Pseudo-Cushing's syndrome: the role of alcohol.
The mechanisms responsible for the genesis of pseudo-Cushing's syndrome are poorly understood. We studied the effect of acute ethanol administration on the hypothalamic-pituitary-adrenal axis in five chronic alcoholic patients and three normal volunteers. Ethanol was administered alone and together with beta 1-24 ACTH given intravenously. Baseline plasma ACTH and cortisol concentrations were significantly higher in the patients than in normal controls (p less than 0.05). Acute ethanol administration produced no significant change in the mean plasma ACTH concentration, failed to augment the effect of exogenous ACTH on the adrenal gland, and produced similar changes in the serum cortisol and aldosterone concentration in both the normal controls and the alcoholic patients. We speculate that pseudo-Cushing's syndrome may represent a state of stress-induced hypercortisolemia secondary to multiple episodes of subacute withdrawal from ethanol.
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000437:Alcoholism / Q000097:blood / Q000150:complications; D000450:Aldosterone / Q000097:blood; D003480:Cushing Syndrome / Q000175:diagnosis* / Q000209:etiology; D003937:Diagnosis, Differential; D000431:Ethanol / Q000494:pharmacology*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008875:Middle Aged
D000431:Ethanol; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone