Overview and Risk Factors
Atopic dermatitis, also known as eczema, is a common chronic skin disease that affects about 20% of people worldwide. It is associated with other markers of atopy, such as asthma, allergic rhinitis, and food allergy. Pathogenesis is not well understood. Signs of disease (inflammation) usually occur early in life and resolve by 6 years of age. However, a significant population has atopic dermatitis that may persist indefinitely.
Presentation varies, depending on patient age and disease severity. In general, children have itching and subsequent erythematous plaques or patches with scaling and papular features on the upper body. Adults tend to have thickened skin with lichenification and excoriated and fibrotic papules, reflecting the chronicity of the disease. Severe cases may present in any distribution. Patients with atopic dermatitis are at increased risk for skin infections.
Family or personal history of atopy. Maternal disease seems to be a stronger risk factor than paternal disease.1 About one-half of those with atopic dermatitis have a relative with allergic asthma. A history of food allergy, allergic rhinitis, or asthma is associated with atopic dermatitis.
Antigens. Variations in antigen exposure may affect risk of disease.2
Some evidence suggests that exclusive breast-feeding for at least the first 3 months of life may be associated with reduced risk among infants with a family history of atopy.3
Diagnosis and Treatment
Major diagnostic criteria for atopic dermatitis include pruritis, relapsing disease, age-appropriate distribution of lesions (face and extensor surfaces in children and flexor surfaces in adults), and a family history of atopy. Nonspecific minor criteria that may aid diagnosis include periorbital darkening, dry skin, and keratosis pilaris on the skin over the triceps region.4 Other diseases, such as hyperimmunoglobulin E syndrome and scabies, can resemble atopic dermatitis in appearance.
No laboratory tests definitively diagnose atopic dermatitis. However, up to 80% of patients will have an elevated serum immunoglobulin E (IgE) and positive skin tests for immediate hypersensitivity reactions to common allergens.5 These tests are not required for diagnosis.
Recurrent skin infections may occur in atopic dermatitis-damaged skin, and they may also exacerbate disease. Skin infections occur much more commonly in atopic dermatitis patients than in psoriasis patients,6 suggesting that factors aside from skin breakdown are involved in predisposition to skin infection.
Initial treatment of atopic dermatitis should seek to eliminate exacerbating agents, such as soaps and detergents, food allergens, and cosmetics. Excessive bathing or use of lotions should be discouraged, as evaporation of water from the skin exacerbates atopic dermatitis. Some patients may be surprised to learn that water-based lotions actually increase evaporation of water from the skin, unlike emollient creams or ointments. Humidifiers may be tried in dry climates.
Emollient creams or ointments should be applied liberally, especially after bathing to lock in moisture. Occlusive bandages or gloves can be worn nightly to aid skin hydration.
Psychological approaches to mitigate stress may help avoid exacerbations.7
Antihistamines may relieve itching symptoms.
Antibiotics may be effective when patients develop a bacterial infection in the affected area or have pustular disease.
Topical corticosteroids should be used in the lowest possible therapeutic strength to treat active atopic dermatitis. Occasional use of topical steroids between episodes reduces the likelihood of recurrence.
Systemic corticosteroids, such as prednisone, may be used for a short duration when exacerbations occur.
Topical tacrolimus and other topical calcineurin inhibitors are second-line agents. They are used less commonly because of concerns about their carcinogenic potential. They may be used in children 2 years old and older who have not responded to other agents. Unlike corticosteroids, they do not cause skin atrophy, so they can be used on sensitive areas, such as the face, eyelids, and underarms. Patients treated with tacrolimus ointment should be aware that a facial flush reaction can occur within 5 to 15 minutes of alcohol ingestion.8
Oral cyclosporine and tacrolimus may be used for severe cases, with close monitoring for systemic side effects. It should be noted, however, that a possible risk of skin and lymph cancers is associated with this drug class.
Immunosuppressants are sometimes used in severe refractory disease.
Phototherapy using ultraviolet light (UVA, UVB, and narrow-band UVB) is usually successful, but may raise the risk of melanoma and other skin cancer.
Desensitization through immunotherapy is not a successful treatment option.
Nutritional modifications that may improve atopic dermatitis have been under study for many years. The following factors are under investigation:
Avoiding Alcohol during Pregnancy
In cases in which both parents had allergic diseases, maternal alcohol intake equivalent to four or more drinks per week increased the risk for atopic dermatitis fourfold.9 Alcohol use during pregnancy carries other major risks and should be avoided completely.
Breast-feeding allows infants to avoid exposure to cow's milk proteins, except insofar as they may be transmitted from the maternal diet through breast milk, as has been demonstrated in studies of colicky infants (see Colic chapter). Avoidance of allergenic foods by a breast-feeding mother may further reduce risk of atopy in the infant. Some have suggested that breast milk supplies specific protective factors as well, notably transforming growth factor Î²2, a cytokine that provides anti-allergenic immunoprotection. Diminished production of this cytokine has been reported in persons with atopic eczema and in the breast milk from mothers with atopy.10
Extensively Hydrolysed Whey Protein Formulas
Hydrolyzed formulas have been used in children who are not breast-fed to reduce the incidence of atopic dermatitis, and are tolerated by at least 90% of infants with documented allergy to cow's milk protein.11 However, these formulas retain some allergenicity, and only amino acid-based formulas can be considered completely nonallergenic.12
Delayed Introduction of Solid Foods
Avoiding the introduction of solid foods until infants have reached 4 to 6 months of age appears to reduce the risk of atopy. A combination of breast-feeding (or hypoallergenic formula) and delayed introduction of solid food appears to be the most effective regimen for atopy prevention in infants.13 This approach may be augmented by environmental controls, such as polyvinyl mattress covers and anti-dust-mite sprays. In a clinical trial, these combined steps were associated with a 67% reduction in dermatitis incidence, compared with a control population.14
Eliminating Allergy-Causing Foods
Eggs, cow's milk, soy, and wheat account for roughly 90% of the allergenic foods in children with atopic dermatitis.15 More than 50% of children with diet-related atopic dermatitis experience both a significant improvement during periods of dietary exclusion and an exacerbation of their condition when challenged with allergen-containing foods.15
Adults with eczema are more likely than children with the condition to experience exacerbations when exposed to foods containing birch pollen, such as apple, carrots, celery, and hazelnuts.15 (See Rheumatoid Arthritis for instructions on elimination diets.)
Double-blind, placebo-controlled food challenges have found that a small fraction of children and adults experience skin reactions when given various additives. These include nitrite, benzoate, and tartrazine, balsam of Peru, and both natural and artificial vanilla.16,17 More than 50% of patients have been reported to improve on diets low in allergens.16
Preliminary evidence indicates that a vegetarian diet results in significant improvement in SCORAD (SCORing Atopic Dermatitis), a clinical tool for objectively assessing the severity of atopic dermatitis. This improvement appears to be related to reductions in circulating blood levels of eosinophils and neutrophils and decreased monocyte production of PGE2, an inducer of IgE and T helper 2 (Th2) cell production.18 A low-energy diet (55% of estimated energy needs) conferred similar benefit to individuals with atopic dermatitis,19 although the practicality of energy-restricted regimens for long-term use is not established.
Prenatal treatment with Lactobacillus in mothers with a family history of atopic disease, combined with postnatal probiotic treatment of their infants, reduced the incidence of infant atopic dermatitis by 50%.20 Probiotic therapy also significantly reduced SCORAD in infants21 and in children.22 An excess of Th2 cells may be involved in IgE synthesis and the development of dermatitis, and diet appears to have a role in this process.18,23 Probiotic treatment (mainly Lactobacillus rhamnosus) may have anti-allergy effects by stimulating Th1 cytokines21 and by down-regulating CD34+ cells involved in the symptoms of dermatitis, while increasing those with anti-inflammatory effects (eg, interferon-Î²3).20
Preliminary data indicate that supplementary vitamin E (400 IU/day) improves symptoms in some adults with this disease.24 Lack of antioxidants may encourage Th2 cell production characteristic of atopy.25 Vitamin E tends to increase Th1 cell production and reduces IgE-mediated responses, which may explain why studies have found inverse associations between vitamin E intake and the risk for atopic eczema.25,26
Elimination diet, if specific triggers for dermatitis have not been found.
What to Tell the Family
Atopic dermatitis is a persistent ailment with a significant hereditary component. Some evidence indicates that the risk for inheriting this disease can be moderated through breast-feeding and allergen avoidance. In persons with established disease, effective management of symptoms is possible through combinations of topical ointments, diet modification, dietary supplements, and, if necessary, systemic anti-inflammatory (corticosteroid) treatment.
1. Ruiz RG, Kemeny DM, Price JF. Higher risk of infantile atopic dermatitis from maternal atopy than from paternal atopy. Clin Exp Allergy. 1992;22:762-766.
2. Trepka MJ, Heinrich J, Wichmann HE. The epidemiology of atopic diseases in Germany: an east-west comparison. Rev Environ Health. 1996;11:119-131.
3. Gdalevich M, Mimouni D, David M, Mimouni M. Breast-feeding and the onset of atopic dermatitis in childhood: A systematic review and meta-analysis of prospective studies. J Am Acad Dermatol. 2001;45:520-527.
4. Hanifin JM, Rajka G. Diagnostic features of atopic dermatitis. Acta Dermatol Venereol. 1980;92:44-47.
5. Jones SM, Sampson HA. The role of allergens in atopic dermatitis. Clin Rev Allergy. 1993;11:471-490.
6. Christophers E, Henseler T. Contrasting disease patterns in psoriasis and atopic dermatitis. Arch Dermatol Res. 1987;279:S48-S51.
7. Pallanti S, Lotti T, Urpe M. Psychoneuroimmunodermatology of atopic dermatitis: from empiric data to the evolutionary hypothesis. Dermatol Clin. 2005;23:695-701.
10. Rautava S, Isolauri E. Cow's milk allergy in infants with atopic eczema is associated with aberrant production of interleukin-4 during oral cow's milk challenge. J Pediatr Gastroenterol Nutr. 2004;39:529-535.
12. Caffarelli C, Plebani A, Poiesi C, Petroccione T, Spattini A, Cavagni G. Determination of allergenicity to three cow's milk hydrolysates and an amino acid-derived formula in children with cow's milk allergy. Clin Exp Allergy. 2002;32:74-79.
13. Muraro A, Dreborg S, Halken S, et al. Dietary prevention of allergic diseases in infants and small children. Part III: Critical review of published peer-reviewed observational and interventional studies and final recommendations. Pediatr Allergy Immunol. 2004;15:291-307.
14. Arshad SH. Primary prevention of asthma and allergy. J Allergy Clin Immunol. 2005;116:3-14.
16. Worm M, Vieth W, Ehlers I, Sterry W, Zuberbier T. Increased leukotriene production by food additives in patients with atopic dermatitis and proven food intolerance. Clin Exp Allergy. 2001;31:265-273.
18. Tanaka T, Kouda K, Kotani M, et al. Vegetarian diet ameliorates symptoms of atopic dermatitis through reduction of the number of peripheral eosinophils and of PGE2 synthesis by monocytes. J Physiol Anthropol Appl Human Sci. 2001;20:353-361.
21. Viljanen M, Savilahti E, Haahtela T, et al. Probiotic effects on fecal inflammatory markers and on fecal IgA in food allergic atopic eczema/dermatitis syndrome infants. Pediatr Allergy Immunol. 2005;16:65-71.
24. Tsoureli-Nikita E, Hercogova J, Lotti T, Menchini G. Evaluation of dietary intake of vitamin E in the treatment of atopic dermatitis: a study of the clinical course and evaluation of the immunoglobulin E serum levels. Int J Dermatol. 2002;41:146-150.
25. Martindale S, McNeill G, Devereux G, Campbell D, Russell G, Seaton A. Antioxidant intake in pregnancy in relation to wheeze and eczema in the first two years of life. Am J Respir Crit Care Med. 2005;171:121-128.