What is eczema (atopic dermatitis)?

Atopic Dermatitis (Eczema): Definition, Pathophysiology, and Management

Atopic dermatitis (eczema) is a chronic, relapsing inflammatory skin condition characterized by intense pruritus, eczematous lesions, and dry skin, affecting 10-20% of children and 2-3% of adults worldwide. 1

Definition and Epidemiology

• Atopic dermatitis (AD) is a chronic inflammatory skin disease that follows a relapsing course, occurring most frequently in children but also affecting adults 1
• Approximately 80% of patients develop symptoms within the first 5 years of life 2
• The prevalence has increased dramatically in recent decades, affecting 10-20% of children and 2-3% of adults globally 1
• AD accounts for 10-20% of all referrals to dermatologists and about 30% of dermatological consultations in general practice 2

Pathophysiology

• AD results from complex interactions between genetic factors, environmental exposures, skin barrier dysfunction, and immunological derangement 1
• The mechanisms involve both "outside-in" (skin barrier dysfunction) and "inside-out" (immunologic aberration triggering barrier disruption) pathways 2
• Cross-talk between skin barrier abnormalities and aberrant immune responses is evidenced by epidermal abnormalities enhancing the release of keratinocyte-derived thymic stromal lymphopoietin, which may enhance Th2 cell differentiation 2
• In acute lesions, Th2 cells produce IL-4, IL-13, and IL-31, which potentiate barrier dysfunction and contribute to pruritus, while in chronic lesions, Th1 cells predominate and secrete interferon gamma and IL-12 3
• Barrier dysfunction from filaggrin gene mutations predisposes patients to AD 3

Clinical Presentation

• The clinical manifestations of AD are variable and age-dependent 4:

  • Infants: Lesions primarily on cheeks, scalp, and extensor surfaces; diaper area is rarely affected 3
  • Young children: Involvement of extremities, cheeks, forehead, and neck 3
  • Older children and adults: Flexural areas (antecubital and popliteal fossae), head, and neck 3

• Key clinical features include:

  • Intense pruritus (itching) 2
  • Eczematous lesions that follow a symmetrical and age-specific distribution pattern 2
  • Dry skin (xerosis) 2
  • Chronic or relapsing disease course 2
  • Personal or family history of atopy (asthma, allergic rhinitis) 2

• Lesion progression 3:

  • Acute: Erythematous papules and serous exudates
  • Subacute: Erythematous scaling papules and plaques
  • Chronic: Lichenification (thickened skin with accentuated markings) and hyperpigmentation

Diagnosis

• AD is diagnosed clinically based on the patient's history, family history, and appearance of the eruption 2
• Diagnostic criteria include an itchy skin condition plus three or more of the following 2:
  • History of itchiness in skin creases (folds of elbows, neck) or cheeks in children under 4 years
  • History of asthma or hay fever (or atopic disease in first-degree relatives for children under 4)
  • General dry skin in the past year
  • Visible flexural eczema (or eczema on cheeks/forehead/outer limbs in children under 4)
  • Onset in the first two years of life (not always applicable in children under 4)
• A skin biopsy is generally not helpful for diagnosis 2

Comorbidities

• AD is associated with other atopic conditions 2:
  • Asthma: Adults with AD are 3 times more likely to have asthma compared to the general population 2
  • Food allergies: 11% of adults with AD have food allergies 2
• More severe AD appears to have a stronger association with asthma than mild or moderate AD 2

Management

Basic Care and Avoidance Strategies

• Emollients/moisturizers are essential for all patients with AD regardless of disease severity 1, 5
• Apply emollients immediately after a 10-15 minute lukewarm bath or shower for maximum benefit 5
• Avoid soaps and detergents as they remove natural lipids from the skin; use dispersible creams as soap substitutes 2
• Keep nails short and wear cotton clothing rather than irritating fabrics like wool to minimize damage from scratching 2, 5
• Avoid extremes of temperature 2

Topical Treatments

• Topical corticosteroids (TCS) are the first-line therapy for acute flares 1, 5:

  • Apply once or twice daily until significant improvement 2
  • Select potency based on patient age, body location, and disease severity 5
  • Use lower potency TCS on sensitive areas (face, neck, skin folds) 5
  • For children, use less potent TCS than those prescribed for adults 5

• Topical calcineurin inhibitors (TCIs) such as pimecrolimus 1% cream and tacrolimus ointment are steroid-sparing alternatives 5:

  • Approved for children aged 2 years and above 5, 6
  • Pimecrolimus (Elidel) is indicated for mild to moderate atopic dermatitis 6
  • Should be used for short periods, with breaks in between treatments 6
  • Not for continuous long-term use due to potential safety concerns 6

• Proactive therapy approach:

  • Twice-weekly application of low to medium potency TCS (e.g., fluticasone or mometasone) to previously affected skin areas for up to 16 weeks may help prevent relapses 2
  • TCIs can also be used proactively to maintain remission 1

Advanced Treatments

• Wet-wrap therapy with TCS is an effective short-term second-line treatment for moderate to very severe AD 5
• Phototherapy (narrowband UVB, broadband UVB, and UVA1) is recommended after failure of topical therapies 1
• Oral antihistamines may be used as adjuvant therapy for reducing pruritus 5
• Topical phosphodiesterase-4 inhibitors have been approved for mild to moderate AD 5

Treatment Cautions

• Long-term application of topical antibiotics is not recommended due to increased risk of resistance and skin sensitization 5
• Topical antihistamines are not recommended due to limited evidence and potential risk of contact dermatitis 5
• The safety of using TCIs like pimecrolimus (Elidel) for long periods is not known 6
• TCIs should not be used on a child under 2 years old 6

Complications and Special Considerations

• Skin infections are common in AD patients 3:

  • Bacterial infections, particularly with Staphylococcus aureus, are suggested by crusting or weeping 2
  • Eczema herpeticum from herpes simplex virus can be life-threatening in AD patients 3
  • Bacterial or viral infections at treatment sites should be resolved before starting treatment with TCIs 6

• Deterioration in previously stable eczema may be due to 2:

  • Secondary bacterial infection
  • Development of contact dermatitis
  • Viral infections (e.g., herpes simplex)

• Patients with AD should minimize or avoid natural or artificial sunlight exposure during treatment with TCIs 6

• The safety of TCIs has not been established in patients with generalized erythroderma or in immunocompromised patients 6