The Online Encyclopedia and Dictionary







Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger similar effects. Glucocorticoids are distinguished from mineralocorticoids and Censored pages by the specific receptors, target cells, and effects. Technically, corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid.

Cortisol (or hydrocortisone) is the most important human glucocorticoid. It is essential for life and regulates or supports a variety of important cardiovascular, metabolic, immunologic, and homeostatic functions. Glucocorticoid receptor s are found in the cells of almost all vertebrate tissues.


Strength of glucocorticoids

A variety of synthetic glucocorticoids, some far more potent than cortisol, have been created for therapeutic use. Glucocorticoid potency, duration of effect, and overlapping mineralocorticoid potency varies (Table).


Name Glucocorticoid potency Mineralocorticoid potency Duration of action (t1/2 in hours)
Hydrocortisone 1 1 8
Cortisone acetate 0.8 0.8 oral 8, intramuscular 18+
Prednisone 3.5-5 0.8 16-36
Prednisolone 4 0.8 16-36
Methylprednisolone 5-7.5 0.5 18-40
Dexamethasone 25-80 0 36-54
Betamethasone 25-30 0 36-54
Triamcinolone 5 0 12-36
Beclomethasone 8 puffs 4 times a day
equals 14 mg oral
prednisone once a day
- -
Fludrocortisone acetate 15 200 -
Deoxycorticosterone acetate (DOCA) 0 20 -
Aldosterone 0.3 200-1000 -

Cortisol (hydrocortisone) is the standard of comparison for glucocorticoid potency. Hydrocortisone is the name used for pharmaceutical preparations of cortisol. Data refer to oral dosing, except when mentioned. Note that oral potency may be less than parenteral potency because significant amounts (up to 50% in some cases) may not be absorbed from the intestine. Note that fludrocortisone, DOCA, and aldosterone are not considered glucocorticoids and are included in this table to provide perspective on mineralocorticoid potency.

Physiologic replacement of glucocorticoid

Any glucocorticoid can be given in a dose that provides approximately the same glucocorticoid effects as normal cortisol production; this is referred to as physiologic, replacement, or maintenance dosing. This is approximately 6-12 mg/m2/day (m2 refers to body surface area (BSA) and is a measure of body size; an average man is 1.7 m2).

Medical uses and effects of high dose glucocorticoids

In much higher doses (termed pharmacologic doses}, glucocorticoids can suppress many inflammatory and immune processes. They are widely used medically for this purpose, especially for suppression of allergic, inflammatory, and autoimmune diseases. They are also given to suppress rejection of transplanted organs.

At these doses, however, many healthy anabolic processes may be impaired. When high dose glucocorticoids are used for too long, they can produce a variety of unwanted side effects.

In high doses, hydrocortisone (cortisol) and those glucocorticoids with appreciable mineralocorticoid potency can exert a mineralocorticoid effect as well, although in physiologic doses this is prevented by rapid degradation of cortisol by 11β-hydroxysteroid dehydrogenase isoenzyme 2 (11β-HSD2) in mineralocorticoid target tissues. Mineralocorticoid effects can include salt and water retention, extracellular fluid volume expansion, hypertension, potassium depletion, and metabolic alkalosis .

The combination of clinical problems produced by prolonged, excess glucocorticoids, whether synthetic or endogenous, is termed Cushing's syndrome.

Adrenal suppression and withdrawal

In addition to the effects listed above, use of high dose steroids for more than a week begins to produce suppression of the patient's adrenal glands because the exogenous glucocorticoids suppress hypothalamic corticotropin releasing hormone (CRH) and pituitary adrenocorticotropic hormone (ACTH). With prolonged suppression the adrenal glands atrophy (physically shrink) and can take months to recover full function after discontinuation of the exogenous glucocorticoid.

During this recovery time, the patient is vulnerable to adrenal insufficiency during times of stress, such as illness. While there is wide individual variation in suppressive dose and time for adrenal recovery, clinical guidelines have been devised to estimate potential adrenal suppression and recovery, to reduce risk to the patient. The following is one example, but many variations exist or may be appropriate in individual circumstances.

  • If a patient has been receiving daily high doses for 5 days or less, they can be abruptly stopped (or reduced to physiologic replacement if patient is adrenal deficient). Full adrenal recovery can be assumed to occur by a week afterward.
  • If high doses were used for 6-10 days, reduce to replacement dose immediately and taper over 4 more days. Adrenal recovery can be assumed to occur within 2-4 weeks of completion of steroids.
  • If high doses were used for 11-30 days, cut immediately to twice replacement, and then by 25% every 4 days. Stop entirely when dose is less than half of replacement. Full adrenal recovery should occur within 1-3 months of completion of withdrawal.
  • If high doses were used more than 30 days, cut dose immediately to twice replacement, and reduce by 25% each week until replacement is reached.
  • Then change to oral hydrocortisone or cortisone as a single morning dose, and gradually decrease by 2.5 mg each week. When a.m. dose is less than replacement, the return of normal basal adrenal function may be documented by checking 0800 cortisol levels prior to the morning dose; stop drugs when 0800 cortisol is 10 μg/dl. It is difficult to predict the time to full adrenal recovery after prolonged suppressive exogenous steroids; some people may take nearly a year.
  • Flare-up of the underlying condition for which steroids are given may require a more gradual taper than outlined above.

Last updated: 02-07-2005 16:43:10
Last updated: 05-03-2005 17:50:55