual impairment of both diastolic function and cardiac morphology.