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Authors’ Response

Walker, W. Allan; Iyengar, Rajashri

Journal of Pediatric Gastroenterology and Nutrition: July 2013 - Volume 57 - Issue 1 - p e9–e10
doi: 10.1097/MPG.0b013e3182923787
Letters to the Editor
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Harvard Medical School, Massachusetts General Hospital, Charlestown

To the Editor:

The response from Bramuzzo et al to our review article examining the complex relation between breast-feeding and allergic disease development underscores several important issues. As highlighted in the response, many infants initially develop atopic dermatitis (AD) because of deficits in their skin barrier that lead to a predisposition to food sensitization. These events can, in turn, serve to initiate the atopic march (1,2). Indeed, approximately 15% to 20% of patients with AD have mutations in filaggrin, a protein that is important in skin barrier function. Filaggrin-deficient mice have demonstrated permissiveness to epicutaneous sensitization to allergenic proteins and exhibit TH17-dominated skin inflammation, which is characteristic of atopic skin lesions (3). Although we agree with this concept outlined in the response from Bramuzzo et al, to state that “atopic” dermatitis is not an allergic disease would be to deny the interplay of this skin condition with multiple exacerbating factors, such as food allergens that have been proven to result directly in AD skin lesions. Approximately 40% of patients with AD have concomitant food allergies (4). Regardless of whether the initial food sensitization occurred through the skin or by another route, studies have also demonstrated the ingestion of implicated allergenic foods in these patients triggers immunologic changes characteristic of allergic responses in the skin that result in the formation of AD skin lesions or “flares” (5). This established concept is supported by the European Academy of Allergy and Clinical Immunology and the consortium of European research centers specialized in allergic diseases (6). In addition, a recent study in 92 exclusively breast-fed infants with established AD demonstrated that 73% of infants showed improvement of skin lesions when their mothers avoided highly allergenic foods such as dairy, tree nuts, and soy (7). In addition, nearly 40% of people with filaggrin mutations do not develop AD (8). Similarly, patients with ichthyosis vulgaris, an inherited dry, scaly skin disorder, who also have filaggrin mutations do not have clinical skin inflammation that is characteristic of AD (9). Therefore, additional factors are necessary to interact with filaggrin in the pathogenesis of AD.

We agree with the authors that future studies of the effects of breast-feeding on the development and expression of allergy should be based on immunoglobulin E–mediated symptoms and not solely on the evaluation of AD. In our review, we stated that future studies examining the association between breast-feeding and allergy development should evaluate for immunoglobulin E–confirmed allergic disease (by examining both clinical symptoms and IgE testing simultaneously) and not just the presence of allergic sensitization. In addition, we recommend that each type of allergic disease be examined separately, rather than being grouped into the same category. This would serve to elucidate more precisely the complex relation between specific breast milk factors and the development of different types of allergic disease.

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REFERENCES

1. Hogan MB, Peele K, Wilson NW, et al. Skin barrier function and its importance at the start of the atopic march. J Allergy (Cairo) 2012; 2012:901940.
2. Zheng T, Yu J, Oh MH, et al. The atopic march: progression from atopic dermatitis to allergic rhinitis and asthma. Allergy Asthma Immunol Res 2011; 3:67–73.
3. Oyoshi MK, Murphy GF, Geha RS. Filaggrin-deficient mice exhibit TH17-dominated skin inflammation and permissiveness to epicutaneous sensitization with protein antigen. J Allergy Clin Immunol 2009; 124:485–493.493.e1.
4. Eigenmann PA, Sicherer SH, Borkowski TA, et al. Prevalence of IgE-mediated food allergy among children with atopic dermatitis. Pediatrics 1998; 101:E8.
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6. Werfel T, Ballmer-Weber B, Eigenmann PA, et al. Eczematous reactions to food in atopic eczema: position paper of the EAACI and GA2LEN. Allergy 2007; 62:723–728.
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8. Henderson J, Northstone K, Lee SP, et al. The burden of disease associated with filaggrin mutations: a population-based, longitudinal birth cohort study. J Allergy Clin Immunol 2008; 121:872–877.e9.
9. Smith FJ, Irvine AD, Terron-Kwiatkowski A, et al. Loss-of-function mutations in the gene encoding filaggrin cause ichthyosis vulgaris. Nat Genet 2006; 38:337–342.
© 2013 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology,