Corticotropin stimulates the synthesis of corticosteroids (of which the most important is hydrocortisone) and to a lesser extent of androgens, by the cells of the adrenal cortex. It has only a minor (transient) effect on aldosterone production, which can proceed independently; in the absence of corticotropin the cells of the inner cortex atrophy.
The release of natural corticotropin by the pituitary gland is controlled by the hypothalamus via corticotropin releasing hormone (CRH or cortico-liberin), production of which is influenced by environmental stresses as well as by the level of circulating hydrocortisone. High plasma concentration of any steroid with glucocorticoid effect
• Cortisol and aldosterone produced in the adrenal cortex have a major role in physiology and pharmacology
• Physiological concentrations of Cortisol are essential for supporting the circulation and glucose production. Physiological concentrations of aldosterone are essential to prevent excessive sodium loss.
• for systemic pharmacological uses, prednisolone or other synthetic adrenocorticosteriods are used because they are more selective glucocorticoids, i.e. have loss sodium-retaining activity.
• For local administration (skin, lung), more potent, fluorinated steroids may be required.
• Glucocorticoids inhibit the transcriptional activation of many of the inflammatory cytokines, giving them a versatile role in the treatment of many types of inflammation.
• Fludrocortisone is a valuable treatment for man* sodium-loisirtgstates.and for most causes of autonomic neuropathy prevents release of corticotropin releasing hormone and so of corticotropin, lack of which in turn results in adrenocortical hypofunction. This is the reason why catastrophe may follow sudden withdrawal of steroid therapy in the chronically treated patient who has an atrophied cortex.
The effects of corticotropin are those of the steroids (hydrocortisone, androgens) liberated by its action on the adrenal cortex. Prolonged heavy dosage causes the clinical picture of Cushing's syndrome.
Uses. Corticotropin is used principally in diagnosis and rarely in treatment. It is inactive if taken orally and has to be injected like other peptide hormones.
Diagnostic use: as a test of the capacity of the adrenal cortex to produce Cortisol; with the short test, the plasma Cortisol (hydrocortisone) concentration is measured before and after an i.m. injection of tetracosactride (Synacthen); a normal response is a rise of more than 200 nanomol/1 in the plasma concentration of hydrocortisone. Longer variants of the test in cases of difficulty involve use of the depot (sustained-release) formulation i.m. For example, 1 mg of the depot is injected daily for 3 days at 9.00 am, with a short tetracosactride test performed on day 3.
Therapeutic use is seldom appropriate because the peptide hormone has to be injected; selective glucocorticoid action (without mineralocorticoid effect) cannot be obtained, and clinical results are irregular. Corticotropin can not be relied on to restore adrenal Cortisol output when a steroid is being withdrawn after prolonged therapy, as it does not restore function in the suppressed hypothalamic/pituitary part of the HPA axis.
Tetracosactride Injection is a powder dissolved in water immediately before injection i.v., i.m. or s.c.
Tetracosactride Zinc Injection (Synacthen Depot) in which the hormone is adsorbed on to zinc phosphate from which it is slowly released. This is the form used in the long tetracosactride test.
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