Eczema (Atopic Dermatitis)

Definition

Epidemiology

• Affects up to 20% of children in developed countries; worldwide cumulative prevalence ~20%
• 50% of cases appear in the first year of life; the vast majority before age 5
• Girls are slightly more affected; in the US, African and Asian infants show increased early risk
• Prevalence plateaued in developed nations in the 1990s but continues rising in developing countries
• Risk is increased by: Western diet, first-born status, cesarean delivery, prenatal antibiotic exposure (all disrupt gut microbiome)
• Dog ownership before age 1 year is protective; cat ownership has no effect
• Eczema resolves or improves in >75% of patients by adulthood

Pathogenesis

Skin Barrier Defect

• Filaggrin (FLG) mutations on chromosome 1q21 are the major genetic defect. Filaggrin is processed into "natural moisturizing factor" (NMF) during keratinocyte differentiation
• Null FLG mutations reduce NMF, increase transepidermal water loss (TEWL), and impair the lipid bilayer (especially ceramide) - causing xerosis
• Inheriting two null FLG mutations dramatically increases risk; 42-79% of carriers develop AD
• FLG mutations are also associated with allergic rhinitis, keratosis pilaris, and hyperlinear palms

Immune Dysregulation (Th2 Skew)

• AD patients show a Th2-dominant immune phenotype: elevated IgE, eosinophils on biopsy, positive skin prick tests
• Key cytokines: IL-4 and IL-13 (drive inflammation and sensitization), IL-31 (binds nerves directly causing itch, also downregulates filaggrin), TSLP (keratinocyte-derived, promotes Th2 response via OX40L)
• The JAK-STAT pathway amplifies the Th2 response and itch signaling
• IL-17 plays a role in some patients, particularly those with more severe/early-onset disease

Diagnostic Criteria (Hanifin & Rajka)

Major Criteria

1. Pruritus
2. Typical morphology and distribution (flexural lichenification in adults; facial/extensor in infants)
3. Chronic or chronically relapsing course
4. Personal or family history of atopic disease

Minor Criteria (selected)

• Xerosis
• Ichthyosis / hyperlinear palms / keratosis pilaris
• Elevated serum IgE / positive RAST
• Early age of onset
• Susceptibility to cutaneous infections (S. aureus, HSV - eczema herpeticum)
• Dennie-Morgan infraorbital fold
• Nipple eczema, cheilitis, recurrent conjunctivitis
• Pityriasis alba, white dermatographism
• Food hypersensitivity, itch with sweating, intolerance to wool

Clinical Presentation by Age

Flexural involvement in childhood atopic dermatitis - Andrews' Diseases of the Skin

Complications

• Eczema herpeticum (Kaposi's varicelliform eruption): widespread HSV superinfection - a dermatologic emergency
• Bacterial superinfection: Staphylococcus aureus (presents with crusting, exudates); treat with cephalexin or dicloxacillin
• Cataracts (anterior subcapsular) and keratoconus (corneal ectasia) in severe/chronic AD
• Progression of the atopic march to asthma and allergic rhinitis

Treatment

1. Lifestyle & Trigger Avoidance

• Avoid harsh soaps, fragrances, alcohol-based products, wool, sweat, and known allergens
• Avoid scratching (itch-scratch cycle perpetuates disease)
• Keep bathing brief (<5 min), lukewarm, with gentle soap; pat dry - do not rub

2. Skin Hydration (Cornerstone)

• Apply emollients within 2 minutes of bathing ("soak and smear")
• Use bland emollients with minimal water content: Vaseline, Aquaphor (avoid lotions - high water content worsens dryness)
• "Wet dressings" for severe cases to increase medication absorption

3. Topical Corticosteroids (First-Line Anti-inflammatory)

• Ointments are the most effective vehicle; creams are acceptable
• Low-medium potency: 7 days per flare; taper afterward
• Avoid high-potency steroids on face, genitalia, or skin folds (atrophy risk)

4. Topical Calcineurin Inhibitors (TCIs)

• Tacrolimus (Protopic) and pimecrolimus (Elidel)
• Steroid-sparing; preferred for face, eyelids, and intertriginous areas
• Can be used as proactive/maintenance therapy 2-3x/week on previously affected skin

5. Anti-itch Measures

• Sedating antihistamines (diphenhydramine, hydroxyzine): useful for nighttime sedation only; little direct effect on AD itch
• Non-sedating antihistamines: helpful for comorbid urticaria/allergic rhinitis, not AD itch itself

6. Bleach Baths

• Diluted bleach baths 1-2x/week (¼ cup bleach in full tub, soak 10 min, rinse) - reduce S. aureus colonization

7. Systemic Treatment (Moderate-Severe / Refractory)

• Oral corticosteroids: short courses for acute severe flares (prednisone 40-60 mg/day adults; 1-2 mg/kg/day children); avoid long-term use
• Dupilumab (anti-IL-4Rα): blocks IL-4 and IL-13 signaling; FDA-approved biologic; highly effective for moderate-severe AD
• JAK inhibitors (abrocitinib, upadacitinib, baricitinib): approved for adults with moderate-severe AD refractory to other treatments
• Cyclosporine, methotrexate, azathioprine, mycophenolate mofetil: older systemic immunosuppressants used off-label
• Phototherapy (UVB, narrowband UVB, PUVA): effective, especially for widespread disease

Key Points Summary