Endogenous glucocorticoid excess underlies the coexistence of bone and vascular diseases

Purpose: Bone and vascular diseases are considered to share pathogenic mechanisms. Excess glucocorticoids, key regulators of cardiovascular and metabolic homeostasis, may promote both diseases simultaneously. We used endogenous Cushing’s syndrome (CS) as a clinically defined model of glucocorticoid excess to investigate whether glucocorticoid excess underlies coexisting bone and vascular diseases. Methods: We included 194 patients with adrenal tumors (ATs): autonomous cortisol secretion (ACS, n=97) and non-functional AT (n=97). ACS was further classified into overt CS (n=17) and subclinical CS (SCS, n=80). Arterial stiffness was defined as a brachial-ankle pulse wave velocity (baPWV) ≥ 1,800 cm/s. Results: Patients with ACS had higher coexistence rates of vertebral fracture and arterial stiffness (23% vs. 2%; p<0.001) and vertebral fracture and abdominal aortic calcification (22% vs. 1%; p<0.001) than those with non-functional AT. In patients with ACS, baPWV was negatively correlated with trabecular bone score (TBS, r=-0.33; p=0.002), but not with bone mineral density, and vertebral fracture was associated with arterial stiffness in the logistic regression analysis. In the multivariate analysis of variance, the degree of cortisol excess (defined as CS, SCS, and non-functional AT) determined the correlation between TBS and baPWV (partial η2=0.07; p