MECHANISMS IN ENDOCRINOLOGY: Endogenous subclinical hypercortisolism and bone: a clinical review

Abstract

In recent years, the condition of subclinical hypercortisolism (SH) has become a topic of growing interest. This is due to the fact that SH prevalence is not negligible (0.8-2% in the general population) and that, although asymptomatic, this subtle cortisol excess is not harmless, being associated with an increased risk of complications, in particular of osteoporosis and fragility fractures. As specific symptoms of hypercortisolism are absent in SH, the SH diagnosis relies only on biochemical tests and it is a challenge for physicians. As a consequence, even the indications for the evaluation of bone involvement in SH patients are debatable and guidelines are not available. Finally, the relative importance of bone density, bone quality and glucocorticoid sensitivity in SH is a recent field of research. On the other hand, SH prevalence seems to be increased in osteoporotic patients, in whom a vertebral fracture may be the presenting symptom of an otherwise asymptomatic cortisol excess. Therefore, the issue of who and how to screen for SH among the osteoporotic patients is widely debated. The present review will summarize the available data regarding the bone turnover, bone mineral density, bone quality and risk of fracture in patients with endogenous SH. In addition, the role of the individual glucocorticoid sensitivity in SH-related bone damage and the problem of diagnosing and managing the bone consequences of SH will be reviewed. Finally, the issue of suspecting and screening for SH patients with apparent primary osteoporosis will be addressed.

Clinical characterization of patients with primary aldosteronism plus subclinical Cushing’s syndrome

“…Regarding bone metabolism impairment in SCS, the risk of developing osteoporosis is enhanced by the overproduction of cortisol in SCS [37,38]. On the other The numbers of patients who remained after the exclusion of 2 patients who had bilateral tumors and who missed the maximum tumor diameter c…”

Nonfunctioning adrenal incidentaloma: A novel predictive factor for metabolic syndrome

“…There is a large body of studies demonstrating that ACS patients present with higher metabolic disorders frequency caused by excess cortisol . Regarding NFAI, its definition includes absence of hypercortisolism as well as any other relevant hormonal activity and the guidelines do not indicate extra care.…”

“…There is a large body of studies demonstrating that ACS patients present with higher metabolic disorders frequency caused by excess cortisol. 5,20,[33][34][35][36][37] Regarding NFAI, its definition includes absence of and their levels usually increase with obesity. 39,40 In agreement, our study demonstrated that even both groups having comparable BMI the signs of insulin resistance were significantly higher in the NFAI group, which might point to a probable difference in the quality of the adipose tissue of these patients or higher circulating levels of me-…”

Cardiovascular events in patients with mild autonomous cortisol secretion: analysis with artificial neural networks

“…The condition of mild autonomous cortisol secretion (ACS) is characterized by an increased cortisol secretion in the absence of the classical signs of overt cortisol excess (1,2), and it is found in up to 20% of patients bearing an incidentally discovered adrenal mass (adrenal incidentaloma, AI) (3,4). In adults, mild ACS has a 0.2-2.0% prevalence and it seems to be associated with an increased risk of fragility fractures, dyslipidemia (DL), type 2 diabetes (T2DM), hypertension (AH), cardiovascular events (CVE) and mortality (5,6,7,8,9,10,11). However, since the improvement of the metabolic complications after the recovery from mild ACS has been not consistently reported (12,13), no widely accepted guidelines are available on how to define mild ACS and to address the treatment in AI patients with subtle hypercortisolism (1,15,16,17,18).…”