ABSTRACT
Described famously in 1932 by Harvey Cushing as “pituitary basophilism,” Cushing’s syndrome refers to the clinical constellation of obesity, diabetes, arterial hypertension, muscular weakness, and adrenal hyperplasia [1]. An elevated serum cortisol is the sine qua non of Cushing’s syndrome. Conversely, symptomatic patients with physiologic hypercortisolism are often described as having “pseudo-Cushing’s syndrome” [2]. All signs and symptoms of Cushing’s syndrome result directly or indirectly from prolonged exposure to excess cortisol. While the full-blown syndrome is unmistakable, the large spectrum of disease and its protean manifestations dictate that Cushing’s syndrome must be considered in the differential diagnosis for many diverse and nonspecific clinical manifestations.
