Atopic dermatitis increases the effect of exposure to peanut antigen in dust on peanut sensitization and likely peanut allergy

How Does Eczema Increase the Risk of Food Allergies?

Eczema, or atopic dermatitis, is an inflammatory skin disorder. In young children, it also is a risk factor for developing food allergies, but why this link exists is unclear.

A new NIH-funded study suggests that exposure to peanut dust increases the risk of peanut allergy, especially for kids with severe eczema. The results lend weight to the idea that exposure to allergens through broken skin may contribute to food allergies for children with eczema.

Atopic dermatitis increases the effect of exposure to peanut antigen in dust on peanut sensitization and likely peanut allergy 

• Helen A. Brough, MSc, FRCPCH^a, 
• Andrew H. Liu, MD^b, 
• Scott Sicherer, MD^c, 
• Kerry Makinson, MSc^a,
• Abdel Douiri, PhD^e, 
• Sara J. Brown, MD^d, 
• Alick C. Stephens, PhD^a, 
• W.H. Irwin McLean, PhD, DSc, FRSE, FMedSci^d, 
• Victor Turcanu, PhD^a, 
• Robert A. Wood, MD^f, 
• Stacie M. Jones, MD^g, 
• Wesley Burks,MD^h, 
• Peter Dawson, PhDⁱ, 
• Donald Stablein, PhDⁱ, 
• Hugh Sampson, MD^c, ∗, 
• Gideon Lack, MD^a, , ∗, 

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Background

History and severity of atopic dermatitis (AD) are risk factors for peanut allergy. Recent evidence suggests that children can become sensitized to food allergens through an impaired skin barrier. Household peanut consumption, which correlates strongly with peanut protein levels in household dust, is a risk factor for peanut allergy.

Objective

We sought to assess whether environmental peanut exposure (EPE) is a risk for peanut sensitization and allergy and whether markers of an impaired skin barrier modify this risk.

Methods

Peanut protein in household dust (in micrograms per gram) was assessed in highly atopic children (age, 3-15 months) recruited to the Consortium of Food Allergy Research Observational Study. History and severity of AD, peanut sensitization, and likely allergy (peanut-specific IgE, ≥5 kU_A/mL) were assessed at recruitment into the Consortium of Food Allergy Research study.

Results

There was an exposure-response relationship between peanut protein levels in household dust and peanut skin prick test (SPT) sensitization and likely allergy. In the final multivariate model an increase in 4 log₂ EPE units increased the odds of peanut SPT sensitization (1.71-fold; 95% CI, 1.13- to 2.59-fold; P = .01) and likely peanut allergy (PA; 2.10-fold; 95% CI, 1.20- to 3.67-fold; P < .01). The effect of EPE on peanut SPT sensitization was augmented in children with a history of AD (OR, 1.97; 95% CI, 1.26-3.09; P < .01) and augmented even further in children with a history of severe AD (OR, 2.41; 95% CI, 1.30-4.47; P < .01); the effect of EPE on PA was also augmented in children with a history of AD (OR, 2.34; 95% CI, 1.31-4.18; P < .01).

Conclusion

Exposure to peanut antigen in dust through an impaired skin barrier in atopically inflamed skin is a plausible route for peanut SPT sensitization and PA.

Key words

• Atopic dermatitis; 
• peanut sensitization; 
• peanut allergy; 
• environmental peanut exposure; 
• dust

Abbreviations used

• AD, Atopic dermatitis; 
• CoFAR, Consortium of Food Allergy Research; 
• EPE, Environmental peanut exposure; 
• FLG, Filaggrin; 
• IQR, Interquartile range; 
• LLQ, Lower limit of quantitation; 
• LR, Logistic regression; 
• OR, Odds ratio; 
• PA, Peanut allergy; 
• sIgE, Specific IgE; 
• SPT, Skin prick test

Funded by Action Medical Research (S/P/4529) and supported by the National Institute for Health Research(NIHR) Biomedical Research Centre at Guy's and St Thomas' NHS Foundation Trust and King's College London and National Institutes of Health (NIH)/National Institute of Allergy and Infectious Disease (NIAID) grants U19AI066738 and U01AI066560. The project was also supported by grants UL1 TR-000154 (National Jewish), UL1 TR-000067 (Mount Sinai), UL1 TR-000039 (Arkansas), UL1 TR-000083 (University of North Carolina), and UL1 TR-000424 (Johns Hopkins) from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH). Its contents are solely the responsibility of the authors and do not necessarily represent the official view of the BRC, NCRR, or NIH. This work was supported by the Wellcome Trust (Intermediate Clinical Fellowship WT086398MA to S.J.B. and Strategic Award 098439/Z/12/Z to W.H.I.M.).

Disclosure of potential conflict of interest: H. A. Brough has received research support from the Department of Health through the National Institute for Health Research (NIHR) comprehensive Biomedical Research Centre award to Guy's & St. Thomas' NHS Foundation Trust in partnership with King's College London and King's College Hospital NHS Foundation Trust, Action Medical Research, UK and Food Allergy Research and Education (FARE), US. S. Sicherer is a member of the American Board of Allergy and Immunology; has consultant arrangements with Food Allergy Research and Education (FARE) and Novartis; has received research support from the National Institute of Allergy and Infectious Disease (NIAID) and Food Allergy Research and Education; has received royalties from UpToDate; and is an Associate Editor for the Journal of Allergy and Clinical Immunology and the Journal of Allergy and Clinical Immunology: In Practice. K. Makinson has received research support from the Immune Tolerance Network, National Institutes of Health(NIH). A. Douiri has received research support from the National Institute for Health Research. S. J. Brown has received research support from the Wellcome Trust Intermediate Clinical Fellowship (WT086398MA) and has received honorarium for speaking at the American Academy of Allergy, Asthma & Immunology annual meetings in 2012 and 2013. W. H. I. McLean has received research support from the Wellcome Trust. R. A. Wood has consultant arrangements with the Asthma and Allergy Foundation of America, is employed by Johns Hopkins University, has received research support from the NIH, and has received royalties from UpToDate. S. M. Jones has received research support from the NIAID, DBV Technologies, and Dyax; has consultant arrangements with the Gerson Lehrman Group; has received payment for lectures from Mercy Children's Hospital, the Greater Kansas City Allergy Society, the European Academy of Allergy and Clinical Immunology, and Riley Children's Hospital. W. Burks is a board member for the American Academy of Allergy, Asthma & Immunology, the Food Allergy Initiative, the Journal of Allergy and Clinical Immunology, the US Food and Drug Administration, and the NIH Study Section; has consultant arrangements with Abbott Laboratories, Dow AgroSciences, McNeill Nutritionals, Merck, Novartis Pharma AG, Schering Plough, GLG Research, ExploraMed Development, Regeneron Pharmaceuticals, and Unilever; is employed by the University of North Carolina; has received research support from Hycor Biomedical; has received payment for lectures from Mylan Specialty; has the following patents: US5558869, US5973121, US6441142, US6486311, US6835824, US7485708, US7879977; receives royalties from UpToDate; has received payment for development of educational presentations from Current Views 2012; and is a minority stockholder in Allertein and Mastcell Pharmaceuticals. P. Dawson has received research support from the NIH. D. Stablein has received research support from the NIH. H. Sampson has received research support from the NIAID and NIH; has received funding supporting clinical trials in milk and wheat allergy from Food Allergy Research and Education; is the chair of the PhARF Award review committee; has consultant arrangements with Allertein Therapeutics, Regeneron, and Danone Research Institute; and has received payment for lectures from Thermo Fisher Scientific, UCB, and Pfizer. G. Lack has received research support from the Department of Health through the National Institute for Health Research (NIHR) comprehensive Biomedical Research Centre award to Guy's & St. Thomas' NHS Foundation Trust in partnership with King's College London and King's College Hospital NHS Foundation Trust and Action Medical Research, UK; is a member of the Scientific Advisory Board for DBV Technologies; has consultant arrangements with the Anaphylaxis Campaign and the National Peanut Board; has received payment for lectures from Sodilac, Novartis, Nestle Nutrition, GlaxoSmithKline, and Serono Symposia International Foundation; and has stock/stock options with DBV Technologies. The rest of the authors declare that they have no relevant conflicts of interest.

Corresponding author: Gideon Lack, MD, Children's Allergy Service, 2nd Floor, Stairwell B, South Wing, Guy's and St Thomas' NHS Foundation Trust, Westminster Bridge Rd, London SE1 7EH, United Kingdom.

∗

These authors contributed equally to this work.

Copyright © 2014 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.

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