Cortisol is the principal human glucocorticoid and a key effector of the hypothalamic-pituitary-adrenal (HPA) axis. It maintains cardiovascular tone, glucose availability, immune modulation, and adaptive responses to physical and psychological stress. Persistent cortisol excess, however, produces a multisystem disorder characterized by central adiposity, hypertension, glucose intolerance, muscle weakness, osteoporosis, skin changes, reproductive dysfunction, and increased susceptibility to infection. This thesis summarizes cortisol physiology, major physiological and pathological causes of elevation, the clinical pattern of hypercortisolism, current diagnostic principles, and contemporary treatment options. Particular attention is paid to distinguishing transient stress-related cortisol elevation from endogenous Cushing syndrome and from exogenous glucocorticoid exposure.
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Xursandova Feruza Sattorovna (2026) studied this question.
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