Cushing Syndrome

Cushing syndrome is the clinical result of prolonged glucocorticoid excess. The excess may be iatrogenic from prescribed glucocorticoids or endogenous: ACTH-dependent disease from a pituitary adenoma or ectopic ACTH secretion, or ACTH-independent disease from an adrenal adenoma or carcinoma. Cortisol excess explains the clustering of progressive hypertension, hyperglycemia, facial rounding, proximal weakness, skin fragility, osteoporosis, infection risk, and mood change; one isolated feature is nonspecific. A detailed medication history comes before biochemical testing because exogenous steroid exposure changes the diagnostic question. Investigate when multiple features are progressive or when an adrenal incidentaloma is at least 1 cm. The work-up follows a clinical sequence: confirm hypercortisolism, interpret ACTH, localize the source, and remove or suppress that source while treating its complications. After cortisol falls, the same physiology creates the opposite danger—temporary or acute cortisol deficiency—so definitive therapy and steroid-replacement planning are inseparable.