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Food Allergy and Atopic Eczema

Gideon Lack, MD
MRC ⁄Asthma UK Centre in Allergic Mechanisms of Asthma, King’s College London
Guy’s & St Thomas’ NHS Foundation Trust, Children’s Allergies Department
London, UK

In analysing the relationship between food allergy (FA) and atopic eczema (AE), there are various possibilities to consider; firstly FA may cause or be an exacerbating factor for AE. The second possibility is that AE may lead to FA. The third possibility is that they mutually contribute to each other.

There is strong evidence of an association between FA and AE. Children with FA more commonly have a history of AE; whereas children with AE very frequently have proven FA. A recent study in 2008 showed that early age of onset and eczema severity were both associated with FA.[1] Furthermore in oral provocation studies done by different groups,[2-4] about half of the positive food challenges resulted in delayed eczematous lesions. These eczematous responses were induced mainly by milk, egg, wheat, and soya. It is therefore surprising that interventional studies to eliminate allergens from the diet of children with AE have had very limited success. Most studies are uncontrolled and suffer from methodological limitations due to lack of blinding, lack of confirmation of FA, selection bias, and different criteria for the diagnosis of AE.[5]

In animal models, there is literature suggesting that cutaneous exposure to allergen can lead to the production of allergen specific IgE, particularly in the context of inflamed or abraded skin.[6,7] More recently, Chan et al[8] showed
that T lymphocyte responses in peanut allergic children were predominant in the CLA+ population consistent with the hypothesis that sensitisation to peanut occurs in the skin. It has also been observed that use of arachis oil is increased in children who develop peanut allergy.[9] More recently, it has been shown that environmental exposure to peanut as measured by a Food Frequency Questionnaire of peanut consumption in the home, was linked to the development of peanut allergy.[10]

The discovery of the importance of filaggrin null mutations in AE provides a biological basis for the possibility of cutaneous sensitisation. These mutations affect up to 50% of Caucasian individuals with moderate to severe AE. Patients with filaggrin null mutations have a deficiency in the skin barrier (irrespective of the presence of eczema), and it has been shown that infants with this mutation have increased Trans Epidermal Water Loss even in the absence of detectable eczema.[11] It has been shown that the filaggrin null mutation increases the risk of peanut allergy (OR 5.3)[12] and the association remained significant after controlling for coexistent AE.

In summary, FA and AE are clearly associated. There is evidence that FA can exacerbate eczema, and perhaps the strongest direct evidence comes from food challenge studies. There is however a lack of well-conducted interventional dietary elimination studies. There is growing circumstantial data to support the potential role of AE and defects in the skin barrier as a cause of FA.

[1.] Hill DJ, Hosking CS, de Benedictis FM, Oranje AP, Diepgen TL, Bauchau V; EPAAC Study Group. Confirmation
of the association between high levels of immunoglobulin E food sensitization and eczema in infancy: an
international study. Clin Exp Allergy. 2008 Jan;38(1):161-8.

[2.] Niggemann B, Reibel S, Roehr CC, Felger D, Ziegert M, Sommerfeld C, et al. Predictors of positive food
challenge outcome in non–IgE-mediated reactions to food in children with atopic dermatitis. J Allergy Clin
Immunol. 2001 Dec;108(6):1053-8.

[3.] Isolauri E, Turjanmaa K. Combined skin prick and patch testing enhances identification of food allergy in infants
with atopic dermatitis. J Allergy Clin Immunol. 1996 Jan;97(1 Pt 1):9-15.

[4.] 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 May;34(5):817-24.

[5.] Fiocchi A, Bouygue GR, Martelli A, Terracciano L, Sarratud T. Dietary treatment of childhood atopic eczema/
dermatitis syndrome (AEDS). Allergy. 2004 Aug;59 Suppl 78:78-85.

[6.] Saloga J, Renz H, Larsen GL, Gelfand EW. Increased airways responsiveness in mice depends on local challenge
with antigen. Am J Respir Crit Care Med. 1994 Jan;149(1):65-70.

[7.] Strid J, Hourihane J, Kimber I, Callard R, Strobel S. Disruption of the stratum corneum allows potent
epicutaneous immunization with protein antigens resulting in a dominant systemic Th2 response. Eur J
Immunol. 2004;34(8):2100.

[8.] Chan SMH, Turcanu V, Stephens AC, Fox AT, Grieve AP, Lack G. Cutaneous lymphocyte antigen and a4b7
T-lymphocyte responses are associated with peanut allergy and tolerance in children. Allergy. In Press.

[9.] Lack G, Fox D, Northstone K, Golding J. Factors associated with the development of peanut allergy in childhood.
N Engl J Med. 2003; 348: 977–985.

[10.] Fox AT, Sasieni P, du Toit G, Syed H, Lack G. Household peanut consumption as a risk factor for the development
of peanut allergy. J Allergy Clin Immunol 2009; 123: 417-23.

[11.] Flohr C, England K, Radulovic S, McLean WH, Campbel LE, Barker J, et al. Filaggrin loss-of-function mutations
are associated with early-onset eczema, eczema severity and transepidermal water loss at 3 months of age.
Br J Dermatol. 2010 Dec;163(6):1333-6.

[12.] Brown SJ, Asai Y, Cordell HJ, Campbell LE, Zhao Y, Liao H, et al. Loss-of-function variants in the filaggrin gene
are a significant risk factor for peanut allergy. J Allergy Clin Immunol. 2011 Mar;127(3):661-7.

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