One of the commonest causes of Cushing syndrome is the administration of "cortisol-like medications" for the treatment of diverse diseases. All other cases of Cushing syndrome are due to the excess production of cortisol by the adrenal gland as, for example, due to:
The symptoms and signs of Cushing's syndrome result directly from chronic exposure to excess glucocorticoid. Establishing the diagnosis is often difficult because few of the symptoms or signs are pathognomonic of the syndrome in isolation. There is a large spectrum of manifestations from subclinical to overt syndrome, depending on duration and intensity of excess steroid production. Furthermore, some of them (such as obesity, hypertension, and glucose intolerance) are common in individuals who do not have adrenal hyperfunction. An important clinical clue to the presence of glucocorticoid excess is the simultaneous development and increasing severity of several of these symptoms.
In those patients not suited for or unwilling to undergo surgery, several drugs have been found to inhibit cortisol synthesis (. ketoconazole , metyrapone ) but they are of limited efficacy. [ citation needed ] Mifepristone is a powerful glucocorticoid type II receptor antagonist and, since it does not interfere with normal cortisol homeostatis type I receptor transmission, may be especially useful for treating the cognitive effects of Cushing's syndrome.  However, the medication faces considerable controversy due to its use as an abortifacient . In February 2012, the FDA approved mifepristone to control high blood sugar levels ( hyperglycemia ) in adult patients who are not candidates for surgery, or who did not respond to prior surgery, with the warning that mifepristone should never be used by pregnant women.