Endocrine Abstracts (2011) 26 S4.1

Subclinical adrenal hyperfunction

G Kaltsas


University of Athens, Athens, Greece.


The adrenal glands secrete a variety of hormones from the cortex (steroids) and the medulla (amines) that when in excess lead to characteristic clinical syndromes. Dysregulation of the secretory pattern of these hormones or hypersecretion not enough to cause a clinically obvious syndrome is termed subclinical hyperfunction and is mainly found in primary adrenal lesions in the form of adrenal incidentalomas (AI). These are adrenal mass lesions usually >1 cm in diameter that are increasingly being discovered during testing, mostly via CT abdominal imaging, for conditions unrelated to adrenal diseases. Their overall incidence ranges between 3 and 10% increasing with age and it is clinically important to identify those that exert clinical or subclinical hormonal activity or have a malignant potential. Subclinical mainly hypercortisolism (Cushing’s) (SC), is the most common hormonal hyperactivity encountered in a significant number of patients with AI; its prevalence ranges according to the diagnostic procedures used and may fluctuate with time. In some patients it may be associated with some of the detrimental effects of continuous autonomous cortisol secretion such as arterial hypertension, dyslipidemia, alterations of carbohydrate metabolism and an increased risk for osteoporotic fractures. It is still unproven whether treatment to reverse autonomous cortisol secretion is beneficial and further mainly prospective controlled studies are required to address this issue. Clinical significant autonomous aldosterone secretion is less common than SC using conventional screening tests, namely the aldosterone to rennin ratio. The introduction of more sophisticated tests based on complex pathophysiological mechanisms may reveal a significantly higher prevalence but further studies are needed to identify significant clinical correlates. Clinically unrecognized or silent pheochromocytomas may be associated with increased morbidity and mortality. However, in the absence of prospective studies correlating hormonal activity with end organ damage, the long term consequences of these syndromes and their management remains largely pragmatic.

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