Endogenous Hypercortisolism describes a clinical state characterized by persistently and pathologically elevated levels of cortisol produced autonomously by the body itself, as opposed to elevation from external medication. This condition is primarily known as Cushing’s syndrome and leads to a distinctive constellation of metabolic, physical, and psychological symptoms due to chronic overexposure to glucocorticoids. Clinical diagnosis requires rigorous endocrine testing to confirm the autonomous, unregulated overproduction of this critical stress hormone.
Origin
The term is a compound of the Greek prefix endo- (meaning within), the steroid hormone cortisol, and the suffix hyper- (meaning excessive) and -ism (meaning a condition). Its clinical recognition is attributed to Harvey Cushing’s initial description of the syndrome in the early 20th century, which linked the pathology to pituitary or adrenal overactivity. Determining the precise source of the cortisol excess is central to selecting the correct clinical intervention.
Mechanism
The underlying mechanism involves a failure of the normal negative feedback inhibition of the hypothalamic-pituitary-adrenal (HPA) axis. In the most common form, a pituitary adenoma over-secretes ACTH, which chronically overstimulates the adrenal glands to produce cortisol. Alternatively, a tumor in the adrenal gland itself may autonomously produce cortisol, or a tumor elsewhere (ectopic) may secrete ACTH. This chronic, unregulated hormonal excess drives profound catabolic effects, suppresses the immune system, and severely alters metabolic pathways, leading to the characteristic systemic dysfunction.
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