The core diagnostic value of tetracosactide injection lies in the precise evaluation of the adrenal cortex's responsiveness to trophic hormones. Its primary uses focus on screening and dynamic assessment of adrenocortical function, providing reliable laboratory evidence for the early diagnosis, etiological differentiation, and disease monitoring of adrenal disorders. Compared with natural ACTH, the product has a shorter half‑life and more targeted action, effectively avoiding hormonal fluctuations potentially caused by natural ACTH. It is also convenient to administer and highly safe, making it one of the first‑line diagnostic agents for clinical adrenocortical function assessment, widely used in endocrinology, emergency medicine, rheumatology and immunology, and other departments.

Adrenocortical insufficiency refers to a group of disorders characterized by insufficient secretion of cortisol, aldosterone, and other hormones by the adrenal cortex, leading to disturbances in metabolism, immunity, water‑electrolyte balance, and other bodily functions. It is classified into primary, secondary, and tertiary types based on etiology. Clinical manifestations commonly include fatigue, weight loss, hypotension, and electrolyte abnormalities. Early symptoms are insidious and easily misdiagnosed, making timely and effective screening critical.

By stimulating the adrenal cortex to secrete cortisol and measuring serum cortisol levels at various time points, the product allows rapid assessment of adrenocortical reserve function and is currently the most common and convenient method for clinical screening of adrenocortical insufficiency. Its core principle is as follows: under normal conditions, injection of tetracosactide activates the adrenal cortex and markedly increases cortisol secretion; in cases of adrenocortical insufficiency, cortisol secretion fails to rise effectively, allowing preliminary disease screening.

Dynamic assessment of adrenal function is an important approach that builds upon adrenocortical insufficiency screening to further define adrenocortical reserve capacity, severity of functional impairment, and etiology (distinguishing primary, secondary, and tertiary adrenocortical insufficiency). Compared with simple screening, dynamic assessment emphasizes dynamic changes in hormone levels, allowing more precise reflection of adrenocortical status and providing detailed evidence for clinical treatment planning and disease monitoring.

As the core stimulating agent, tetracosactide injection enables dynamic monitoring of adrenal function through combinations of varying dosages, administration routes, and sampling time points, mainly including short‑term and long‑term dynamic assessments for different clinical scenarios.

Short‑term dynamic assessment is mainly used to evaluate the immediate responsiveness of the adrenal cortex and determine the severity of functional impairment. The procedure is refined from basic screening: in addition to baseline and 30‑minute post‑injection cortisol measurements, cortisol is also tested at 60 and 90 minutes to observe dynamic trends.

Normally, cortisol peaks at 30 minutes and remains elevated at 60 and 90 minutes. Mild impairment may show delayed peaking (at 60 minutes) with reduced but still suprathreshold levels. Severe impairment results in persistently subthreshold peaks with no meaningful increase. Such dynamic monitoring effectively differentiates mild, moderate, and severe adrenocortical insufficiency and guides treatment dosage adjustment.

Long‑term dynamic assessment is used for etiological differentiation and disease monitoring, especially for secondary and tertiary adrenocortical insufficiency. The common method is the long‑acting tetracosactide (Synacthen Depot) stimulation test: 1 mg of long‑acting tetracosactide is administered intramuscularly, and serum cortisol is measured at baseline, 0.5, 1, 2, 3, 4, and 5 hours post‑injection for continuous 5‑hour monitoring. In primary adrenocortical insufficiency, intrinsic adrenal damage prevents meaningful cortisol elevation even under prolonged stimulation. In secondary insufficiency (due to insufficient ACTH secretion from pituitary dysfunction), the adrenal cortex is intact, and cortisol gradually rises with a potentially delayed but ultimately normal peak. In tertiary insufficiency (due to insufficient CRH secretion from hypothalamic dysfunction), cortisol rises more slowly with a lower peak, requiring correlation with ACTH levels for further differentiation.