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Atopic dermatitis
is an immune-mediated inflammation of the skin arising from an interaction
between genetic and environmental factors. Recent research suggests
that a heritable epidermal barrier defect is a primary cause, and defects
in the filaggrin gene have been specifically implicated.
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. Atopic dermatitis frequently
resolves completely by age 30.
Etiology
Atopic dermatitis (AD) primarily affects children in urban areas or developed countries; at least 5% of children in the US are affected. Like asthma, it may be linked to proallergic/proinflammatory T-cell immune responses. Such responses are becoming more common in developed countries because trends toward smaller families, cleaner indoor environments, and early use of vaccinations and antibiotics deprive children of the early exposure to infections and allergens that otherwise suppress proallergic T cells and thereby induce tolerance to various antigens.
Pathophysiology
AD can be divided into 2 forms:
Extrinsic AD:
This form occurs when environmental exposures trigger immunologic, usually allergic (ie, IgE-mediated), reactions in genetically susceptible people. Common environmental triggers include
AD is common within families, suggesting a genetic component. 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, research has shown that skin affected by AD is deficient in ceramides, which increases transepidermal water loss.
Intrinsic AD:
This form is not mediated by IgE. Intrinsic AD is nonfamilial and idiopathic, and its pathophysiology is generally not well understood.
Symptoms and Signs
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 antecubital and popliteal fossae and on the eyelids, neck, and wrists and may occasionally become generalized. Lesions slowly resolve to dry scaly macules (xerosis) that can fissure and facilitate exposure to irritants and allergens. In older children or 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.
Complications:
Secondary bacterial infections, especially staphylococcal and streptococcal, and regional lymphadenitis are common.
Eczema herpeticum (Kaposi's 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 the patient to many potential allergens, and contact dermatitis may aggravate and complicate AD, as may the generally dry skin that is common among these patients.
Diagnosis
Diagnosis is clinical (see Table 1: Dermatitis: 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. For example, psoriasis is usually extensor rather than flexurally distributed, may involve the fingernails, and has a shinier (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.
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Table 1
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Clinical Findings in Atopic
Dermatitis*
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Common features
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Chronic or chronically relapsing symptoms
Eczema, typically on the face and extensor surfaces in infants and children and flexural surfaces in adolescents and adults
Personal or family history of atopic disease
Pruritus
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Frequent features
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Cutaneous infections
Early onset
Elevated serum IgE
Nonspecific dermatitis of hands and feet
Positive type I allergy skin tests
Xerosis
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Occasional features
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Cataracts (anterior subcapsular)
Facial erythema
Food intolerance
Ichthyosis
Infraorbital folds
Itching with sweating
Keratoconus
Nipple eczema
Pityriasis alba
Recurrent conjunctivitis
White dermatographism
Wool intolerance
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*Diagnosis requires ≥ 3 common features plus ≥ 3 frequent or occasional features.
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There is no definitive laboratory test for AD. However, allergic precipitants of AD can be identified with skin testing, measurement of allergen-specific IgE levels, or both.
Prognosis
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 completely by age 30. AD may have long-term psychologic sequelae as children confront many challenges of living with a visible, sometimes disabling, skin disease during formative years.
Treatment
Treatment can usually be given at home, but patients who have exfoliative dermatitis (see Dermatitis: 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 moisturizing. Bathing and hand washing should be infrequent, and lukewarm (not hot) water should be used; soap use should be minimized on dermatitic areas because it may be drying and irritating. Colloidal oatmeal baths can be helpful. When toweling dry, the skin should be blotted or patted dry rather than rubbed.
Body oils or emollients such as white petrolatum, vegetable oil, or hydrophilic petrolatum (unless the patient is allergic to lanolin) applied immediately after bathing may help retain skin moisture and reduce itching. Continuously wet dressings (not wet-to-dry) are an alternative 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 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.
Avoidance of
precipitating factors:
Household antigens can be controlled by 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; and 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 ) and oral (eg, dicloxacillin , cephalexin , erythromycin [all 250 mg qid]), 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:
Corticosteroids are the mainstay of therapy. Creams or ointments applied 2 times a day 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 or, 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.
Other therapies:
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 2 times a day. 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.
Light therapy 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 and Scaling Diseases: Phototherapy) therapy is reserved for extensive, refractory AD. Adverse effects include sun damage (eg, PUVA lentigines, nonmelanoma skin cancer). Because of these adverse effects, PUVA is rarely indicated for children or young adults.
Systemic immune modulators effective in at least some patients include cyclosporine , interferon-γ, 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 this is suspected, an ophthalmology consult should be obtained.
Last full review/revision September 2009 by Karen McKoy, MD, MPH
Content last modified September 2009
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