Food allergy: A trigger for atopic dermatitis?

September 23, 2019

Recommendations for whether to test for and treat food allergy in the setting of atopic dermatitis have changed.

Pediatricians might know that food allergy and atopic dermatitis (AD) often coexist. What they might not realize is that food allergy rarely is a primary cause of AD, or eczema, according to Pooja Varshney, MD, clinical assistant professor of Pediatrics at Dell Medical School at the University of Texas at Austin and a pediatric allergist at Dell Children’s Medical Center, Austin.

“We know that AD and food allergy often travel with each other, along with other allergic conditions like rhinitis and asthma. The question often presented to pediatricians is whether a food allergy is causing a child’s AD or causing it to flare,” says Varshney, who spoke on the topic in July during the Society for Pediatric Dermatology 44th Annual Meeting in Austin, Texas.

Cow’s milk, hen’s egg, peanut, wheat, soy, tree nuts, fish, and shellfish are responsible for more than 90% of food allergy in children.1 Nearly 40% children with moderate-to-severe AD have immunoglobulin E- (IgE-) mediated food allergy.2

Pediatricians should keep in mind that patients with AD, especially those with more severe disease, are likely to have or develop food allergy, according to Varshney, and it’s important to identify whether AD patients have food allergy with IgE-mediated symptoms, which is seen soon after eating foods. “Ask food allergy screening questions in children that have AD, certainly if it is moderate-to-severe,” she says. This is a test of the emergency system. Please be advised that in the case of a real emergency

However, whether foods are actually triggering AD can be much harder to determine. A history of eczema flaring soon after ingestion of a food, either through the child’s diet or through the diet of a breastfeeding mother, is difficult to differentiate from the natural waxing and waning of AD disease.

What’s a pediatrician to do?

There isn’t much evidence to support eliminating foods from moms’ or children’s diets to help their eczema improve, and elimination diets have real risks, according to Varshney.

“The risk-to-benefit ratio is really changing. Recent studies have shown that elimination of foods from a child’s diet rarely improves AD and [a child] very well may have increasing risk of developing anaphylactic food allergy if he or she avoids a food unnecessarily. This is particularly true of a child who was previously able to eat the food without any immediate or anaphylactic symptoms,” Varshney says.3,4

The recommendation to avoid unnecessary elimination diets is a paradigm shift in thinking, Varshney says. A recent guideline published by the National Institute of Allergy and Infectious Diseases (NIAID) helps guide pediatricians and others in the care of young children who have AD in how to introduce foods. The current NIAID guidelines help pediatricians identify patients that may most benefit from allergy evaluation, as well as guide patients at no or low risk for peanut allergy.5

“I think a main take-home of the guidelines is if a baby has mild-to-moderate AD, we really do not need to test before food introduction. We really want these assessments and conversations to be happening early-at the 4- to 6-month well checks,” Varshney says. “In those infants who have severe AD, testing is recommended before giving the baby peanut. We really are looking to identify babies with severe AD or those who already have a food allergy, particularly to egg, as they are at highest risk of peanut allergy but also stand to benefit most from early introduction if not allergic. That’s when early testing is suggested.”5

Varshney also points pediatricians to a recent American Academy of Pediatrics (AAP) guideline looking specifically at nutritional interventions for prevention of atopic disease. The guideline reports no benefit from using hydrolyzed formulas or changing maternal diet for the development of allergy, according to Varshney.6 It’s a field that’s constantly evolving, she says.

The diagnosis of food allergy tends to be more reliable when it’s based on and guided by a thorough history and physical exam. Whereas allergy testing is useful to confirm IgE-mediated food allergy, it has its limitations. Food IgE panels are not recommended because they can result in misdiagnosis of food allergy, Varshney says.

There’s also unnecessary and potentially harmful testing going on. Varshney says some naturopathic and nontraditional providers utilize inappropriate or disproven testing, including food immunoglobulin G (IgG) panels and muscle testing. These tests are not recommended and often lead to unnecessary elimination diets. Pediatricians need to firmly but gently educate their patients about the pitfalls of such testing and risks of inappropriate elimination diets in children, she says.

Testing is most useful when pediatricians determine or suspect that a patient has an immediate or IgE-type food allergy, Varshney says.

“All patients with a suspected food allergy should be seen by a board-certified allergist trained in food allergy. Whether the pediatrician orders any blood testing or defers the full evaluation to the allergist is dependent on the physician. Consultation with an allergist allows for additional testing like skin prick testing, food challenge, as well as follow-up because we know that certain food allergies-particularly milk and egg-are commonly outgrown,” Varshney says. “Testing can help determine the course of a particular child’s food allergy. Peanut allergy is less commonly outgrown but is outgrown in about 20% of kids, so we do need to follow these kids.”

Pediatricians should recommend that patients with IgE-type food allergy strictly avoid the food until seeing the allergist and consider prescribing injectable epinephrine in case of a severe reaction.

Eczema and food allergy often coexist

Varshney says there are a few theories about why eczema and food allergy often coexist.

The idea of the “atopic march” is one. The theory describes the progression of allergic disease seen in many children who have allergies, starting with AD and food allergy early on. Then these children typically go on to develop other allergic conditions such as allergic rhinitis and allergic asthma.

Another idea has to do with sensitization through the skin. So, children with a defective skin barrier, which is a big part of AD, are more susceptible to allergens, including food allergens, that penetrate the skin and activate the immune system to develop an abnormal or allergic response to food.7

Still other theories revolve around the thinking that these conditions aren’t actually a cause-and-effect but rather travel together, perhaps due to genetic predisposition.8

“We know genetic abnormalities and certain mutations exist with both those conditions. So perhaps the conditions are just different expressions of a particular patient’s genetic predisposition to developing allergic disease,” Varshney says. “This is an active area of research looking at how early intervention for AD may reduce the rate of food allergy development.”

That includes ongoing research looking at whether starting treatments such as dupilumab early in life can help prevent or halt the atopic march, she says.

In the meantime, attention to the skin barrier with thick emollients and moisturizers is a low-cost and low-risk intervention that pediatricians can recommend early on. It might be an intervention to help prevent the atopic march for at-risk infants, according to Varshney, but that’s not yet clear.

Disclosures:

Dr. Varshney discloses the following: Food Allergy Research and Education, clinical network grant, principal investigator and medical director; Aimmune, principal investigator; DBV Technologies, principal investigator.

References:

1. Bergmann MM, Caubet JC, Boguniewicz M, Eigenmann PA. Evaluation of food allergy in patients with atopic dermatitis. J Allergy Clin Immunol Pract. 2013;1(1):22-28.

2. Eigenmann PA, Beyer K, Lack G, et al. Are avoidance diets still warranted in children with atopic dermatitis? Pediatr Allergy Immunol. July 5, 2019. Epub ahead of print.

3. Du Toit G, Roberts G, Sayre PH, et al; LEAP Study Team. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med. 2015;372(9):803-813.

4. Fleischer DM, Bock SA, Spears GC, et al. Oral food challenges in children with a diagnosis of food allergy. J Pediatr. 2011 Apr;158(4):578.e1-583.e1.

5. 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.e7-173.e7.

6. Greer FR, Sicherer SH, Burks AW; Committee on Nutrition; Section on Allergy and Immunology. The effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, hydrolyzed formulas, and timing of introduction of allergenic complementary foods. Pediatrics. 2019;143(4):e20190281.

7. Natsume O, Ohya Y. Recent advancement to prevent the development of allergy and allergic diseases and therapeutic strategy in the perspective of barrier dysfunction. Allergol Int. 2018;67(1):24-31.

 

8. Kim J, Kim BE, Leung DYM. Pathophysiology of atopic dermatitis: clinical implications. Allergy Asthma Proc. 2019;40(2):84-92.