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Wednesday, August 13, 2025

Eczema (atopic)


Introduction

Atopic dermatitis (AD), commonly referred to as atopic eczema, is a chronic, relapsing, inflammatory skin disorder characterized by pruritus, eczematous lesions, xerosis, and a defective skin barrier. It is a central component of the “atopic triad,” along with allergic rhinitis and asthma, and is strongly associated with immune dysregulation.

The condition affects both children and adults, with the majority of cases presenting in early childhood. AD significantly impacts quality of life due to chronic itch, sleep disturbance, cosmetic concerns, and the psychosocial burden it imposes.

Epidemiology

  • Prevalence: ~15–20% in children; 2–10% in adults worldwide.

  • Onset: 60% of cases present before age 1, 90% before age 5.

  • Gender: Slight female predominance in childhood.

  • Geography: More common in urban and developed countries.

Etiology and Pathophysiology

1. Skin Barrier Dysfunction

  • Mutations in the filaggrin gene (FLG) and other epidermal structural proteins reduce the integrity of the skin barrier.

  • Leads to increased transepidermal water loss (TEWL) and greater penetration of allergens, irritants, and microbes.

2. Immune Dysregulation

  • Skewing toward Th2 immune response in acute phases (↑ IL-4, IL-5, IL-13) and Th1/Th22/Th17 activation in chronic phases.

  • Overproduction of IgE and eosinophilia in many patients.

3. Environmental Triggers

  • Allergens (dust mites, pollen, animal dander)

  • Irritants (soaps, detergents, synthetic fabrics)

  • Microbial factors (Staphylococcus aureus colonization)

  • Climate (low humidity, cold weather)

  • Stress

4. Genetic and Familial Factors

  • Family history of atopy increases risk.

  • FLG mutations strongly associated with early-onset and severe AD.

Clinical Features

Core Features

  • Pruritus: Hallmark symptom; often worse at night.

  • Eczematous Lesions:

    • Acute: Erythematous, edematous papules/plaques, oozing, crusting.

    • Subacute/Chronic: Lichenification, excoriation, hyperpigmentation, fissures.

  • Xerosis: Dry, scaly skin even in unaffected areas.

Age-related Distribution

  • Infants: Cheeks, scalp, extensor limbs, trunk.

  • Children: Flexural surfaces (antecubital, popliteal fossae), neck, wrists, ankles.

  • Adults: Hands, eyelids, neck, flexures; diffuse xerosis.

Complications

  • Secondary bacterial infection: Impetiginization, cellulitis (commonly S. aureus).

  • Viral infections: Eczema herpeticum (HSV), molluscum contagiosum.

  • Fungal infections: Dermatophytes, Malassezia.

  • Sleep disturbance, growth impairment (in severe pediatric cases).

Diagnosis

AD is diagnosed clinically; no specific lab test confirms it.

Diagnostic Criteria (Hanifin and Rajka)

  • Major features (≥3 required):

    • Pruritus

    • Typical morphology and distribution

    • Chronic or relapsing course

    • Personal or family history of atopy

  • Minor features: Xerosis, ichthyosis, keratosis pilaris, hand/foot dermatitis, nipple eczema, elevated serum IgE, early onset, recurrent conjunctivitis, Dennie–Morgan folds.

Management

Treatment goals: reduce symptoms, prevent flares, repair skin barrier, control inflammation, and minimize complications.

1. Education and Lifestyle

  • Avoid known triggers (fragrances, harsh soaps, wool clothing).

  • Keep nails short to reduce excoriation damage.

  • Maintain indoor humidity if possible.

2. Skin Barrier Repair

  • Regular emollient use: Apply liberally at least twice daily, ideally immediately after bathing (“soak and seal” method).

    • Examples: Petrolatum, ceramide-based creams, mineral oil.

  • Bathing practices:

    • Short lukewarm baths/showers (5–10 min).

    • Use non-soap cleansers or mild syndet bars.

3. Topical Anti-inflammatory Therapy

Topical Corticosteroids (TCS)

  • First-line for flares.

  • Potency based on site and severity:

    • Mild: Hydrocortisone 1% cream.

    • Moderate: Betamethasone valerate 0.05–0.1%, triamcinolone acetonide 0.1%.

    • Potent/very potent for resistant areas (short-term): Clobetasol propionate 0.05%.

  • Apply once or twice daily for 1–2 weeks, then taper.

Topical Calcineurin Inhibitors (TCIs)

  • Tacrolimus 0.03% (children ≥2 yrs), 0.1% (adults).

  • Pimecrolimus 1% cream.

  • Useful for sensitive sites (face, eyelids, genitalia) and long-term maintenance.

4. Anti-pruritic Measures

  • Oral antihistamines (cetirizine, loratadine) mainly for sleep disturbance due to itch.

  • Wet wrap therapy for severe flares.

5. Infection Control

  • Topical or systemic antibiotics if secondary infection present (e.g., flucloxacillin, cephalexin).

  • Antiviral therapy (acyclovir) for eczema herpeticum.

6. Systemic and Advanced Therapies

  • Phototherapy (narrowband UVB) for widespread disease unresponsive to topicals.

  • Systemic immunosuppressants for severe, refractory cases:

    • Cyclosporine: 3–5 mg/kg/day (short-term).

    • Methotrexate: 10–25 mg weekly.

    • Azathioprine: 1–3 mg/kg/day.

    • Mycophenolate mofetil: 1–3 g/day.

  • Biologics:

    • Dupilumab: IL-4 receptor alpha antagonist; 600 mg SC loading, then 300 mg every 2 weeks.

7. Maintenance Therapy

  • Proactive intermittent use of low-potency TCS or TCIs on previously affected areas.

  • Continued daily emollient use.

Prognosis

  • Many children outgrow or experience reduced severity with age.

  • Adult-onset cases may be more persistent.

  • With appropriate treatment, most achieve good disease control.



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