Many difficulties can be encountered in the management of patients with Cushings syndrome or suspected Cushings syndrome.
In the first step of the diagnosis strategy, establishing the state of chronic hypercortisolism may be hampered by a number of pitfalls: drug interaction (inducers of high CBG levels, liver enzyme inducers, glucocorticoids, antiglucocorticoid RU 486, Glycyrrhetinic acid); intercurrent pathologic states (obesity, thyroid dysfunction, renal failure). Various pathologic or physiologic conditions may be associated with biochemical, and sometimes clinical, evidences of endogenous glucocorticoid excess creating the pseudo-Cushing syndrome (depression, anorexia nervosa, alcoholism, strenuous exercise, pregnancy). Familial resistance to glucocorticoids, a rare inherited condition, is associated with excess glucocorticoid, androgen, and mineralocorticoid production with no clinical manifestations of Cushings syndrome. Normal suppression with the classic low-dose dexamethasone test can be observed in authentic Cushings disease.
Once the positive diagnosis of Cushings syndrome has been convincingly established, one may deal with numerous etiologic pitfalls. Cushings disease mimicking an autonomous adrenocortical tumor, severe Cushings disease mimicking the classic ectopic ACTH syndrome, mild ectopic ACTH syndrome mimicking the classic Cushings disease.
These various situations, and the ways to avoid pitfalls, will be presented and discussed using illustrating clinical cases.