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REVIEW  UNILATERAL NON-ALDOSTERONE-PRODUCING ADRENOCORTICAL TUMORS 

Minerva Endocrinologica 2019 March;44(1):33-42

DOI: 10.23736/S0391-1977.18.02884-5

Copyright © 2018 EDIZIONI MINERVA MEDICA

lingua: Inglese

Autonomous hypercortisolism: definition and clinical implications

Giuseppe REIMONDO , Soraya PUGLISI, Anna PIA, Massimo TERZOLO

Unit of Internal Medicine and Endocrinology, Department of Clinical and Biological Sciences, San Luigi Gonzaga University Hospital, University of Turin, Orbassano, Turin, Italy



In current practice, an adrenal adenoma usually comes as an unexpected byproduct of an imaging study performed for unrelated reasons, without any prior suspect of adrenal disease. Therefore, these tumors currently represent a public health challenge because they are increasingly recognized due to the widespread use of high-resolution cross-sectional imaging for diagnostic purposes. In radiology series, the prevalence of adrenal adenomas increases steeply with age, from around 3% below the age of 50 years up to 10% in the ageing population. These tumors may have clinical relevance because they are able to secrete cortisol autonomously, independently from the pituitary control, in up to 20-30% of patients. In most of the cases the resulting cortisol excess is insufficient to produce a typical Cushing phenotype but may have clinical consequences, such as hypertension, diabetes, obesity, dyslipidemia and osteoporosis. Despite some controversy on the most effective diagnostic algorithm to define this subtle hypercortisolism, there is mounting evidence that a simple approach by using the 1-mg overnight dexamethasone suppression test (DST) may stratify patients for their cardiovascular risk. Cross-sectional, retrospective studies showed that patients with increasingly higher cortisol following DST have an adverse cardiovascular risk profile and are at increased risk of death. Therefore, also a subtle autonomous cortisol excess is associated with increased morbidity and mortality, mainly of cardiovascular origin.


KEY WORDS: Adrenocortical adenoma - Cushing Syndrome - Adrenocortical hyperfunction

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