title: Endocrine evaluation of incidentally discovered adrenal masses (incidentalomas)
abstract: Since 1989, 45 patients [pts; 26 females and 19 males, aged 19-79 yr (median, 58)] bearing incidentally discovered adrenal masses were studied. The aim of the study was to verify the prevalence of hormone activity in clinically silent adrenal masses. Endocrine work-up included determination of urinary catecholamines and their metabolites, measurement of PRA and aldosterone levels in clino- and orthostatic posture, and basal and dynamic [dexamethasone (dex) suppression and ovine CRH stimulation] evaluation of hypothalamic-pituitary-adrenal axis. The most frequent finding was the reduction of dehydroepiandrosterone sulfate (DHEA-S) levels below the third percentile of controls in 19 (42%) pts. DHEA-S levels were significantly lower in pts than in controls [68 (range, 5-1000) vs. 208 (34-326) micrograms/dL; 1.8 (0.1-27.1) vs. 5.6 (0.9-8.8) mumol/L; P < 0.001]. Three pts (7%) had high 24-h mean serum cortisol levels, and 6 (14%) had blunted day-night amplitude of cortisol rhythm. Defective dex suppressibility was found in 15% of pts vs. 8% of controls (P < 0.05). ACTH and cortisol responses to ovine CRH did not significantly differ between pts and controls, although blunted ACTH responses were found in 22% of the cases. The above-mentioned endocrine alterations could be accounted for by autonomous cortisol secretion by the adrenal nodule at a rate not sufficient to give clinical expression, but able to inhibit to some extent the hypothalamic-pituitary-adrenal axis. These results indicate that silent cortisol hypersecretion is frequently observed in pts with adrenal incidentaloma even if progression to overt Cushing's syndrome seems unlikely. Indeed, the size of the mass and the hormone pattern remained substantially unchanged in 9 pts followed up for 12 months. From merely a cost/benefit ratio, the evaluation of DHEA-S levels and dex suppression has sufficient sensitivity to identify the occurrence of silent hypercortisolism.
authors.affiliation: Department of Clinical and Biological Sciences, University of Turin, S. Luigi Hospital, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Osella
authors.forename: M
authors.initials: M
authors.lastname: Terzolo
authors.forename: G
authors.initials: G
authors.lastname: Borretta
authors.forename: G
authors.initials: G
authors.lastname: Magro
authors.forename: A
authors.initials: A
authors.lastname: Alí
authors.forename: A
authors.initials: A
authors.lastname: Piovesan
authors.forename: P
authors.initials: P
authors.lastname: Paccotti
authors.forename: A
authors.initials: A
authors.lastname: Angeli
mesh_terms: D000236:Adenoma / Q000175:diagnosis / Q000378:metabolism / Q000473:pathology; D000310:Adrenal Gland Neoplasms / Q000175:diagnosis / Q000378:metabolism* / Q000473:pathology; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D002277:Carcinoma / Q000175:diagnosis / Q000378:metabolism / Q000473:pathology; D002395:Catecholamines / Q000652:urine; D003346:Corticotropin-Releasing Hormone; D003687:Dehydroepiandrosterone / Q000031:analogs & derivatives / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate; D003907:Dexamethasone; D005260:Female; D006728:Hormones / Q000378:metabolism*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D008875:Middle Aged; D010673:Pheochromocytoma / Q000175:diagnosis / Q000378:metabolism / Q000473:pathology; D012083:Renin / Q000097:blood; D014057:Tomography, X-Ray Computed; D014463:Ultrasonography
chemical_list: D002395:Catecholamines; D006728:Hormones; D003687:Dehydroepiandrosterone; D000450:Aldosterone; D019314:Dehydroepiandrosterone Sulfate; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D012083:Renin; D006854:Hydrocortisone