“…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].…”