Food Allergy in Atopic Dermatitis

Sandipan Dhar and Sahana M Srinivas1

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Abstract
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Introduction
What was known?
Food allergy can exacerbate atopic dermatitis and hence routine diet elimination would
decrease the severity of AD.
Atopic dermatitis (AD) is a chronic, relapsing, inflammatory skin disease characterized by
pruritus and eczematous skin lesions. It is often associated with increased serum IgE levels
and personal and family history of “atopic diathesis” which includes type 1 allergies, allergic
rhinitis, and asthma.[1,2,3] The pathogenesis of AD is complex with multifactorial etiology
involving genetic, immunological, and environmental factors leading to disrupted skin barrier
and immune system.[4] Environmental factors include microbes, irritants, and extremes of
temperature, psychological stress, and food allergens.[5,6] There are many studies
demonstrating the role of food allergens in triggering or exacerbating in small set of AD
patients. Around 60% of children develop AD by 1st year of life with food allergies
developing early in this group.
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Food Allergy and Atopic Dermatitis

Clinical studies have documented the prevalence of food allergy in AD from 20% to 80%.[7]
Common food allergens triggering AD are milk and milk products, peanuts, eggs, soy, wheat,
seafood, and shellfish.[8] Many studies have documented that food allergy plays an important
role in exacerbating severe form of AD and diet elimination will decrease the severity. An
open pilot study conducted by Dhar and Banerjee on the effects of dietary elimination in AD
in 100 Indian children showed statistically significant decrease in the severity score after
dietary elimination alone. A group of 100 children without systemic disease and not on
systemic steroids were assessed for severity of AD by SCORAD index. They were advised to
strictly avoid diet containing milk and milk products, nuts, nut containing foods, egg, sea fish
and prawns, brinjal, and soybean, for 3 weeks. To maintain proper nutrition, they were asked
to take lots of dal, rohu fish, chicken, and fruits. After 3 weeks, the severity of AD was
measured and showed significant improvement.[9]
Werfel et al., compiled the results of eight studies and found a prevalence of food allergy
proven by double-blind placebo-controlled food challenge (DBPCFC) to be 33%–63%.[10]
In a study of Japanese nursery school children, increased serum IgE levels, maternal history
of atopy, and food allergy was linked to developing AD in children <6 months of age.[11] On
the contrary, there are few studies with no temporal association of food allergy and AD.
Guillet, et al. in a study of cohort of 250 children found a direct correlation between food
allergy and increased severity of AD.[12] Few studies have shown that patients suffering
from food allergy have been significantly associated with allergic rhinitis, bronchial asthma,
and persistent eczematous reactions.[13]
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Pathophysiology of Aggravation of Atopic Dermatitis with Food

Raw food ingestion and effects of foodborne microbes on the intestinal flora may affect the
development of food allergy in AD. Skin barrier plays an important role as it prevents entry
of pathogens and allergens. Filaggrin gene defect in AD increases the risk of AD. In AD,
there is an epidermal barrier dysfunction leading to entry of food allergens and subsequent
percutaneous and mucosal sensitization.[14] The pathogenesis of AD associated food allergy
is complex. Due to the break in the skin, Langerhans cell gets exposed to allergens, which
trigger an immediate or delayed type of reaction causing inflammation.[15]
Exacerbation of AD by food occurs by increased binding of antigen to immature gut
microvillus, increased intestinal permeability that initiates immune responses, with primarily
altered antigen transfer. The gut bacterial pathogen acts as infectious agent and superantigen
thus exacerbating AD by food.[16,17] Through sensitization, atopic march can result in food
allergies, environmental allergies, asthma, and eosinophilic esophagitis. Immediate types of
allergic reactions are IgE mediated type III, activating the complement system whereas
delayed reactions are mediated by T-cells and activated eosinophils.[17]
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Clinical Features
Food allergy in AD may result in IgE-mediated immediate and non-IgE mediated late
eczematous reactions. 40%–60% constitute IgE-mediated food allergy. Food allergy can
manifest as flares, hives, pruritus, and other cutaneous symptoms in the absence of AD flare.
Reactions can occur in the skin, oropharynx, gastrointestinal, respiratory, and cardiovascular
systems.[8] Immediate IgE-mediated reactions occur within few minutes to hours after
ingestion of food. Cutaneous reactions include urticaria, angioedema, pruritus, erythema,
morbilliform eruptions, contact urticaria, and allergic contact dermatitis. The most common
reactions are acute urticaria with or without angioedema. These reactions give rise to pruritus
and in return exacerbate or worsen preexisting AD. Nondermatological manifestations
include vomiting, diarrhea, abdominal pain, rhinitis, asthma, and anaphylaxis.[18] In a study
of 113 children with severe AD, 63 children had developed symptoms after food challenge
within 2 h with a recurrence of pruritus in few after 6–8 h.[19] In a recent study of soy allergy
in patients suffering from AD, early reactions was seen in 2.8% cases. One-third of patients
(27.2%) were sensitized to soy without clinical symptoms.[20]
Late non-IgE mediated eczematous reactions rarely occur, and their pathogenesis is not very
clear. Delayed reactions develop after 2-6 days following ingestion of allergen food. This
reaction has also been described as “food responsive eczema.” Late reactions can occur as
isolated phenomenon or along with immediate type reaction.[21] Only few studies have
documented the late phase reactions. Rowlands et al. in their study, described that out of the
58 DBPCFCs only 1 had eczematous food reactions.[22] Breuer et al. in his study of food
challenge in 106 children for cow's milk, hen's egg, wheat, soy; isolated eczematous reaction
was seen in 6% and combined reactions in 21%.[21]
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Diagnosis
Diagnosis of food allergy is not based on history or clinical examination. Parents giving a
history of exacerbation of AD due to food should not be taken as a reliable indicator. There
are many tests available but must be interpreted properly as there is a high rate of false-
positive reaction with low predictive value. An expert panel set up for publishing guidelines
for AD reviewed the literature and found that multiple studies demonstrated 50%–90% of
presumed food allergy are not allergies.[23] Many patients may have sensitization but may
not develop symptoms. Diagnoses of IgE-mediated reactions require sensitization and
development of symptoms. In recent guidelines put forward by American Academy of
Dermatology, they have recommended testing of children younger than 5 years for food
allergy with intractable pruritus.[24]
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Investigations
Several investigations done to confirm food allergy are increased serum IgE, skin prick test
(SPT), skin application food test, radio allergen sorbent test, atopic patch test, and oral
challenge test (DBPCFC). IgE-mediated immediate reactions can be evaluated by SPT and
allergen-specific serum IgE tests. These tests done alone are not diagnostic as the give false
positive reaction and have low predictive value. The gold standard test for confirmation of
food allergy is DBPCFC.[8,25] Non-IgE mediated eczematous reactions are not assessed and
documented in many studies. In a study by Breuer et al., 106 children were administered with
DBPCFC; 43% were immediate reactions, 45% were immediate and late eczematous
reactions, and 12% were late eczematous reactions.[21] In another study of DBPCF C, 10%
of positive food challenges were not associated with food-specific IgE. In the same trial,
children were given exclusion diet of egg and milk and AD improved significantly.[26] In an
Indian study by Dhar and Saxena, SPT positivity to common food allergens were egg white,
fish, milk, brinjal, dal, groundnut, and banana.[27] Different studies have shown variation in
positive predictive value for atopic patch testing, hence not routinely performed. Routine
testing for food allergies is not recommended. It should be considered in young children with
intractable AD or with a history of a reaction following a specific food. A diagnostic
elimination diet may be helpful to improve AD.
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Dietary Elimination and Risk

Dietary elimination is not recommended routinely as there is not much evidence that has
demonstrated improvement in AD. Few studies have shown good improvement in AD with
dietary elimination. A Cochrane systematic review based on randomized controlled trials
(RCTs) have shown that eliminating egg or cow's milk did not show any benefit and do not
support the concept of dietary elimination.[28] Avoidance of food with proven food allergy
and confirmed by oral challenge elimination diet may be useful. In an RCT, 55 children with
AD with egg allergy proven by oral challenge showed good improvement with the exclusion
of egg in diet. In an open pilot Indian study of dietary elimination in 100 children, they
showed significant improvement in AD.[9]
Although food elimination is beneficial in one subset of AD, it has its own risk. Effects of
elimination diet include nutritional deficiency, affects growth and development of the child,
causes social isolation, may cause anaphylaxis following reintroduction of restricted food,
and low-quality health.[29] Food allergies decrease with age except with nuts. The patient
develops immunological tolerance to restricted food when reintroduced to the diet after
restriction for 6–12 months.[30] Parents should be advised to give complementary foods rich
in nutrients if elimination diet is followed.
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Conclusion
Food allergies are common in AD. A careful history and clinical approach are necessary to
detect food allergy as food elimination may give rise to a severe nutritional deficiency in
children. There is sufficient evidence in literature that food allergies exacerbate AD;
however, it should be diagnosed only after proven specific allergen tests. Although dietary
elimination improves AD, DBPCFC is the gold standard test to diagnose food allergies.
Parents should be counseled about the risks of food elimination and educated about myths
associated with food allergy.

Financial support and sponsorship

Nil.

Conflicts of interest
There are no conflicts of interest.
What is new?
There is not much evidence that food elimination routinely improves atopic dermatitis.
Avoidance of food with proven food allergy can be beneficial in improving moderate to
severe AD and hence food elimination is not recommended for management of AD.
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References
1. Dhar S, Banerjee R. Atopic dermatitis in infants and children in India. Indian J Dermatol
Venereol Leprol. 2010;76:504–13. [PubMed]
2. Dhar S, Kanwar AJ, Nagaraja Personal and family history of atopy in children with atopic
dermatitis in North India. Indian J Dermatol. 1997;42:9–13.
3. Dhar S, Malakar R, Chattopadhyay S, Dhar S, Banerjee R, Ghosh A. Correlation of the
severity of atopic dermatitis with absolute eosinophil counts in peripheral blood and serum
IgE levels. Indian J Dermatol Venereol Leprol. 2005;71:246–9. [PubMed]
4. Ring J, Alomar A, Bieber T, Deleuran M, Fink-Wagner A, Gelmetti C, et al. Guidelines for
treatment of atopic eczema (atopic dermatitis) part I. J Eur Acad Dermatol
Venereol. 2012;26:1045–60. [PubMed]
5. Dhar S, Kanwar AJ, Kaur S, Sharma P, Ganguly NK. Role of bacterial flora in the
pathogenesis & management of atopic dermatitis. Indian J Med Res. 1992;95:234–
8.[PubMed]
6. Morren MA, Przybilla B, Bamelis M, Heykants B, Reynaers A, Degreef H. Atopic
dermatitis: Triggering factors. J Am Acad Dermatol. 1994;31(3 Pt 1):467–73. [PubMed]
7. Werfel T, Breuer K. Role of food allergy in atopic dermatitis. Curr Opin Allergy Clin
Immunol. 2004;4:379–85. [PubMed]
8. Katta R, Schlichte M. Diet and dermatitis: Food triggers. J Clin Aesthet
Dermatol. 2014;7:30–6. [PMC free article] [PubMed]
9. Dhar S, Malakar R, Banerjee R, Chakraborty S, Chakraborty J, Mukherjee S. An
uncontrolled open pilot study to assess the role of dietary eliminations in reducing the
severity of atopic dermatitis in infants and children. Indian J Dermatol. 2009;54:183–5.[PMC
free article] [PubMed]
10. Werfel T, Ballmer-Weber B, Eigenmann PA, Niggemann B, Rancé F, Turjanmaa K, et al.
Eczematous reactions to food in atopic eczema: Position paper of the EAACI and
GA2LEN. Allergy. 2007;62:723–8. [PubMed]
11. Fukiwake N, Furusyo N, Takeoka H, Toyoda K, Kubo N, Kido M, et al. Association
factors for atopic dermatitis in nursery school children in Ishigaki Islands – Kyushu
University Ishigaki Atopic Dermatitis Study (KIDS) Eur J Dermatol. 2008;18:571–
4.[PubMed]
12. Guillet G, Guillet MH. Natural history of sensitizations in atopic dermatitis. A 3-year
follow-up in 250 children: Food allergy and high risk of respiratory symptoms. Arch
Dermatol. 1992;128:187–92. [PubMed]
13. Celakovská J, Bukac J. Analysis of food allergy in atopic dermatitis patients –
Association with concomitant allergic diseases. Indian J Dermatol. 2014;59:445–50.[PMC
free article] [PubMed]
14. De Benedetto A, Kubo A, Beck LA. Skin barrier disruption: A requirement for allergen
sensitization? J Invest Dermatol. 2012;132(3 Pt 2):949–63. [PMC free article][PubMed]
15. Hanifin JM. Evolving concepts of pathogenesis in atopic dermatitis and other eczemas. J
Invest Dermatol. 2009;129:320–2. [PubMed]
16. Majamaa H, Isolauri E. Evaluation of the gut mucosal barrier: Evidence for increased
antigen transfer in children with atopic eczema. J Allergy Clin Immunol. 1996;97:985–
90. [PubMed]
17. Thestrup-Pedersen K, Ring J. Atopic dermatitis: Summary of the 1st Georg Rajka
Symposium 1998 and a literature review. Acta Derm Venereol. 1999;79:257–64.[PubMed]
18. Wüthrich B. Food-induced cutaneous adverse reactions. Allergy. 1998;53(46 Suppl):131–
5. [PubMed]
19. Sampson HA, McCaskill CC. Food hypersensitivity and atopic dermatitis: Evaluation of
113 patients. J Pediatr. 1985;107:669–75. [PubMed]
20. Jarmila C, Kvetuše E, Karel E, Jaroslava V, Josef B. Soy allergy in patients suffering
from atopic dermatitis. Indian J Dermatol. 2013;58:325. [PMC free article] [PubMed]
21. Breuer K, Heratizadeh A, Wulf A, Baumann U, Constien A, Tetau D, et al. Late
eczematous reactions to food in children with atopic dermatitis. Clin Exp
Allergy. 2004;34:817–24. [PubMed]
22. Rowlands D, Tofte SJ, Hanifin JM. Does food allergy cause atopic dermatitis? Food
challenge testing to dissociate eczematous from immediate reactions. Dermatol
Ther. 2006;19:97–103. [PubMed]
23. Boyce JA, Assa’ad A, Burks AW, Jones SM, Sampson HA, Wood RA, et al. Guidelines
for the diagnosis and management of food allergy in the United States: Summary of the
NIAID-Sponsored expert panel report. J Am Acad Dermatol. 2011;64:175–92. [PubMed]
24. Sidbury R, Tom WL, Bergman JN, Cooper KD, Silverman RA, Berger TG, 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;71:1218–
33. [PMC free article] [PubMed]
25. Mohajeri S, Newman SA. Review of evidence for dietary influences on atopic
dermatitis. Skin Therapy Lett. 2014;19:5–7. [PubMed]
26. Niggemann B, Sielaff B, Beyer K, Binder C, Wahn U. Outcome of double-blind, placebo
controlled food challenge tests in 107 children with atopic dermatitis. Clin Exp
Allergy. 1999;29:91–6. [PubMed]
27. Dhar S, Saxena A. Evaluating of prick test in atopic dermatitis and chronic
urticaria. Indian J Dermatol. 1995;42:148–51.
28. Bath-Hextall F, Delamere FM, Williams HC. Dietary exclusions for established atopic
eczema. Cochrane Database Syst Rev. 2008;1:CD005203. [PubMed]
29. Przybilla B, Ring J. Food allergy and atopic eczema. Semin Dermatol. 1990;9:220–
5. [PubMed]
30. Sampson HA. The immunopathogenic role of food hypersensitivity in atopic
dermatitis. Acta Derm Venereol Suppl (Stockh) 1992;176:34–7. [PubMed]