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Atopic Dermatitis (Eczema)

(Atopic Eczema; Infantile Eczema)

By Mercedes E. Gonzalez, MD, Clinical Assistant Professor;Medical Director, University of Miami, Department of Dermatology, Miller School of Medicine;Pediatric Dermatology of Miami

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Atopic dermatitis (AD, often referred to as eczema) is a chronic inflammatory skin disorder with a complex pathogenesis involving genetic susceptibility, immunologic and epidermal barrier dysfunction, and environmental factors. Pruritus is the primary symptom; skin lesions range from mild erythema to severe lichenification. Diagnosis is by history and examination. Treatment is moisturizers, avoidance of allergic and irritant triggers, and often topical corticosteroids or immune modulators. Childhood atopic dermatitis frequently resolves or lessens significantly by adulthood.

Etiology

Atopic dermatitis primarily affects children in urban areas or developed countries, and prevalence has increased over the last 30 yr; up to 20% of children and 1 to 3% of adults in developed countries are affected. Most people with the disorder develop it before age 5, many of them before age 1. The unproven hygiene hypothesis is that decreased early childhood exposure to infectious agents (ie, because of more rigorous hygiene regimens at home) may increase the development of atopic disorders and autoimmunity to self-proteins; many patients or family members who have AD also have asthma or allergic rhinitis.

Pathophysiology

All of the following contribute to the development of AD:

  • Genetic factors

  • Epidermal barrier dysfunction

  • Immunologic mechanisms

  • Environmental triggers

Genes implicated in AD are those encoding epidermal and immunologic proteins. A major predisposing factor for AD is the existence in many patients of a mutation in the gene encoding for the filaggrin protein, which is a component of the cornified cell envelope produced by differentiating keratinocytes.

Known epidermal barrier defects in skin affected by AD also include decreased ceramides and antimicrobial peptides and increased transepidermal water loss, which increase penetration of environmental irritants and allergens, and microbes, triggering inflammation and sensitization.

In acute AD lesions, Th2 T cell cytokines (IL-4, IL-5, IL-13) predominate, whereas in chronic lesions Th1 T cell cytokines (IFN-gamma, IL-12) are present. Numerous other cytokines, including thymic stromal lipoprotein, CCL17, and CCL22, play a role in the inflammatory reaction in AD. New treatments targeting specific cytokines are helping to identify the specific immune pathways in AD.

Common environmental triggers include

  • Foods (eg, milk, eggs, soy, wheat, peanuts, fish)

  • Airborne allergens (eg, dust mites, molds, dander)

  • Staphylococcus aureus colonization on skin due to deficiencies in endogenous antimicrobial peptides

  • Topical products (eg, cosmetics, fragrances, harsh soaps)

  • Sweating

  • Rough fabrics

Symptoms and Signs

Atopic dermatitis usually appears in infancy, typically by 3 mo.

In the acute phase, lesions are red, edematous, scaly patches or plaques that may be weepy. Occasionally vesicles are present.

In the chronic phase, scratching and rubbing create skin lesions that appear dry and lichenified.

Distribution of lesions is age specific. In infants, lesions characteristically occur on the face, scalp, neck, and extensor surfaces of the extremities. In older children and adults, lesions occur on flexural surfaces such as the neck, and the antecubital and popliteal fossae.

Intense pruritus is a key feature. Itch often precedes lesions, and itch worsens with allergen exposures, dry air, sweating, local irritation, wool garments, and emotional stress.

Complications

Secondary bacterial infections (superinfections), especially staphylococcal and streptococcal infections (eg, cellulitis and regional lymphadenitis) are common. Exfoliative dermatitis can develop.

Eczema herpeticum (also called Kaposi varicelliform eruption) is a diffuse herpes simplex infection occurring in patients with AD. It manifests as grouped vesicles in areas of active or recent dermatitis, although normal skin can be involved. High fever and adenopathy may develop after several days. Occasionally, this infection can become systemic, which may be fatal. Sometimes the eye is involved, causing a painful corneal lesion.

Fungal and nonherpetic viral skin infections (eg, common warts, molluscum contagiosum) can also occur.

Patients with long-standing AD may develop cataracts in their 20s or 30s.

Frequent use of topical products exposes patients to many potential allergens, and contact dermatitis caused by these products may aggravate and complicate AD, as may the generally dry skin that is common among these patients.

Diagnosis

  • Clinical evaluation

  • Sometimes testing for allergic triggers with skin prick testing, radioallergosorbent testing levels, or patch testing

Atopic dermatitis is often hard to differentiate from other dermatoses (eg, seborrheic dermatitis, contact dermatitis, nummular dermatitis, psoriasis), although a family history of atopy and the distribution of lesions are helpful. The following distribution patterns can help with differentiation:

  • Psoriasis is usually extensoral rather than flexural, may involve the fingernails, and has a thicker and whiter (micaceous) scale.

  • Seborrheic dermatitis affects the face (eg, nasolabial folds, eyebrows, glabellar region, scalp) most commonly.

  • Nummular dermatitis is not flexural, and lichenification is rare.

Because patients can still develop other skin disorders, not all subsequent skin problems should be attributed to AD.

Pearls & Pitfalls

  • Clues to atopic dermatitis include a flexural distribution and personal or family history of allergic rhinitis, asthma, or allergies.

  • Bacterial superinfection is a common complication in atopic dermatitis and may be easily confused with eczema herpeticum.

Diagnostic Clinical Features in Atopic Dermatitis*

Essential features

Pruritus

Dermatitis (eczema)— acute, subacute, or chronic, with

  • Typical age-specific patterns

  • Chronic or relapsing history

Important features

Early age of onset

Personal or family history of atopic disease

IgE reactivity

Xerosis

Associated features (help to suggest the diagnosis)

White dermatographism

Pityriasis alba

Hyperlinear palms

Facial pallor

Infraorbital folds

Nipple dermatitis

Perifollicular accentuation

Lichenification

Prurigo lesions

Delayed blanch response

Certain regional changes (eg, perioral changes, periauricular changes)

On the face, neck, and extensor surfaces in infants and children; flexural surfaces in any age group; spares groin and axillae.

There is no definitive laboratory test for AD. However, precipitating environmental allergens of AD can be identified with skin testing, measurement of allergen-specific IgE levels, or both. Routine cultures for S. aureus are not done because that organism is present in skin lesions of > 75% of AD patients (vs in < 25% of unaffected people). However, nasal and skinfold cultures are done in patients with recurrent, unresponsive, and possibly antimicrobial-resistant infections.

Prognosis

Atopic dermatitis in children often abates by age 5 yr, although exacerbations are common throughout adolescence and into adulthood. Girls and patients with severe disease, early age of onset, family history, and associated allergic rhinitis or asthma are more likely to have prolonged disease. Even in these patients, AD frequently resolves or lessens significantly by adulthood. AD may have long-term psychologic sequelae as children confront the many challenges of living with a visible, sometimes disabling, skin disease during their formative years.

Treatment

  • Supportive care (eg, moisturizers and dressings, antihistamines for pruritus)

  • Avoidance of precipitating factors

  • Topical corticosteroids

  • Topical immune modulators

  • In severe disease, systemic immunosuppressants

  • Sometimes ultraviolet (UV) therapy

  • Treatment of superinfections

Treatment can usually be given at home, but patients who have exfoliative dermatitis, cellulitis, or eczema herpeticum may need to be hospitalized.

(See also the American Academy of Dermatology Association’s Guidelines of Care for Atopic Dermatitis.)

Supportive care

Skin care involves the following measures:

  • Hydrating with water

  • Use of nonsoap cleansers that are neutral- to- low pH, hypoallergenic, and fragrance free

  • Taking baths with diluted bleach or colloidal oatmeal

  • Applying moisturizers (eg, white petrolatum ointments or creams)

  • Wearing wet wraps

Bathing should not be done more than once daily. Bathing with diluted bleach 2 times/wk plus nasal application of mupirocin can reduce S. aureus colonization and decrease the severity of AD (1). Colloidal oatmeal is sometimes soothing. When toweling dry, the skin should be blotted or patted dry rather than rubbed.

Moisturizers (ointments such as white petrolatum or hydrophilic petrolatum [unless the patient is allergic to lanolin] or thick creams) are applied immediately after bathing to help retain skin moisture and reduce itching.

Wet wraps (a topical corticosteroid or immunomodulator applied to wet skin, wrapped with a moist layer, and then overlaid with a dry layer) are helpful for severe, thick, and recalcitrant lesions.

Antihistamines can help relieve pruritus via their sedating properties. Options include hydroxyzine 25 mg po tid or qid (for children, 0.5 mg/kg q 6 h or 2 mg/kg in a single bedtime dose) and diphenhydramine 25 to 50 mg po at bedtime. Low-sedating H1 receptor blockers (such as loratadine 10 mg po once/day, fexofenadine 60 mg po bid or 180 mg po once/day, and cetirizine 5 to 10 mg po once/day) may be useful, although their efficacy has not been defined. Doxepin (a tricyclic antidepressant also with H1 and H2 receptor blocking activity) 25 to 50 mg po at bedtime may also help, but its use is not recommended for children < 12 yr. Fingernails should be cut short to minimize excoriations and secondary infections.

Treatment reference

  • Huang JT, Abrams M, Tlougan B, et al: Treatment of Staphylococcus aureus colonization in atopic dermatitis decreases disease severity. Pediatrics 123(5):e808-814, 2009. doi: 10.1542/peds.2008-2217.

Avoidance of precipitating factors

Household antigens can be controlled by the following measures:

  • Using synthetic fiber pillows and impermeable mattress covers

  • Washing bedding in hot water

  • Removing upholstered furniture, soft toys, carpets, and pets (to reduce dust mites and animal dander)

  • Using air circulators equipped with high-efficiency particulate air (HEPA) filters in bedrooms and other frequently occupied living areas

  • Using dehumidifiers in basements and other poorly aerated, damp rooms (to reduce molds)

Reduction of emotional stress is useful but often difficult. Extensive dietary changes intended to eliminate exposure to allergenic foods are unnecessary and probably ineffective; food hypersensitivities rarely persist beyond childhood.

Corticosteroids

Topical corticosteroids are the mainstay of therapy. Creams or ointments applied twice daily are effective for most patients with mild or moderate disease. Moisturizers are liberally applied after corticosteroid applications to all skin. Systemic corticosteroids should be avoided whenever possible, because disease rebound is often severe and topical therapy is safer. Prolonged topical use can lead to thinning of the skin and striae. Prolonged, widespread use of high-potency corticosteroid creams or ointments should be avoided in infants because adrenal suppression may ensue.

Other therapies

Topical tacrolimus and pimecrolimus are T-cell inhibitors effective for AD. They can be used for mild to moderate AD or when corticosteroid adverse effects such as skin atrophy, striae formation, or adrenal suppression is a concern. Tacrolimus ointment or pimecrolimus cream is applied twice daily. Burning or stinging after application is usually transient and abates after a few days. Flushing is less common.

Repair of the stratum corneum and barrier function may help alleviate AD. Research has shown that skin affected by AD is particularly deficient in ceramides and that a deficiency in ceramides increases transepidermal water loss. Several ceramide-containing emollient products are considered helpful for AD control.

Phototherapy is helpful for extensive AD. Natural sun exposure ameliorates disease in many patients, including children. Alternatively, therapy with ultraviolet A (UVA) or B (UVB) may be used. Narrowband UVB therapy is proving more effective than traditional broadband UVB therapy and is also effective in children. Psoralen plus UVA (PUVA—see Psoriasis : Phototherapy) therapy is reserved for extensive, refractory AD. Adverse effects include sun damage (eg, PUVA lentigines, nonmelanoma skin cancer). Because of these adverse effects, phototherapy, particularly PUVA, is avoided when possible in children or young adults.

Systemic immune modulators effective in at least some patients include cyclosporine, interferon gamma, mycophenolate, methotrexate, and azathioprine. All downregulate or inhibit T-cell function and have anti-inflammatory properties. These agents are indicated for widespread, recalcitrant, or disabling AD that fails to abate with topical therapy and phototherapy.

Antistaphylococcal antibiotics, both topical (eg, mupirocin, fusidic acid [applied for ≤ 2 wk]) and oral (eg, dicloxacillin, cephalexin, erythromycin [all 250 mg qid for 1 to 2 wk]), are used to treat bacterial skin superinfections such as impetigo, folliculitis, or furunculosis. Nasal mupirocin can also be used to decrease carriage of S. aureus and the severity of AD.

Eczema herpeticum is treated with acyclovir. Infants receive 10 to 20 mg/kg IV q 8 h; older children and adults with mild illness may receive 200 mg po 5 times/day. Involvement of the eye is considered an ophthalmic emergency, and if eye involvement is suspected, an ophthalmology consult should be obtained.

Key Points

  • Atopic dermatitis (AD) is common, particularly in developed nations, affecting 15 to 30% of children and 2 to 10% of adults.

  • Common triggers include airborne allergens (eg, pollen, dust), sweat, harsh soaps, rough fabrics, and fragrances.

  • Common findings include pruritus and erythematous patches and plaques and lichenification in the antecubital and popliteal fossae and on the eyelids, neck, and wrists.

  • Superinfections (particularly S. aureus infections and eczema herpeticum) are common.

  • AD often improves by adulthood.

  • First-line treatments include moisturizers, topical corticosteroids, and antihistamines as needed for pruritus.

Resources In This Article

* This is the Professional Version. *