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HealthConsider > Blog > Healthcare > Eczema (Atopic Dermatitis): Clinical Review for Health Professionals
Healthcare

Eczema (Atopic Dermatitis): Clinical Review for Health Professionals

Last updated: September 28, 2025 6:11 am
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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.

Contents
  • Introduction
  • Epidemiology and Risk Factors
  • Pathophysiology
  • Clinical Features
    • Acute Phase
    • Chronic Phase
  • Diagnosis and Severity Assessment
  • Differential Diagnosis
  • Management
    • Basic Measures
    • Topical Therapies
    • Systemic Therapies
    • Phototherapy
    • Infection Management
  • Patient Education and Adherence
  • Monitoring and Follow-Up
  • Conclusion

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.

The information provided on HealthConsider.com is for general informational and educational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Always seek the guidance of your physician or other qualified health provider with any questions you may have regarding a medical condition or treatment.

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