Cushingoid

Cushingoid describes the collection of physical features associated with Cushing’s syndrome, not a distinct disease itself. The term denotes a phenotype that results from prolonged exposure to elevated cortisol levels, whether from endogenous overproduction or exogenous glucocorticoid therapy.

Typical features include central obesity with a dorsocervical fat pad, a rounded "moon" face, abdominal striae, proximal muscle weakness, thinning of the skin, easy bruising, and hypertension. Additional signs may include glucose intolerance, hirsutism, menstrual irregularities in women, facial fullness, and secondary osteoporosis. The severity and combination of signs vary among individuals, and these features can resemble other conditions, so evaluation by a clinician is important.

Causes of a Cushingoid appearance most commonly arise from exogenous glucocorticoid use. Endogenous causes include ACTH-dependent Cushing’s syndrome (pituitary adenoma producing ACTH) and ectopic ACTH secretion from nonpituitary tumors, as well as ACTH-independent causes such as adrenal adenoma or carcinoma.

Diagnosis involves biochemical confirmation of hypercortisolism, typically with elevated 24-hour urinary free cortisol, loss of normal diurnal cortisol variation, or failure to suppress cortisol on an overnight dexamethasone test. Differentiating the cause relies on measuring ACTH levels, performing high-dose dexamethasone suppression testing, and imaging of the pituitary and adrenal glands.

Management targets the underlying cause. In cases of exogenous steroids, tapering or stopping the drug is primary. Tumors may require surgical removal, with radiotherapy or medical therapies (such as ketoconazole or metyrapone) used in some scenarios. Ongoing care addresses metabolic complications and cosmetic concerns. Prognosis depends on duration of cortisol excess and the success of treating the underlying cause.