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The Cushing Syndrome: Quest for the Holy Grail

David N. Orth, MD
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Vanderbilt University Medical Center; Nashville, TN 37232-2250 Grant Support: In part by NIH Research Grants DK46070 and RR00095.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1994;121(5):377-378. doi:10.7326/0003-4819-121-5-199409010-00012
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The endogenous Cushing syndrome results from excessive cortisol secretion that is usually secondary to excessive adrenocorticotropin (ACTH) secretion. About 85% of patients with the ACTH-dependent Cushing syndrome have ACTH-secreting pituitary microadenomas (Cushing disease). Most of the remaining patients have ACTH-secreting nonpituitary tumors (the ectopic ACTH syndrome), usually small-cell lung carcinomas, and follow an acute clinical course different from that of patients with Cushing disease [1]. However, about one fifth of patients with the ectopic ACTH syndrome have indolent tumors (usually bronchial carcinoids) and may present with a clinical picture indistinguishable from that of Cushing disease. Further, the classic test for distinguishing between the two, the high-dose dexamethasone suppression test [2], is unreliable in at least half of patients with bronchial carcinoids [35].

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