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Source: Smith SM, Gums JG. Adrenal Gland Disorders. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 8th ed. Accessed May 27, 2012.

  • Hypercortisolism

  • Clinical features resulting from chronic exposure to excess glucocorticoids of any cause.

  • Pituitary adenomas (Cushing's disease)
  • Ectopic ACTH-secreting tumors
  • Adrenal adenomas or carcinomas

  • Results from effects of supraphysiologic levels of glucocorticoids caused by exogenous administration or endogenous overproduction by adrenal gland (adrenocorticotropic hormone [ACTH]-dependent) or by abnormal adrenocortical tissues (ACTH-independent).
  • Ectopic ACTH syndrome is excessive ACTH production resulting from endocrine or nonendocrine tumor, usually of pancreas, thyroid, or lung.
  • ACTH-independent Cushing’s syndrome usually caused by adrenal adenomas and carcinomas.

  • Annual incidence of Cushing’s syndrome: 13 cases per million people.
  • Approximately 70% of cases due to Cushing’s disease, 15% to ectopic ACTH-secreting tumors, and 15% to adrenal tumors.

  • Chronic corticosteroid use
  • Age 20–50 years
  • Female sex

Signs and Symptoms

  • Central obesity and facial rounding (90% of patients)
  • Peripheral obesity and fat accumulation (50%)—fat accumulation in dorsocervical area (buffalo hump); moon facies.
  • Myopathy (65%) or muscular weakness (85%)
  • Striae along lower abdomen that may have red to purple color.
  • Hypertension (75–85%)
  • Glucose intolerance (60%)
  • Psychiatric changes (55%)
  • Osteoporosis (50–60%)
  • Gonadal dysfunction with amenorrhea in up to 75% of women
  • Excess androgen secretion with hirsutism in 80% of women

Laboratory Tests

  • 24-hour urinary free cortisol (UFC), midnight plasma cortisol, late-night (11 pm) salivary cortisol, and/or low-dose dexamethasone suppression test (DST) can identify hypercortisolism.
  • Plasma ACTH test; metyrapone stimulation test; corticotropin-releasing hormone (CRH) stimulation test; and inferior petrosal sinus sampling may be performed.


  • High-resolution CT and MRI may identify pituitary and adrenal masses.

Differential Diagnosis

  • Primary and secondary aldosteronism

  • Limit morbidity and mortality.
  • Return patient to normal functional state by removing source of hypercortisolism without causing pituitary or adrenal deficiencies.

  • See Table 1 for treatment plans based on etiology.

Table 1. Possible Treatment Plans in Cushing’s Syndrome Based on Etiology

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