Generic Name

Hydrocortisone

Mechanism

• Receptor binding: Activates the cytosolic glucocorticoid receptor (GR) at the 11β‑hydroxyl group.
• Nuclear translocation: GR‑hydrocortisone complex migrates into the nucleus, binds glucocorticoid response elements (GREs).
• Gene regulation
• Trans‑activation of anti‑inflammatory genes (e.g., lipocortin‑1 → inhibition of phospholipase A₂).
• Trans‑repression of pro‑inflammatory mediators (cytokines, chemokines, COX‑2, iNOS, adhesion molecules).
• Vascular effects: Induces selective vasoconstriction, reducing dermal edema.

Pharmacokinetics

• Absorption: Highly lipophilic; dermal penetration varies with formulation (ointment > cream > gel).
• Systemic exposure: Low (<5 % of applied dose), but can increase with occlusion, large surface area, damaged skin.
• Metabolism: First‑pass hydroxylation to inactive metabolites (hydrocortisone‑prednisone, mitotane).
• Half‑life: Intracellular GR‑complex ~12 h; systemic drug half‑life ∼7 h.
• Excretion: Renal elimination of metabolites (~90 %).

Indications

• Dermatitis: Contact, atopic, seborrheic, irritant.
• Seborrheic dermatitis (non‑ocular).
• Psoriasis (minor lesions).
• Eczema (– mild‑to‑moderate).
• Dermatologic pruritus.
• Allergic reactions (localized e.g., urticaria).
• Pre‑operative skin prep (short‑term).

Contraindications

• Absolute contraindications
• Known hypersensitivity to hydrocortisone or any steroid excipient.
• Untreated infections of the skin (e.g., impetigo, candidiasis).
• Ocular use in active uveitis or uncontrolled glaucoma.
• Relative warnings
• Systemic corticosteroid requirement or prolonged high‑dose therapy (>2 weeks).
• Pregnancy & lactation: category C/C2 – use only if benefit outweighs risk.
• Adjunctive therapy with immunosuppressants (risk of systemic absorption).

Dosing

• Formulations: 0.5 % (cream/ointment), 1 % (cream/ointment).
• Application
• Wash, dry skin → apply thin film to affected area.
• Frequency: 2–3× daily (unless higher potency or special instructions).
• Duration: Shortest effective period (≤ 7–10 days for most indications).
• Special considerations
• Avoid burning, blistering sites.
• Use non‑preserved formulations for mucosal surfaces.
• Occlusion: Use only in short bursts (≤ 48 h) to avoid systemic absorption.

Adverse Effects

• Local (common)
• Skin atrophy, striae, telangiectasia, hypopigmentation.
• Contact dermatitis to excipients.
• Burning or stinging at application.
• Systemic (rare)
• Cushingoid changes with extensive use.
• HPA axis suppression (especially in infants or high‑dose regimens).
• Hypoglycaemia (in diabetic patients).

Monitoring

• Clinical: Assess lesion improvement; document any signs of skin atrophy.
• Systemic: For infants or long‑term use—measure serum cortisol, blood pressure, fasting glucose.
• Adjunctive: Ophthalmology referral if used on eyelids or for ocular indications.

Clinical Pearls

• Use the lowest effective concentration; 0.5 % cream is often adequate for most eczema flares.
• Apply on the “look‑of‑skin” zone (rather than onto the surface film) to maximize penetration.
• Choose non‑preserved ointments for acne or sensitive areas—preservatives can trigger contact dermatitis.
• Short‑term occlusion (2 h) can boost potency but keep cumulative exposure < 14 days to prevent systemic side‑effects.
• In infants (< 6 months) limit area to < 5 % of body surface area per dose.
• Before eye use ensure all ocular surface disease is controlled; high‑potency steroids (e.g., flavonolone) are preferred for active inflammation.
• Patch test when a patient reports prior steroid reaction; hydrocortisone‐0.1 % can be used for screening.
• Store position: Keep at room temperature and away from heat or direct sunlight to prevent degradation.

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• *This drug card provides quick, evidence‑based reference for clinicians and students: *Hydrocortisone Topical* – low‑potency, first‑line anti‑inflammatory steroid.