Adrenocortical suppression
Glucocorticoid therapy suppresses the release of adrenocorticotrophic hormone (ACTH) from the pituitary gland. This can cause gradual atrophy of ACTH–dependent tissue in the adrenal cortex, leading to adrenocortical suppression and subsequent dependence on exogenous glucocorticoid therapy. A patient who is dependent on exogenous glucocorticoid therapy is at risk of cortisol deficiency if the glucocorticoid is stopped or the dose is reduced quickly. They are also at risk of cortisol deficiency during periods of stress, such as surgery or illness, because the usual response of increased adrenal cortisol production does not occur.
A single morning cortisol concentration within the reference range does not exclude adrenocortical suppression. However, an ambulatory morning cortisol concentration above 400 nanomol/L makes clinically significant adrenocortical suppression unlikely, provided the patient is not taking a drug that can interfere with the test (eg estrogen therapy). The morning cortisol should be measured before 9am and at least 24 hours after the last dose of glucocorticoid. A normal response to short Synacthen test definitively excludes adrenocortical suppression.
To prevent glucocorticoid deficiency in a patient who has, or is at risk of, adrenocortical suppression:
- slowly taper the glucocorticoid dose if stopping treatment, allowing at least 1 week between each dose reduction
- increase the dose of glucocorticoid therapy during periods of stress (see Glucocorticoid replacement during intercurrent illness and surgery for recommended doses). If the patient’s regular dose is equal to or higher than the dose recommended for their illness or surgery, the dose does not need to be increased further.