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Corticosteroids

Corticosteroids are synthetic analogs of adrenal cortex hormones used for potent anti-inflammatory and immunosuppressive effects.

They mimic:

Cortisol (glucocorticoid activity)
Aldosterone (mineralocorticoid activity — varies by agent)

This page focuses on pharmacology. For disease-specific management, see linked clinical pages below.

Classification

Systemic Glucocorticoids

Inhaled / Intranasal

Topical

Multiple potency classes (dermatologic use)

Mechanism of Action

Corticosteroids act via intracellular glucocorticoid receptors.

Stepwise:

1) Drug diffuses across cell membrane
2) Binds cytoplasmic glucocorticoid receptor
3) Complex translocates to nucleus
4) Alters gene transcription

Primary effects:

↓ IL-1, IL-2, IL-4, IL-5, IL-6, TNF-α
↓ Eosinophil survival
↓ T-cell activation
↓ Mast cell mediator release
↓ Phospholipase A2 → ↓ prostaglandins & leukotrienes

Result:

Broad suppression of inflammatory pathways.

Onset:

Hours to days (genomic effect)

Glucocorticoid vs Mineralocorticoid Activity

Drug	Glucocorticoid Potency	Mineralocorticoid Activity
Hydrocortisone	Low	Moderate
Prednisone	Moderate	Low
Methylprednisolone	Moderate	Minimal
Dexamethasone	High	None

Clinical implications:

Mineralocorticoid activity → fluid retention, edema, hypertension
Dexamethasone preferred when fluid retention undesirable

Pharmacologic Roles Across Systems

Corticosteroids are used in many disease states:

This reflects their broad anti-inflammatory and immunosuppressive activity.

Adverse Effects

Short-term:

Hyperglycemia
Mood changes
Fluid retention
Insomnia
Increased appetite

Long-term:

Adrenal suppression
Osteoporosis
Cushingoid features
Muscle wasting
Increased infection risk
Peptic ulcer disease
Skin thinning

Mechanism:

Systemic metabolic and immune suppression.

HPA Axis Suppression

Chronic systemic corticosteroid use suppresses endogenous cortisol production.

Abrupt discontinuation may cause:

Adrenal insufficiency
Hypotension
Fatigue
Adrenal crisis (severe cases)

Taper required when:

Therapy > 2–3 weeks
Moderate to high doses
Cushingoid features present

Clinical Pearls

Intranasal corticosteroids are first-line for nasal congestion in allergic rhinitis.
Inhaled corticosteroids are foundational in asthma management.
Steroids suppress late-phase allergic inflammation.
Epinephrine, not steroids, is first-line in anaphylaxis.
Always consider HPA suppression in prolonged systemic therapy.