HE pathological or iatrogenic state of glucocorticoid excess combined with its clinical and biochemical findings is known as CS. Endogenous CS results from prolonged exposure to excess glucocorticoids produced by the adrenal cortex or an adrenal tumor. To understand the causes of CS it is appropriate to classify the hypercortisolemic state by its dependence on corticotropin (ACTH). Pituitary corticotrophic adenomas account for about 80 to 90% of all noniatrogenic adult cases of CS. Cortisol-producing adrenal as well as non-pituitary ACTHsecreting lesions such as lung carcinoid, small cell lung carcinoma, pheochromocytoma, medullary thyroid carcinoma, pancreatic islet tumors, and rare ovarian tumors account for the majority of the balance. Ectopic CRH-producing lesions such as hypothalamic gangliocytomas are exceedingly rare. A subset of patients with CS presents with variable hormonogenesis, which may or may not exhibit overt clinical expression. During the nadir of hormonogenesis, serum hormone levels may be elevated, normal, or subnormal. The variability of these cycles may be regular or irregular. Definition of Cyclic CS Although not identified in most large series of patients with CS, the presence of cyclic CS is being increasingly
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