Atopic Dermatitis

Etiologies​

Diet                                                                                                                                                                                                                  

• Broadly speaking, diet and food allergies as a cause of atopic dermatitis are uncommon and essentially never the sole cause of atopic dermatitis.  There are a couple of very good review articles and commentaries on this topic that I have come across. 

  • One is by Dr. Peter Lio who a is a pediatric dermatologist at Northwestern and proponent of alternative medicine, originally published in Cutis and then reprinted in Practical Dermatology. (36638380)  He does a good job providing a balanced paradigm for how diet relates to atopic dermatitis.  First, he acknowledges that there is a significant focus on diet as cause of disease which leads to 90% of parents believing their child's AD is caused by foods.  He is careful to point out that foods can contribute to AD, however, even trigger a flare, but that this is different than being causative.  For example, there are a number of foods that can cause nonimmunologic skin irritation due to their acidity or other properties, precipitating a flare of AD when contacting the skin.  Foods that may have that potential include:

    • ​citrus, corn, radish, mustard, garlic, onion, pineapple, many spices, food additives and preservatives​​

  • Dr. Lio points out the two main diagnostic modalities for identifying IgE-mediated food allergies which manifest with urticaria, angioedema, and potentially anaphylaxis.  ​Immunoenzymatic serum assay for IgE antibodies and intradermal skin prick testing are used to identify the potential for these allergies.  Allergies identified by this method, if accompanied by signs and symptoms of pruritus and histamine release after food ingestion, may contribute to AD flares by initiating scratching and leading to the itch-scratch-AD flare cycle.  

  • He describes the gold standard for identifying food-induced AD which is the double-blind placebo-controlled food challenged (DBPCFC).  In trials using this method, <1% of participants had immediate AD flares alone when ingesting foods, and the rates were no different from placebo.  However, 4% of participants developed AD flares along with other non-AD skin findings, which was greater than placebo.  This demonstrates that AD alone is an uncommon immediate manifestation of food allergy, but that if accompanied by other non-AD signs and symptoms it could contribute to a flare.  Delayed onset manifestations of AD occurred in 2.2% of participants and was no different than placebo.  Conclusion: exacerbation of AD in the absence of other signs of food allergy is unlikely to be related to food intake.  

• Another review article written primarily by allergists (mitigating potential specialty bias in favor of one's specialty being the more integral to the disease process), "Are avoidance diets still warranted in children with atopic dermatitis?" published in Pediatric Allergy and Immunology, advocates for limited testing for food allergens as a cause of atopic dermatitis.  The abstract provides a nice summary (31273833), but main points included:​​

  • 40% of children with moderate-severe AD have clinically significant food allergies.  Many children will demonstrate positive reactions on tests but have no clinically significant reaction. 

  • Postulates that IgE sensitization of oral food allergies may occur via the skin and not ingestion (i.e., skin contact with peanuts primes immune system, then peanut allergy is observed on first challenge with peanuts).  

  • They advocate the following plan:

    • First, good skin care routine.  Emollients, topical steroids, anti-itch plan.  Role of food often becomes minor if skin is addressed

    • Next, food history.  Tomato, eggplant, and parmesan cheese among many others may provoke just perioral erythema and does not warrant food allergy testing.  

    • If allergy testing warranted, restrict it to a subset of suspected foods based on history, often egg, milk, wheat, and rarely soy. Tests have good negative predictive value but like patch testing positive results must be clinically correlated.  Testing for other foods that could be a cause of severe anaphylactic reactions like peanuts, although not likely a cause of AD, may be warranted given the association between AD, food allergies that may contribute to AD, and anaphylactic food allergies.

    • If foods are identified via history and testing, a 2-3 week elimination trial can be attempted while continuing skin care.  Elimination may improve symptoms, but also may lead to progression of the allergy towards an anaphylactic response.  If no response is seen, food allergy is not proven.  If improvement is seen, rechallenge to establish the cause.  

    • Avoidance diets do not need to be complete.  Small amounts of a food like eggs or milk cooked in a baked good may be tolerable, prevent worsening of the allergy, and complete elimination will not likely lead to any additional improvement.

Contact Dermatitis                                                                                                                                                                                        

• The prevalence of contact dermatitis in children with atopic dermatitis appears to be higher, with ~50% greater odds of having more than 1 positive reaction.  Reaction to cocamidopropyl betaine was 3.7x more likely in AD patients than those without AD. 37768237

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