Food Allergy and Atopic Dermatitis: Fellow Travelers or Triggers?
Many children with atopic dermatitis also have an allergy to one or more foods, but the presence of these two conditions in an individual does not necessarily indicate a causal link between them. Testing and interpretation, sometimes with specialist consultation, may be required to discern whether food allergy is present in a child with atopic dermatitis and—if it is present—whether the food is triggering or exacerbating signs and symptoms of atopic dermatitis. Recent milestone trials have demonstrated that early introduction of peanuts can reduce the development of peanut allergy in at-risk children. Parents may benefit from education about current revised guidelines that now recommend offering peanut-containing foods to most children at the time he or she is ready for solid food.
Semin Cutan Med Surg 36(supp4):S95-S97
© 2017 published by Frontline Medical Communications
Atopic dermatitis; avoidance; food allergy; peanut
Food allergy is common among children with atopic dermatitis. About one-quarter to one-third of children with atopic dermatitis have immunoglobulin E (IgE)-mediated
clinical reactivity to food proteins.1,2 For comparison, about 5% of infants and young children and 2% of adults in the United States have food allergies.3 Analysis of 18 popula- tion-based studies determined that the rate of food allergy was as much as 6 times higher in children 3 months of age with atopic dermatitis compared with healthy controls (odds ratio, 6-18; 95% confidence interval 2.94-12.98; P<0.001). Some data suggest that food allergy is linked to relatively severe atopic dermatitis.4
Conversely, atopic dermatitis is more common in those with food allergy than it is in the general population, with an estimated 35% to 71% of patients with food allergy also having atopic dermatitis.5
Participants should read the activity information, review the activity in its entirety, and complete the online post-test and evaluation. Upon completing this activity as designed and achieving a passing score on the post-test, you will be directed to a Web page that will allow you to receive your certificate of credit via e-mail or you may print it out at that time.The online post-test and evaluation can be accessed at http://tinyurl.com/atopicdermsupl2017.
Inquiries about CME accreditation may be directed to the University of Louisville Office of Continuing Medical Education & Professional Development (CME & PD) at [email protected] or (502) 852-5329.
Lawrence F. Eichenfield, MD
Linda F. Stein Gold, MD
Wynnis L. Tom, MD
Physicians: This activity has been planned and implemented in accor- dance with the requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of the University of Louisville and Global Academy for Medical Education, LLC. The University of Louisville is accredited by the ACCME to provide continuing medical education for physicians.
The University of Louisville Office of Continuing Medical Education & Professional Development designates this enduring material for a maximum of 1.75 AMA PRA Category 1 CreditTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Nurses: Postgraduate Institute for Medicine is accredited with distinction as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation.This educational activity for 1.6 contact hour is provided by the Postgraduate Institute for Medicine. Designated for 0.8 contact hours of pharmacotherapy credit for Advance Practice Nurses.
Recent research into the pathophysiology of atopic dermatitis has yielded two new treatments—the first ones to receive US Food and Drug Administration (FDA) approval for management of this condition in more than a decade. Both new therapies offer novel mechanisms of action. Crisaborole, a topical medi- cation that inhibits the phosphodiesterase-4 (PDE-4) enzyme, is approved for the treatment of mild to moderate disease in adults and children as young as 2 years old. Dupilumab, the first biologic therapy approved for use in atopic dermatitis, inhibits interleukin (IL)-4 and IL-13. It is indicated for the treatment of moderate to severe disease in adults whose disease is inadequately controlled with topical prescription therapies, or when those therapies are inadvisable.
Awareness of the substantial impact atopic dermatitis can have on quality of life can facilitate patient-clinician conversations about treatment goals. Such discussions may influence shared decision-making about therapeutic choices.
Therapeutic patient education has been applied to a variety of conditions and is now being studied in atopic dermatitis.
Food allergy and infection represent common comorbidities in patients with atopic dermatitis. New information about the benefit of the early introduction of peanuts to the diet has surfaced in recent years. Alterations in the skin microbiome may underlie the association of colonization and infection in atopic dermatitis. Preliminary research attempts to deploy the atopic patient’s “good” bacteria to reduce Staphylococcus aureus colonization.
Brief, expert reviews of the literature in these areas can help busy providers stay current in a rapidly evolving field, and can facilitate the translation of research into clinical practice to improve outcomes.
By reading and studying this supplement, participants should be better able to:
- Demonstrate an understanding of how atopic dermatitis can affect patient sleep, quality of life, daily activities, risk of comorbidities, and health care utilization/cost
- Explain the mechanism of action and clinical trials data supporting recently approved treatments for atopic dermatitis
- Discuss investigation therapies for atopic dermatitis
- Apply recent recommendations for evaluation of candidates for systemic treatment of atopic dermatitis
- Explain the benefit of providing patients with a written action plan
- Analyze the relationships of food allergy and infection to atopic dermatitis.
Individuals in a position to control the content of this educational activity are required to disclose: 1) the existence of any relevant financial relationship with any entity producing, marketing, re-selling, or distributing health care goods or services consumed by, or used on, patients with the exemption of non-profit or government organizations and non-health care related companies, within the past 12 months; and 2) the identification of a commercial product/device that is unlabeled for use or an investigational use of a product/device not yet approved.
Lawrence F. Eichenfield, MD, Advisory Board/Speaker: Valeant Pharmaceuticals North America LLC. Consultant: Eli Lilly and Company, Genentech, Inc., Otsuka America Pharmaceutical, Inc./Medimetriks Pharmaceuticals, Inc., Pfizer Inc., Sanofi Genzyme/Regeneron Pharmaceuticals, TopMD, Valeant. Investigator: Sanofi Genzyme/Regeneron.
Linda F. Stein Gold, MD, Consultant: Pfizer. Grant/Research: GlaxoSmithKline and Pfizer. Data Monitoring Committee: Otsuka.
Wynnis L. Tom, MD, Consultant: Pfizer. Grant/Research: Pfizer, Celgene Corporation, Pfizer, and Regeneron.
University of Louisville CME & PD Advisory Board and Staff Disclosures:
The CME & PD Advisory Board and Staff have nothing to disclose.
CME/CE Reviewers: University of Louisville Cindy England Owen, MD, has nothing to disclose. The Postgraduate Institute of Medicine planners and managers Trace Hutchison, PharmD; Samantha Mattiucci, PharmD, CHCP; Judi Smelker-Mitchek, MBA, MSN, RN; and Jan Schultz, MSN, RN, CHCP, have nothing to disclose.
Global Academy for Medical Education Staff: Eileen McCaffrey, MA; Tristan M. Nelsen, MNM, CMP, HMCC; Sylvia H. Reitman, MBA, DipEd; and Ron Schaumburg have nothing to disclose.
Off-Label/Investigational Use Disclosure
This CME/CE activity discusses the off-label use of certain approved medica- tions as well as data from clinical trials on investigational agents. Any such material is identified within the text of the articles.
This continuing medical education (CME/CE) supplement was developed from a satellite symposium held at the Skin Disease Education Foundation’s 18th Annual Las Vegas Dermatology Seminar, November 3, 2017, in Las Vegas, Nevada. The Guest Editors acknowledge the editorial assistance of Global Academy for Medical Education and Eileen McCaffrey, MA, medical writer, in the development of this supplement. The manuscript was reviewed and approved by the Guest Editors as well as the Editors of Seminars in Cutaneous Medicine and Surgery. The ideas and opinions expressed in this supplement are those of the Guest Editors and do not necessarily reflect the views of the supporter, Global Academy for Medical Education, the University of Louisville, Postgraduate Institute for Medicine, or the Publisher.
Eigenmann PA, Sicherer SH, Borkowski TA, Cohen BA, Sampson HA. Prevalence of IgE-mediated food allergy among children with atopic dermatitis. Pediatrics. 1998;101(3):E8.
Mavroudi A, Karagiannidou A, Xinias I, et al. Assessment of IgE-mediated food allergies in children with atopic dermatitis. Allergol Immunopathol (Madr). 2017;45(1):77-81.
FDA. Food Allergen Labeling and Consumer Protection Act of 2004. http://www. fda.gov/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/ Allergens/ucm106890.htm. Accessed October 23, 2017.
Tsakok T, Marrs T, Mohsin M, et al. Does atopic dermatitis cause food allergy? A systematic review. J Allergy Clin Immunol. 2016;137(4):1071-1078.
Boyce JA, Assa’ad A, Burks AW, et al. Guidelines for the diagnosis and manage- ment of food allergy in the United States: report of the NIAID-sponsored expert panel. J Allergy Clin Immunol. 2010;126(6 Suppl):S1-58.
Sidbury R, Tom WL, Bergman JN, et al. Guidelines of care for the management of atopic dermatitis: section 4. Prevention of disease flares and use of adjunctive therapies and approaches. J Am Acad Dermatol. 2014;71(6):1218-1233.
Eller E, Kjaer HF, Host A, Andersen KE, Bindslev-Jensen C. Food allergy and food sensitization in early childhood: results from the DARC cohort. Allergy. 2009;64(7):1023-1029.
Spergel JM, Boguniewicz M, Schneider L, Hanifin JM, Paller AS, Eichenfield LF. Food allergy in infants with atopic dermatitis: limitations of food-specific IgE measurements. Pediatrics. 2015;136(6):e1530-1538.
Fleischer DM, Bock SA, Spears GC, et al. Oral food challenges in children with a diagnosis of food allergy. J Pediatr. 2011;158(4):578-583.e571.
Chang A, Robison R, Cai M, Singh AM. Natural history of food-triggered atopic dermatitis and development of immediate reactions in children. J Allergy Clin Immunol Pract. 2016;4(2):229-236.e221.
American Academy of Pediatrics. Committee on Nutrition. Hypoallergenic infant formulas. Pediatrics. 2000;106(2 Pt 1):346-349.
Greer FR, Sicherer SH, Burks AW. Effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, timing of introduction of complementary foods, and hydrolyzed formulas. Pediatrics. 2008;121(1):183-191.
Du Toit G, Katz Y, Sasieni P, et al. Early consumption of peanuts in infancy is associated with a low prevalence of peanut allergy. J Allergy Clin Immunol. 2008;122(5):984-991.
Katz Y, Rajuan N, Goldberg MR, et al. Early exposure to cow’s milk protein is protective against IgE-mediated cow’s milk protein allergy. J Allergy Clin Immunol. 2010;126(1):77-82.e71.
Koplin JJ, Osborne NJ, Wake M, et al. Can early introduction of egg prevent egg allergy in infants? A population-based study. J Allergy Clin Immunol. 2010; 126(4):807-813.
Du Toit G, Roberts G, Sayre PH, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med. 2015;372(9):803-813.
Du Toit G, Sayre PH, Roberts G, et al. Effect of avoidance on peanut allergy after early peanut consumption. N Engl J Med. 2016;374(15):1435-1443.
Togias A, Cooper SF, Acebal ML, et al. Addendum guidelines for the prevention of peanut allergy in the United States: report of the National Institute of Allergy and Infectious Diseases-sponsored expert panel. Ann Allergy Asthma Immunol. 2017;118(2):166-173.e7.
*Associate Clinical Professor of Dermatology and Pediatrics, University of California, San Diego School of Medicine, Rady Children’s Hospital, San Diego, California
Publication of this CME/CE article was jointly provided by University
of Louisville, Postgraduate Institute for Medicine, and Global Academy for Medical Education, LLC, and is supported by an educational grant from Pfizer Inc. Dr Tom has received an honorarium for her participation in this activity. She acknowledges the editorial assistance of Eileen McCaffrey, MA, medical writer, and Global Academy for Medical Education in the development of this continuing medical education journal article.
Wynnis L. Tom, MD, Consultant: Pfizer. Grant/Research: Pfizer, Celgene Corporation, Pfizer, and Regeneron.
Address reprint requests to: Wynnis Tom, MD, Rady Children’s Hospital, 8010 Frost Street, San Diego, CA 92123; [email protected]
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