Abstract
Introduction: ACTH-independent Cushing's syndrome (CS) can be associated to the expression of ectopic- or overexpression of eutopic adrenal receptors. These receptors activate adenylate cyclase and subsequently stimulate steroid synthesis, resulting in ACTH-independent CS and growth promotion with hyperplasia or macronodular adrenal changes. Excess cortisol (Co)-secretion better correlates with variations of ligands for the aberrant receptors than the suppressed circulating ACTH.
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