Eczema (Atopic Dermatitis): Clinical Review for Health Professionals

Introduction

Eczema, commonly referred to as atopic dermatitis (AD) when of atopic origin, is a chronic inflammatory skin disease characterized by relapsing pruritic lesions. It affects up to 20% of children and 3% of adults worldwide, imposing significant burden on quality of life, sleep, and psychosocial health. Eczema results from a complex interplay of genetic predisposition, impaired skin barrier function, immune dysregulation, and environmental triggers.

Epidemiology and Risk Factors

• Prevalence: AD typically arises in early childhood; 60% of cases present within the first year of life and 90% by age five. Adult-onset cases account for a growing subset.
• Genetic Factors: Mutations in the filaggrin gene (FLG) compromise barrier function. Family history of atopy (asthma, allergic rhinitis, eczema) increases risk.
• Environmental Triggers: Temperature and humidity extremes, irritants (soap, detergents), allergens (dust mites, pollens, foods), microbial exposure (Staphylococcus aureus colonization), and psychosocial stress exacerbate disease.

Pathophysiology

1. Skin Barrier Dysfunction: Filaggrin deficiency and lipid abnormalities increase transepidermal water loss, facilitating allergen and microbial penetration.
2. Immune Dysregulation: Acute lesions are driven by Th2-biased cytokines (IL-4, IL-13, IL-31) promoting IgE production and pruritus. Chronic disease shows a mixed Th1/Th17 profile with skin remodeling and lichenification.
3. Microbial Factors: High levels of S. aureus colonize lesional and nonlesional skin, releasing superantigens that amplify inflammation.

Clinical Features

Acute Phase

• Morphology: Erythematous, edematous papules and vesicles; weeping and crusting common.
• Distribution: In infants—cheeks, scalp, extensor surfaces; in older children/adults—flexural areas (antecubital and popliteal fossae), neck, wrists, ankles.
• Symptoms: Intense pruritus leading to excoriation and secondary infection.

Chronic Phase

• Morphology: Lichenified plaques with accentuated skin markings, hyperpigmentation in darker skin types.
• Distribution: Flexural predominance continues; hand eczema may be severe in manual workers.
• Symptoms: Persistent itch-scratch cycle, xerosis, and potential fissuring.

Diagnosis and Severity Assessment

• Diagnosis: Clinical—based on pruritus, characteristic morphology and distribution, chronic relapsing course, and personal/family history of atopy.
• Severity Scoring: Use validated tools such as SCORAD (SCORing Atopic Dermatitis), EASI (Eczema Area and Severity Index), or POEM (Patient-Oriented Eczema Measure) to guide treatment decisions and monitor response.

Differential Diagnosis

• Contact dermatitis (allergic or irritant)
• Psoriasis (inverse or guttate morphology)
• Seborrheic dermatitis
• Scabies and other pruritic infestations
• Ichthyosis, cutaneous T-cell lymphoma (erythroderma in adults)

Management

Basic Measures

• Skin Care: Regular use of emollients (ointments, creams) to restore barrier function—apply liberally (30–50 g/week for adults).
• Bathing Practices: Short (5–10 minutes) lukewarm baths with gentle, fragrance-free cleansers; pat dry and apply emollient within 3 minutes.

Topical Therapies

• Topical Corticosteroids (TCs): First-line anti-inflammatory agents. Use low- to mid-potency TCs for face and flexural areas; higher potency for lichenified plaques. Apply once or twice daily, tapered based on response.
• Topical Calcineurin Inhibitors (TCIs): Tacrolimus and pimecrolimus for sensitive areas (face, intertriginous) or steroid-sparing in long-term management.
• Topical Crisaborole: A phosphodiesterase-4 inhibitor indicated for mild-to-moderate AD in patients ≥2 years old.

Systemic Therapies

• Antihistamines: Sedating antihistamines (e.g., hydroxyzine) may aid sleep by reducing nocturnal itch, though they do not modify disease.
• Systemic Corticosteroids: Reserved for severe, flaring disease; short courses (<2 weeks) due to adverse effects.
• Immunosuppressants: Cyclosporine, methotrexate, azathioprine, or mycophenolate mofetil for moderate-to-severe refractory AD—monitor labs and organ function regularly.
• Biologics: Dupilumab (IL-4Rα antagonist) is approved for moderate-to-severe AD in adults and adolescents, showing significant improvement in EASI and quality of life scores. Emerging agents targeting IL-13, IL-31, and JAK pathways are under investigation.

Phototherapy

• Narrow-band UVB (NB-UVB): Effective for widespread disease; monitor for skin aging and carcinogenesis with long-term use.
• Excimer Laser (308 nm): Targeted therapy for recalcitrant plaques.

Infection Management

• Topical Antimicrobials: Mupirocin for localized S. aureus infections.
• Systemic Antibiotics: For overt bacterial superinfection—culture-guided therapy, typically antistaphylococcal agents.

Patient Education and Adherence

• Demonstrate proper application techniques for emollients and topical medications.
• Set realistic expectations: AD is chronic and requires long-term maintenance.
• Encourage regular follow-up and use of severity scores to track progress.
• Address psychosocial impact: Provide support for sleep disturbances, school/work accommodations, and referral to counseling when needed.

Monitoring and Follow-Up

• Short-term: Reassess 2–4 weeks after treatment initiation to adjust regimen.
• Long-term: Periodic evaluation every 3–6 months in stable patients; more frequent reviews for those on systemic agents or biologics.
• Safety Monitoring: Regular lab tests (CBC, liver/renal function) for patients on systemic immunosuppressants or biologics.

Conclusion

Eczema (atopic dermatitis) is a multifaceted disease requiring a comprehensive, individualized approach. Emphasis on barrier repair, tailored anti-inflammatory therapy, patient education, and psychosocial support optimizes disease control and quality of life for affected individuals.