Domino_5-Minute Clinical Consult, 33e

DERMATITIS, ATOPIC Dennis E. Hughes, DO, FACEP

BASICS

• Food allergies may be seen in association with AD, but there is no conclusive common origin. Studies of breastfeeding conveying decreased risk versus increased risk are mixed in conclusion. • Exposure to tobacco smoke • Some evidence suggests that repeated exposure to water high in mineral content may exacerbate the condition. • Family history of atopy – Asthma – Allergic rhinitis COMMONLY ASSOCIATED CONDITIONS • Food sensitivity/allergy in many cases. Strong as sociation with asthma and allergic rhinitis; atopic march—clinical succession of AD with subsequent development of allergic rhinitis followed by asthma (1) • Association with both cutaneous and extra cutaneous infections: URI, OM, UTI, cellulitis, erysip elas, zoster, endocarditis, both methicillin-resistant and susceptible stains of Staphylococcus aureus , pharyngitis, and rarely sepsis • Hyper-IgE syndrome (Job syndrome) – AD – Elevated IgE – Recurrent pyodermas – Decreased chemotaxis of mononuclear cells • Presence of major symptoms including relapsing of condition, family history, typical distribution, and morphology necessary to make diagnosis of AD • Most prevalent symptoms: itch (54%), dryness and scaling (19.6%), inflamed skin (7.2%), skin pain (8.2%), sleep disturbance (11.4%) PHYSICAL EXAM Primarily skin manifestations • Distribution of lesions – Infants: trunk, face, and extensor surfaces; diaper sparing – Children: antecubital and popliteal fossae, wrists and ankle locations – Adults: hands, feet, face, neck, upper chest, and genital areas as well as flexor surfaces • Morphology of lesions – Infants: erythema and papules; may develop oozing, crusting vesicles – Children and adults: Lichenification and scaling are typical with chronic eczema as a result of persistent scratching and rubbing (lichenification is rare in infants). • Associated signs – Facial erythema, mild to moderate – Perioral pallor – Infraorbital fold (Dennie–Morgan fold)—atopic pleat DIAGNOSIS Clinical diagnosis HISTORY

– Dry skin progressing to ichthyosis – Increased palmar linear markings – Pityriasis alba (hypopigmented asymptomatic areas on face and shoulders) – Keratosis pilaris DIFFERENTIAL DIAGNOSIS • Photosensitivity rashes • Contact dermatitis (especially if only the face is involved) • Scabies • Seborrheic dermatitis (especially in infants) • Psoriasis or lichen simplex chronicus if only localized disease is present in adults • Rare conditions of infancy – Histiocytosis X – Wiskott-Aldrich syndrome – Ataxia-telangiectasia syndrome • Ichthyosis vulgaris DIAGNOSTIC TESTS & INTERPRETATION Initial Tests (lab, imaging) • No test is diagnostic. • Serum IgE levels are elevated in as many as 80% of affected individuals, but test is not routinely ordered or indicated. • Eosinophilia tends to correlate with disease severity. • Scoring AD (SCORAD) is a scoring system for AD, comprising scores for area, intensity, and subjective symptoms. TREATMENT GENERAL MEASURES • Minimize flare-ups and control the duration and intensity of flare-up. • Avoid agents that may cause irritation (e.g., wool, perfumes). • Minimize sweating. • Lukewarm (not hot) bathing. No evidence signifi cantly guides frequency of bathing, but a minimum of twice weekly and when hygiene dictates for with postbath skin emollients. • Avoid alkaline soaps. Use hypoallergenic cleans ers with a slightly acidic (pH 5 to 6) with gentle mechanical removal of crusts, scale, and bacterial skin contaminants. • Sun exposure may be helpful. • Humidify the house. • Avoid excessive contact with water. • Avoid lotions that contain alcohol. • If very resistant to treatment, search for a coexisting contact dermatitis. Pediatric Considerations Chronic potent fluorinated corticosteroid use may cause striae, hypopigmentation, or atrophy, especially in children.

DESCRIPTION • A chronic, relapsing, inflammatory, intensely pruritic skin disease • Early-onset cases have coexisting allergen sensitiza tion more often than late-onset cases. • Clinical phenotypical presentation is highly variable, suggesting multifactorial pathophysiology. • May have significant effect on quality of life for pa tient and family—recurrent symptoms affect lifestyle and mental health EPIDEMIOLOGY • 45% of all cases begin in the first 6 months of life with 80–95% onset prior to age of 5 years. • 50–66% of affected children will have a spontane ous remission before adolescence. • Also, may have late-onset dermatitis in adults or relapse of childhood condition—primarily hand eczema • Darker pigmented individuals are affected more often than whites. • 60% incidence if one parent is previously affected and rises to 80% if both parents are previously affected. Monozygotic twins have 80% concordance for the disorder. Incidence Varies worldwide, but all countries’ populations are affected. The only consistent signal favored lower incidence in rural versus urban locations (exceptions are Canada and Mexico). Prevalence Approaching 20% prevalence in children and 10% in young adults; still present in later adulthood 2% ETIOLOGY AND PATHOPHYSIOLOGY • Current understanding is atopic dermatitis (AD) is a systemic T-helper cell driven disorder. • Alteration in stratum corneum results in transepider mal water loss and defect in barrier function. • Epidermal adhesion is reduced either as a result of (i) genetic mutation resulting in altered epidermal proteins or (ii) defect in immune regulation causing an altered inflammatory response. • Interleukin-31 (IL-31) upregulation is thought to be a major factor in pruritus mediated by cytokines and neuropeptides rather than histamine excess. Genetics • Recent discovery of association between AD and mutation in the filaggrin gene ( FLG ), which codes for a skin barrier protein • Both epidermal and immune coding are likely involved. RISK FACTORS • “Itch–scratch cycle” (stimulates histamine release) • Skin infections • Emotional stress

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• Irritating clothes and chemicals • Excessively hot or cold climate

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