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Atopic Dermatitis (Eczema)
Atopic dermatitis (AD) is an immune-mediated inflammation of the skin arising from an interaction between genetic and environmental factors. The genetic factors involve both epidermal barrier function as well as the immune system. 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.
AD 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 allergic reactions to environmental allergens and autoimmunity to self-proteins. Many patients or family members who have AD also have asthma or allergic rhinitis.
AD has been historically divided into 2 forms: extrinsic or IgE-mediated (70 to 80% of cases) and intrinsic or non‒IgE-mediated (the remainder). However, both forms are now often thought to be different phases of the same disorder. Many patients with AD have a mutation in the gene encoding for the filaggrin protein, which is a component of the cornified cell envelope produced by differentiating keratinocytes. Also, skin affected by AD is deficient in ceramides, which increases transepidermal water loss. One hypothesis is that the non-IgE form is the initial phase resulting from poor barrier function of the epidermis; subsequently, in most patients, IgE-mediated sensitization occurs to a variety of environmental allergens. Also, some autosensitization may result from IgE autoantibodies produced to autoantigens released from damaged skin cells.
Common environmental antigens include
Manifestations of intrinsic and extrinsic AD are similar. AD usually appears in infancy, typically by 3 mo.
In the acute phase, lasting 1 to 2 mo, red, weeping, crusted lesions appear on the face and spread to the neck, scalp, extremities, and abdomen.
In the chronic phase, scratching and rubbing create skin lesions (typically erythematous macules and papules that lichenify with continued scratching). Lesions typically appear in the antecubital and popliteal fossae and on the eyelids, neck, and wrists and may occasionally become generalized. Lesions slowly resolve to dry scaly macules that can fissure and facilitate exposure to irritants and allergens. In older children and adults, intense pruritus is the key feature. Patients have a reduced threshold for perceiving itch, and itch worsens with allergen exposures, dry air, sweating, local irritation, wool garments, and emotional stress.
Secondary bacterial infections, especially staphylococcal and streptococcal infections (eg, cellulitis—see Cellulitis ), and regional lymphadenitis (see Lymphadenitis ) are common. Exfoliative dermatitis (see Exfoliative Dermatitis ) can develop.
Eczema herpeticum (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 is clinical (see Table: Clinical Findings in Atopic Dermatitis*). AD 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:
Because patients can still develop other skin disorders, not all subsequent skin problems should be attributed to AD.
Clinical Findings in Atopic Dermatitis*
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. Patients with severe, unresponsive disease should have nasal and skinfold cultures for S. aureus as a possible precipitant.
AD 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 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 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. )
Skin care involves the following measures:
Bathing should not be done more than once daily. Bathing with diluted bleach (to reduce S. aureuscolonization and decrease the severity of AD) or colloidal oatmeal is sometimes helpful. When toweling dry, the skin should be blotted or patted dry rather than rubbed.
Emollients such as white petrolatum, vegetable oil, or hydrophilic petrolatum (unless the patient is allergic to lanolin) are applied immediately after bathing to help retain skin moisture and reduce itching.
Continuously wet dressings (not wet-to-dry dressings) worn after topical corticosteroids have been applied to inflamed areas are helpful for severe lesions.
Coal tar cream or oil can be an effective topical antipruritic but also can be inconvenient because it stains clothing.
Antihistamines can help relieve pruritus. 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 H2receptor 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.
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. 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]), can control S. aureus nasal colonization and are indicated in patients with severe disease unresponsive to specific therapies and positive nasal cultures. Extensive dietary changes intended to eliminate exposure to allergenic foods are unnecessary and probably ineffective; food hypersensitivities rarely persist beyond childhood.
Corticosteroids are the mainstay of therapy. Creams or ointments applied twice daily are effective for most patients with mild or moderate disease. Emollients are applied between corticosteroid applications and can be mixed with them to decrease the corticosteroid amount required to cover an area. Systemic corticosteroids (prednisone 60 mg [for children, 1 mg/kg] po once/day for short courses of 7 to 14 days) are indicated for extensive or refractory disease but should be avoided whenever possible, because disease often recurs and topical therapy is safer. Prolonged, widespread use of high-potency corticosteroid creams or ointments should be avoided in infants because adrenal suppression may ensue.
Tacrolimus and pimecrolimus are T-cell inhibitors effective for AD. They should be used when patients do not respond to corticosteroids and tar or when corticosteroid adverse effects such as skin atrophy, striae formation, or adrenal suppression is a concern. Tacrolimus 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 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.
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.
Atopic dermatitis (AD) is common, particularly in developed nations, affecting 15 to 30% of children and 2 to 10% of adults.
Common triggers include foods, airborne allergens, S. aureuscolonization, and topical products.
Common findings include pruritus and erythematous macules, papules, and lichenification in the antecubital and popliteal fossae and on the eyelids, neck, and wrists.
AD often improves by adulthood.
First-line treatments include moisturizers, topical corticosteroids, and antihistamines as needed for pruritus.
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