• Systemic Glucocorticoid
• Synthetic corticosteroid

Parent class:

• Corticosteroids

Prednisone is converted in the liver to its active form, prednisolone.

It:

• Binds intracellular glucocorticoid receptors
• Alters gene transcription
• ↓ Pro-inflammatory cytokines (IL-1, IL-2, IL-4, IL-5, IL-6, TNF-α)
• ↓ Eosinophils
• ↓ T-cell activation
• ↓ Prostaglandins and leukotrienes (via phospholipase A2 suppression)

Full signaling pathway:

• Glucocorticoid Signaling

Net effect:

Broad anti-inflammatory and immunosuppressive activity.

• Oral administration
• Prodrug (converted to prednisolone in liver)
• Hepatic metabolism
• Renal excretion of metabolites
• Duration: intermediate acting

Caution in severe hepatic impairment (may require prednisolone instead).

Used across many inflammatory conditions:

• Asthma (exacerbations)
• Urticaria
• Anaphylaxis (adjunct)
• Rheumatoid Arthritis
• Inflammatory Bowel Disease
• Autoimmune diseases
• Transplant rejection

Not first-line for acute bronchospasm (no immediate bronchodilation).

Highly condition-specific.

Examples:

• Asthma exacerbation: 40–60 mg daily (short course)
• Autoimmune disease: variable dosing
• Physiologic replacement: lower dosing

Morning dosing preferred to mimic natural cortisol rhythm.

• Hyperglycemia
• Mood changes
• Insomnia
• Fluid retention
• Increased appetite

• HPA axis suppression
• Osteoporosis
• Cushingoid appearance
• Muscle wasting
• Increased infection risk
• Hypertension
• Peptic ulcer disease
• Cataracts

Mechanism:

Systemic glucocorticoid effects on metabolism and immune function.

Chronic prednisone suppresses ACTH production.

Abrupt discontinuation may cause:

• Adrenal insufficiency
• Hypotension
• Fatigue
• Adrenal crisis (severe cases)

Taper required if:

• Used >2–3 weeks
• Moderate/high doses
• Cushingoid features present

See:

• HPA Axis Physiology

• NSAIDs → ↑ GI bleeding risk
• CYP3A4 inducers ↓ steroid levels
• CYP3A4 inhibitors ↑ steroid levels
• Live vaccines contraindicated in high-dose therapy

• Prednisone is a prodrug; prednisolone is active form.
• Morning dosing reduces adrenal suppression.
• Short “burst” courses typically do not require taper.
• Long-term therapy requires bone protection.
• Treat inflammation — not immediate bronchospasm.

Prednisone has:

• Moderate glucocorticoid potency
• Low mineralocorticoid activity

Compare:

• Dexamethasone (higher potency, no mineralocorticoid effect)
• Hydrocortisone (lower potency, more mineralocorticoid effect)

• Corticosteroids
• Glucocorticoid Signaling
• Asthma