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
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. 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.
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 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. 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.
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. It has been shown that the filaggrin null mutation increases the risk of peanut allergy (OR 5.3) 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.
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