Key Points

• Cushing's syndrome is categorized into ACTH-dependent or ACTH-independent cases. Pituitary ACTH-dependent Cushing's syndrome is Cushing's disease.

• The diagnosis is established when the clinical findings of Cushing's syndrome are associated with laboratory documentation of excess cortisol production.

• Measurement of 24-hour urinary cortisol excretion is a good screening tool.

• Comparison of serum ACTH concentration with serum cortisol level can help determine the cause of hypercortisolism.

• Treatment of Cushing's syndrome is directed at the cause of hypercortisolism. The treatment of choice for Cushing's disease is selective transsphenoidal resection.

Hypercortisolemia (also hypercortisolism, hyperadreno-

corticism), caused by either exogenous administration of cortisol or other synthetic glucocorticoids or endogenous overproduction of Cortisol, leads to a constellation of clinical and biochemical findings referred to as Cushing's syndrome (Arnaldi et al., 2003; Findling and Raff, 2005). The multiple causes include pituitary adenomas, excess production of CRH leading to hyperplasia of corticotropes in the pituitary, ectopic production of ACTH and CRH, and adrenocortical adenomas and carcinomas. The term Cushing's disease specifically refers to pituitary-dependent cortisol hypersecretion (Biller et al., 2008). Pituitary, ACTH-dependent Cushing's disease accounts for at least 70% of endogenous cases, while the most common cause of ACTH-independent Cushing's syndrome is prolonged glucocorticoid therapy.

Patients who have undergone bilateral adrenalectomy for hypothalamic-pituitary-dependent Cushing's syndrome may develop pituitary tumors associated with marked skin pigmentation. This condition is known as Nelson's syndrome. The skin hyperpigmentation occurs because of excess production of melanocyte-stimulating hormone (MSH), a product of the gene that also encodes ACTH and beta endorphin.

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