Treating atopic dermatitis

Key Points

Atopic dermatitis (AD) is caused by a disorder of the inborn immune system resulting in a chronic skin disease with pruritus as a core and essential symptom. Rubbing and scratching results in inflammation and irritation. AD has been reported to occur in up to 21% of infants and children up to age 30 months.¹

AD has no gender preference, but there seem to be genetic factors that predispose susceptible individuals to the development of AD in certain environmental settings. For example, children with a family history of AD, asthma, or environmental allergies, or who have specific mutations in the filaggrin gene, which is partially responsible for normal skin barrier function, are at increased risk of developing AD.² Moreover, the increased incidence of AD in infants and children in industrialized countries support an environmental trigger.³

The clinical picture of AD is that of an interrupted skin barrier due to scratching. Symmetrically distributed scaly erythematous patches constitute the classic presentation of AD lesions.

Investigators continue to argue the role of food and other allergens in the pathogenesis of AD. AD cannot be solely attributed to the activation of an IgE-mediated response, the pathway involved with food allergies.⁵ Genetics play a part in immune irregularities as well, as do environmental allergens and bacterial antigens. The interplay of these factors activates both the immediate and delayed cellular immune hypersensitivity response pathways.⁶

Histories

Treatment pathways should be derived from taking a thorough history, which should include family history, environmental history, skin care history, social history, and diet history.

If a food allergy is suspected, the clinician should attempt to distinguish between food allergy and food sensitivity or intolerance. If food allergy is suspected, a family and postnatal maternal history of food allergy should be included in a dietary history. The top known food allergens are egg, milk, fish, wheat, soy, and nuts. Breastfed infants may be sensitive to the mother's ingestion of high-caffeinated beverages and gas-producing foods. With infants with a family history of food allergy, ask about the amount of cow's milk, eggs, nuts, wheat, or soy in the diet.

Studies have shown no correlation between a prenatal maternal elimination diet and the development of AD.⁷ A recent study reported the possible positive impact of probiotics taken by the mother prenatally and continued postnatally by the infant in a decrease of IgE-associated AD.⁸ In rare cases, referral to a nutritionist may be warranted for a breastfeeding mother with food allergies who has an infant with severe recalcitrant atopic dermatitis.

The impact of AD on patients and their families needs to be empathetically acknowledged: it is not "just eczema." The chronic and unpredictable nature of the disease, interrupted sleep patterns, and social stigma can and should be assessed and quantified. Quality of life concerns should be addressed at regular intervals to help identify and manage the physical and psychosocial stressors endured by these patients and their families.⁹ In two British studies, quality of life and family impact assessment tools for patients and their caregivers were developed, tested for reliability, and found useful for family counseling as an adjunct to medical therapy with emollients and prescribed topicals.^10,11

Treatment modalities

The cornerstone of effective treatment is the frequent application of bland emollients. The vehicle (ointment vs. cream) is individualized based on the patient's skin tolerance and personal preference. Alternative topicals such as lavender oil and other topical herbal preparations have not been evaluated in controlled studies. If a parent or caregiver would like to try an alternative topical agent, be sure to recommend application to a small test area first to minimize the risk of an adverse event.