Synthetic glucocorticoids are a group of drugs with anti-inflammatory, immunosuppressant, metabolic, and endocrine effects. These drugs are structurally and functionally similar to the endogenous glucocorticoid hormone cortisol. Glucocorticoids have immediate effects (e.g., vasodilation) that do not depend on DNA interaction. However, they exert their main antiinflammatory and immunosuppressive actions by binding to glucocorticoid receptors, which causes complex changes in gene transcription. These genomic effects only begin to manifest after several hours. Similarly, glucocorticoids bind to mineralocorticoid receptors, but, for most glucocorticoid drugs, high doses are required for a significant mineralocorticoid effect. Systemic glucocorticoids are used for hormone replacement therapy (e.g., in Addison disease), for acute or chronic inflammatory diseases (e.g., rheumatoid arthritis), and for immunosuppression (e.g., after organ transplants). Local glucocorticoids are used to treat conditions like dermatoses, asthma, and anterior uveitis. Side effects include metabolic and endocrine disturbances, weight gain, skin reactions, hypertension, and psychiatric disorders. Contraindications for systemic glucocorticoids include systemic fungal infections and, in the case of dexamethasone, cerebral malaria. Status asthmaticus is a contraindication for inhaled glucocorticoids. Topical and ophthalmic glucocorticoids are usually contraindicated if there are preexisting local infections.
- Corticosteroids: a class of steroid hormones that includes glucocorticoids and mineralocorticoids 
Endogenous corticosteroids: hormones synthesized from cholesterol in the adrenal cortex 
- Endogenous glucocorticoids (e.g., cortisol): synthesized in the zona fasciculata with antiinflammatory, immunosuppressant, metabolic, and endocrine effects
- Endogenous (i.e., aldosterone): synthesized in the zona glomerulosa and primarily functions to regulate the renin-angiotensin system and maintain electrolyte and water balance
- Synthetic corticosteroids: structural and functional analogs of endogenous corticosteroids that are used in the treatment of a variety of conditions 
- Corticosteroids that are administered orally, intravenously, or intramuscularly
- Act systemically as they are distributed throughout the body
- Examples: See table below.
- Local corticosteroids (local glucocorticoids)
systemic corticosteroids  of
- Hydrocortisone is the synthetic equivalent of endogenous cortisol and its glucocorticoid and mineralocorticoid potency is considered to be “1” (see table below).
- Relative to hydrocortisone, systemic corticosteroids differ in potency of their glucocorticoid effects (relative glucocorticoid potency) and mineralocorticoid effects (relative mineralocorticoid potency) for a given dose.
|Relative potency of systemic corticosteroids |
|Duration of action|| |
| Common routes |
| Short-acting |
|Hydrocortisone|| || || || |
|Cortisone|| || || || |
| Intermediate-acting |
| || || |
|Methylprednisolone|| || || || |
|Triamcinolone|| || || || |
| Long-acting |
| || || || |
|Betamethasone|| || || || |
|Fludrocortisone|| || || || |
- Summary of effects of systemic corticosteroids
Anti-inflammatory and immunosuppressive
- Acute effects (within minutes)
Long-term effects (within hours) : Glucocorticoids bind to cytoplasmic glucocorticoid receptors (GRs)
- → inhibition of neutrophil apoptosis; and demargination; (loss of neutrophil binding to adhesive endothelial integrin molecules)→ neutrophilic leukocytosis
- → Promotion of apoptosis in eosinophils, monocytes, and lymphocytes
- → ↑ Inhibition of phospholipase A2,; which decreases the production of arachidonic acid derivatives.
- → ↑ Inhibition of transcription factors (e.g., NF-κB) → ↓ expression of pro-inflammatory genes
- → Translocation to the cell nucleus and binding to glucocorticoid responsive elements (GREs) within the promoters of anti-inflammatory genes (e.g., interleukin-10) → ↑ expression of anti-inflammatory genes
- Mineralocorticoid properties: e.g., reduced sodium excretion, increased potassium excretion
- Antiproliferative: triggers cell apoptosis; , and inhibits fibroblast proliferation
- Anabolic-androgenic effects with steroid abuse : increase in muscle mass and strength
Both acute and long-term effects lead to inhibition of inflammatory processes and to immunosuppression!
Glucocorticoid toxicity depends on the dose that is administered over a certain period of time. Therefore even low doses can have toxic effects if administered long-term. If glucocorticoids are administered once or only briefly (e.g., for treatment of anaphylactic shock), there are usually no significant side effects even in high doses.
|Metabolism, electrolytes and endocrine system|
|CNS and psyche|
Many of the side effects listed above are also features of iatrogenic !
|Topical glucocorticoids||Inhaled glucocorticoids|
|Eyes|| || |
Local side-effects of inhaled glucocorticoids can be avoided by reducing the dose to the lowest effective amount, rinsing with mouthwash after each puff, improving the inhalation technique and compliance, and keeping vaccinations up to date!
We list the most important adverse effects. The selection is not exhaustive.
- Adrenocortical insufficiency ()
- Systemic symptomatic treatment
- Local symptomatic treatment: anterior uveitis; , dermatoses, ; , and osteoarthritis or juvenile idiopathic arthritis
- Organ transplant
- Preterm delivery
- General: hypersensitivity
- Dermatological: bacterial, viral or fungal infection of the mouth or throat (triamcinolone)
- Inhalation: status asthmaticus or acute asthma; episode requiring intensive measures (beclomethasone, budesonide)
We list the most important contraindications. The selection is not exhaustive.
Tapering to avoid toxicity
- Short-term administration (≤ 3 weeks): no tapering necessary
- Long-term administration (> 3 weeks): tapering regimen based on patient age and condition and on duration/dose of prior glucocorticoid administration → e.g., tapering over 2 months
- Sudden discontinuation after chronic use should be avoided because of the risk of adrenal insufficiency (adrenal crisis) secondary to long-term hypothalamic-pituitary-adrenal axis suppression.
- IM application
- Tapering to avoid toxicity
If the Cushing threshold is exceeded over a longer period of treatment, the glucocorticoid dose should be gradually decreased to minimize the risk of adrenocortical insufficiency.
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