Cushing’s syndrome can be caused by partially autonomous pituitary tumors secreting ACTH (ACTH-dependent Cushing’s syndrome) or by autonomous adrenal or ectopic tumors secreting Cortisol (ACTH-independent Cushing’s syndrome). ACTH- independent Cushing’s syndrome is associated with feedback suppression of ACTH secretion.

Major clinical manifestations of Cushing’s syndrome (hypercorti- solism) include hypertension due to Na+ retention, hyperglycemia (due to gluconeogenesis insulin resistance, and hyper- insulinemia), increased plasma levels of DHEA and increased urinary excretion of 17-ketosteroids.

Other features include osteoporosis, weight gain with centripetal obesity, muscle wasting and weakness. Sex-related problems include amenorrhea and hirsutism (in women) impotency (in men) and decreased libido (in both). Psychological problems include depression, irritability, insomnia, psychosis, manic depression.

Overall, glucocorticoids bring about a redistribution of fat together with an increase in total body fat. There is characteristic centripetal distribution of fat i.e., an accumulation of fat in the central axis of the body (truncal obesity) with wasting of the extremities.

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As the thin skin of the abdomen is stretched by the increased subcutaneous depot, the subdermal tissues rupture to form prominent reddish-purple stria. The deposition of fat in the facies is called “moon face.” The deposition of fat in the suprascapular region is referred to as “buffalo hump” or “dowager’s hump” (dowager = elderly woman). Excessive fat distribution leads to a pendulous abdomen. Chronic excess of glucocorticoids lead to hyperlipidemia and hypercholesterolemia.