Cushing’s Syndrome
Chronic glucocorticoid excess leads to development of symptoms and physical features known as Cushing’s syndrome or hypercortisolism. The most common cause is iatrogenic, resulting from chronic glucocorticoid therapy. Spontaneous Cushing’s syndrome is caused by abnormalities of the pituitary or adrenal gland or because of adrenocorticotropic hormone (ACTH) secretion by nonpituitary tumors. Cushing’s disease is defined as the specific type of Cushing’s syndrome caused by excessive pituitary ACTH secretion from a pituitary tumor.
Causes
In about 70% of patients, Cushing’s syndrome results from excess production of ACTH and consequent hyperplasia of the adrenal cortex. ACTH overproduction may stem from pituitary hypersecretion. More females than males are affected. An ectopic ACTH-producing tumor in another organ (particularly bronchogenic or pancreatic carcinoma), or administration of synthetic glucocorticoids or ACTH, causes about 15% of cases. Hypokalemia and hyperpigmentation are found in this group. In the remaining patients, Cushing’s syndrome results from a cortisol-secreting adrenal tumor, which is usually benign.
Complications
The stimulating and catabolic effects of cortisol produce the complications of Cushing’s syndrome. Increased calcium resorption from bone may lead to osteoporosis and pathologic fractures. Peptic ulcer may result from increased gastric secretions, pepsin production, and decreased gastric mucus. Increased hepatic gluconeogenesis and insulin resistance can cause impaired glucose tolerance. Overt diabetes mellitus occurs in fewer than 20% of patients.
Frequent infections or slow wound healing because of decreased lymphocyte production and suppressed antibody formation may occur. Suppressed inflammatory response may even mask a severe infection.
Hypertension due to sodium and water retention is common and may lead to ischemic heart disease and heart failure. Menstrual disturbances and sexual dysfunction also occur. Decreased ability to handle stress may result in psychiatric problems, ranging from mood swings to frank psychosis.
Assessment
The patient may report using synthetic steroids. She may complain of fatigue, muscle weakness, sleep disturbances, water retention, amenorrhea, decreased libido, irritability, and emotional lability. Additionally, she may list symptoms similar to those of hypoglycemia. Inspection may reveal a spectrum of characteristic signs, including thin hair, a moon-shaped face from fluid retention, hirsutism, acne, a buffalo-humplike back, and thin extremities from muscle wasting. Other observable features are petechiae, ecchymoses, and purplish striae; delayed wound healing; and swollen ankles. Auscultation typically reveals hypertension.
Diagnostic tests
Diagnosis of Cushing’s syndrome depends on a demonstrated increase in cortisol production and the failure to suppress endogenous
cortisol secretion after administration of dexamethasone. The patient should remain in the same time zone for 30 days to facilitate specimen collection during the test. Initial screening may consist of a 24-hour urine test to determine free cortisol excretion rate in addition to the tests described below. Failure to suppress plasma and urine cortisol levels confirms the diagnosis of Cushing’s syndrome.
cortisol secretion after administration of dexamethasone. The patient should remain in the same time zone for 30 days to facilitate specimen collection during the test. Initial screening may consist of a 24-hour urine test to determine free cortisol excretion rate in addition to the tests described below. Failure to suppress plasma and urine cortisol levels confirms the diagnosis of Cushing’s syndrome.
A high-dose dexamethasone suppression test
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