Endocrine Abstracts

Many difficulties can be encountered in the management of patients with Cushing’s syndrome or suspected Cushing’s 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 Cushing’s syndrome. Normal suppression with the classic low-dose dexamethasone test can be observed in authentic Cushing’s disease.

Once the positive diagnosis of Cushing’s syndrome has been convincingly established, one may deal with numerous etiologic pitfalls. Cushing’s disease mimicking an autonomous adrenocortical tumor, severe Cushing’s disease mimicking the classic ectopic ACTH syndrome, mild ectopic ACTH syndrome mimicking the classic Cushing’s disease.

These various situations, and the ways to avoid pitfalls, will be presented and discussed using illustrating clinical cases.