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Glucocorticoids

Last updated: June 3, 2021

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Synthetic glucocorticoids are a group of drugs with antiinflammatory, immunosuppressant, metabolic, and endocrine effects. These drugs are structurally and functionally similar to the endogenous glucocorticoid hormone cortisol. Glucocorticoids have immediate effects (e.g., vasoconstriction) 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. Adverse effects include metabolic and endocrine disturbances, weight gain, skin reactions, hypertension, and psychiatric disorders; using the lowest dose possible for the shortest period of time, patient education, and regular screening can help lower the incidence of adverse effects and ensure early detection if they do occur. 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.

This article describes the pharmacology of synthetic glucocorticoids in detail; accordingly, glucocorticoids refer here to the drug class rather than the endogenous hormone.

Relative potency of systemic corticosteroids [1][3]
Duration of action

Drug

Common routes
of administration
Equivalent
doses
Relative
glucocorticoid
potency
Relative
mineralocorticoid
potency
Systemic glucocorticoids
Short-acting
(8–12 hours)
Hydrocortisone
  • Oral
  • Injectable
  • Topical
  • 20 mg
  • 1
  • 1
Cortisone
  • Oral
  • Injectable
  • 25 mg
  • 0.8
  • 0.8
Intermediate-acting
(12–36 hours)

Prednisolone

  • 5 mg
  • 4
  • 0.8
Prednisone
Methylprednisolone
  • Oral
  • Injectable
  • 4 mg
  • 5
  • 0.5
Triamcinolone
  • Injectable [5][6][7]
  • Topical
  • 4 mg
  • 5
  • 0
Long-acting
36–72 hours

Dexamethasone

  • Oral
  • Injectable
  • Topical
  • 0.75 mg
  • 30
  • 0
Betamethasone
  • Oral
  • Injectable
  • Topical
  • 0.6 mg
  • 30
  • 0
Systemic mineralocorticoid

Intermediate-acting
12–36 hours

Fludrocortisone
  • Oral
  • 0.1 mg
  • 10–15
  • 125–150

Fludrocortisone is not used for glucocorticoid activity but as a mineralocorticoid substitute in the management of adrenal insufficiency. [3][8]

  1. Anti-inflammatory and immunosuppressive
  2. Mineralocorticoid properties
    • Cortisol can bind to mineralocorticoid receptors at high concentrations [9]
    • Effects include, e.g., reduced sodium excretion, increased potassium excretion
  3. Antiproliferative: triggers cell apoptosis, and inhibits fibroblast proliferation [10]
  4. Anabolic-androgenic effects with steroid abuse: : increase in muscle mass and strength

Both acute and long-term effects of glucocorticoids lead to inhibition of inflammatory processes and to immunosuppression.

References:[11][12][13][14][15]

Systemic glucocorticoids

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 adverse effects even at high doses.

Organ/System of organs Effects
Skin
Cardiovascular system
Metabolism, electrolytes and endocrine system
GI system
CNS and psyche
Eyes
Other

Many of the adverse effects listed above are also features of iatrogenic Cushing syndrome.

The tibia is BIGgA than the FIBula: cortisol increases Blood pressure, Insulin resistance, Gluconeogenesis, and Appetite; and decreases Fibroblast activity, Immune response, and Bone formation.

Local glucocorticoids [20]

Topical glucocorticoids Inhaled glucocorticoids
Local effects
Eyes
  • Ocular reactions
Other

-

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.

References:[22]

We list the most important contraindications. The selection is not exhaustive.

  • Systemic administration
    • Tapering to avoid toxicity
      • Short-term administration (≤ 3 weeks): usually 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

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.

An intratendinous injection carries the risk of bacterial spread and iatrogenic bacterial arthritis.

References:[2][23]

Complications are most common with long-term systemic treatment but can also occur with higher-dose topical and inhaled steroids. The risk of complications can be reduced by keeping treatment durations short or doses low. [24]

Approach [25]

Risk assessment

Risk factors for complications of glucocorticoid therapy
Adrenal suppression and adrenal insufficiency [28][29][30]
Osteoporosis [24]
  • Systemic therapy at any dose ≥ 3 months
Peptic ulcer disease [31]
  • Systemic therapy for at least 7–28 days increases the risk of bleeding.
Diabetes and hyperglycemia [32][33][34]
  • Increased risk of hyperglycemia within 24–48 hours of starting systemic treatment
Infections [35]
  • Systemic therapy for at least 2–4 weeks at doses > 20 mg/day
Cardiovascular disease [36][37][38][39][40]
  • Hypertension can result from any medium- to high-dose systemic steroid regimen.
  • Alterations to lipid levels usually require at least 2 weeks of systemic therapy.
Ocular disease [41][42]
  • Glaucoma can result from several weeks of any form of steroid administration.
  • The risk of cataracts increases after > 1 year of high-dose systemic therapy.
Psychiatric complications [43][44]
  • Typically within 2 weeks of starting systemic therapy, particularly with very high-dose therapy

Measures to prevent complications

Measures to prevent complications of glucocorticoid therapy
Complication to prevent Before therapy During therapy
Adrenal suppression and adrenal insufficiency [3][45]
Osteoporosis [26]
  • For all patients taking ≥ 2.5 mg/day prednisone (or equivalent) for ≥ 3 months
Peptic ulcer disease [47]
Diabetes and hyperglycemia [24]
  • Obtain baseline HbA1c. [24]
  • Consider home glucometer for patients on long-term moderate- and high-dose steroids.
Infections
Cardiovascular disease [24]
Ocular disease [24][41][55]
  • Regular eye examinations [42]
  • Educate patients on the symptoms of glaucoma.
Psychiatric disease [3][24]
  • Screen patients for psychiatric comorbidities, e.g., depression. [24]
  • Review within a week of initiating steroid therapy for mood changes. [43]
  • Avoid split-dose regimens to prevent sleep disruption.

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