1987
DOI: 10.1016/0002-9343(87)90028-3
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Alcohol-induced pseudo-cushing's syndrome mimicking cushing's disease in a patient with an adrenal mass

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Cited by 25 publications
(20 citation statements)
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“…We were able to retrieve 35 cases of alcohol-induced pseudo-Cushing's syndrome, two of whom were not clinically cushingoid (1,2,12,18,(37)(38)(39)(40)(41)(42)(43)(44)(45). In these reports, endocrinological testing was performed when the subjects had been abstinent for widely varying periods (range 1-60 days).…”
Section: Studies In Abstinent Alcoholic Subjectsmentioning
confidence: 99%
“…We were able to retrieve 35 cases of alcohol-induced pseudo-Cushing's syndrome, two of whom were not clinically cushingoid (1,2,12,18,(37)(38)(39)(40)(41)(42)(43)(44)(45). In these reports, endocrinological testing was performed when the subjects had been abstinent for widely varying periods (range 1-60 days).…”
Section: Studies In Abstinent Alcoholic Subjectsmentioning
confidence: 99%
“…The challenge in the evaluation of alcohol-induced hypercortisolism and its differentiation from patients with pathologic Cushing's syndrome is heightened because some patients can be less than forthright about the magnitude of their chronic alcohol consumption. Although the majority of patients with alcohol-induced Cushing's syndrome have either normal or increased plasma ACTH, adrenal nodular disease and subnormal plasma ACTH has been reported (33).…”
Section: Alcohol-induced Hypercortisolismmentioning
confidence: 99%
“…On the other hand, some patients with alcohol-induced hypercortisolism may have obvious clinical features of Cushing's syndrome including facial fullness with plethora, violaceous striae and proximal myopathy and edema (18,28,32,33). Most patients with pathologic hypercortisolism have objective clinical manifestation of cortisol excess such as hypertension, diabetes/pre-diabetes, low bone density with fracture and hirsutism/oligomenorrhea.…”
Section: Clinical Differentiation: Physiologic Vs Pathologic Hypercormentioning
confidence: 99%
“…The syndrome may, in addition, be caused by ectopic corticotropin releasing hormone (CRH) secretion [10, 11, 12], bilateral primary pigmented nodular adrenal dysplasia (PPNAD) or macronodular adrenal hyperplasia [13], the ectopic actions of gastric inhibitory peptide or catecholamines [14, 15, 16], and other adrenal-dependent processes associated with adrenocortical hyperfunction such as the McCune-Albright syndrome and Carney’s complex [13, 17]. Pseudo-Cushing’s states, which may have similar clinical presentations together with evidence of hypercortisolaemia, may be caused by alcohol dependence [18, 19, 20, 21, 22]and/or depression [23, 24, 25, 26]. It may also be necessary to differentiate Cushing’s syndrome from other clinical presentations with ‘cushingoid’ features, such as cases of simple obesity in which some cushingoid clinical features may be present [27, 28, 29, 30, 31, 32].…”
Section: Definitions and Aetiologymentioning
confidence: 99%