Posted by: Indonesian Children | April 14, 2010

Food allergy and atopic eczema.

Curr Opin Allergy Clin Immunol. 2010 Apr 6. [Epub ahead of print]

Food allergy and atopic eczema.

Worth A, Sheikh A.

Allergy & Respiratory Research Group, Centre for Population Health Sciences: General Practice Section, The University of Edinburgh, Edinburgh, Scotland, UK.


PURPOSE OF REVIEW: To review recent developments on the inter-relationship between food allergy and atopic eczema, with a particular focus on understanding the role of filaggrin gene defects. RECENT FINDINGS: Filaggrin gene defects have recently been identified as a major risk factor for the development of atopic eczema. These skin barrier defects increase the risk of early onset, severe and persistent forms of atopic eczema. They also increase the risk of allergic sensitization, and asthma and allergic rhinitis in those with co-existent eczema. These skin barrier defects are also likely to increase the risk of food allergy. SUMMARY: Atopic dermatitis and food allergy are frequently herald conditions for other manifestations of ‘the allergic march’. They commonly co-exist, particularly in those with early onset, severe and persistent atopic eczema. Filaggrin gene defects substantially increase the risk of atopic eczema. The increased skin permeability may increase the risk of sensitization to food and other allergens, this pointing to the possible role of cutaneous allergen avoidance in early life to prevent the onset of atopic eczema and food allergy. Emerging evidence also indicates that oral exposure to potentially allergenic foods may be important for inducing immunological tolerance.


Allergol Immunopathol (Madr). 2002 May-Jun;30(3):120-6.

[Etiologic implication of foods in atopic dermatitis: evidence against]

[Article in Spanish]

Martorell Aragonés A.

Jefe de la Sección de Alergia. Servicio de Pediatría. Hospital General Universitario de Valencia. Profesor Asociado de Pediatría. Facultad de Medicina. Universidad de Valencia. Spain.


Atopic dermatitis is a typical chronic inflammatory skin disease that usually occurs in individuals with a personal or family history of atopy. Children with atopic dermatitis frequently present IgE-mediated food sensitization, the most commonly involved foods being egg and cow’s milk. However, controversy currently surrounds whether food allergy is an etiological factor in atopic dermatitis or whether it is simply an associated factor, accompanying this disease as one more expression of the patient’s atopic predisposition. Approximately 40 % of neonates and small children with moderate-to-severe atopic dermatitis present food allergy confirmed by double-blind provocation tests but this allergy does not seem to be the cause of dermatitis since in many cases onset occurs before the food responsible for allergic sensitization is introduced into the newborn’s diet.Studies of double-blind provocation tests with food in patients with atopic dermatitis demonstrate mainly immediate reactions compatible with an IgE-mediated allergy. These reactions occur between 5 minutes and 2 hours and present mainly cutaneous symptoms (pruritus, erythema, morbilliform exanthema, wheals) and to a lesser extent, digestive manifestations (nausea, vomiting, abdominal pain, diarrhea), as well as respiratory symptoms (wheezing, nasal congestion, sneezing, coughing). However, these reactions do not indicate the development of dermatitis.Some authors believe that responses to the food in provocation tests may also be delayed, appearing mainly in the following 48 hours, and clinically manifested as exacerbation of dermatitis. However, delayed symptoms are difficult to diagnose and attributing these symptoms to a particular foodstuff may not be possible.Delayed reactions have been attributed to a non-IgE-mediated immunological mechanism and patch tests with food have been proposed for their diagnosis. In our experience and in that of other authors, the results of patch tests with cow’s milk do not seem very specific and could be due, at least in part, to the irritant effect of these patches on the reactive skin of children with atopic dermatitis.The involvement of foods in atopic dermatitis will always be difficult to demonstrate given that an exclusion diet is not usually required for its resolution. Food is just one among several possible exacerbating factors and consequently identification of its precise role in the course of the disease is difficult. Further double-blind prospective studies are required to demonstrate the effectiveness of exclusion diets in the treatment of atopic dermatitis.Apart from the controversy surrounding the etiological role of foods, the most important point in atopic dermatitis is to understand that the child is atopic, that is, predisposed to developing sensitivity to environmental allergens; in the first few years of life to foods and subsequently to aeroallergens. Consequently, possible allergic sensitization to foods should be evaluated in children with atopic dermatitis to avoid allergic reactions and to prevent the possible development of allergic respiratory disease later in life.


Allergol Immunopathol (Madr). 2002 May-Jun;30(3):114-20.

[Etiologic implication of foods in atopic dermatitis: evidence in favor]

[Article in Spanish]

Fernández-Benítez M.

Consultora del Departamento de Alergología e Inmunología Clínica de la Clínica Universitaria. Profesora Adjunta de la Facultad de Medicina. Universidad de Navarra. Spain.


Some of the immunopathologic mechanisms involved in IgE responses are currently being identified; Th2 lymphocytes are known to be activated in patients with atopic dermatitis with subsequent production of the cytokines interleukin (IL)-4 and IL-5, which are responsible for IgE production and eosinophil recruitment. Nevertheless, T cell activation in this disease takes place in two phases. In the first phase, Th2 cells are activated and IL-4, IL-5 and IL-13 are produced; this first stage is produced with the initial activation induced by the antigen. In the second phase there are chronic lesions, Th1 lymphocytes are activated and IFg is produced. This chronic phase is associated with the presence of eosinophils and macrophages that produce IL-12.Numerous articles have demonstrated food sensitization to be an etiopathogenic factor in atopic dermatitis. The prevalence of sensitization varies, depending on the patient’s age and the severity of the disease. Children with moderate-to-severe atopic dermatitis have been observed to have a positive skin test and high IgE concentrations to various foods. Nevertheless, a positive skin test to foods in such children does not always implicate these foods as the cause of the clinical manifestations; moreover, in children showing subsequent tolerance to these foods, skin tests can sometimes remain positive and high levels of specific IgE can persist. It is now known that IgE not only participate in the degranulation of mastocyte cells but also in reactions mediated by T cells and other antigen-presenting cells (dendritic cells) which have high-affinity receptors for IgE.The immediate IgE response is well known but it is also known that in addition to the immediate response, a delayed response is also involved, evidenced by the presence of antigen-specific T cells to foods or other allergens such as inhalant allergens. After a strict exclusion diet, children with atopic dermatitis and sensitivity to foods such as milk, egg, flour and soya can develop tolerance; for this reason provocation tests with the food in question should be repeated every 2-3 years. In children with sensitivity to other foods such as dried fruits, fish, and shellfish, sensitivity can sometimes persist into adulthood without tolerance being achieved. In conclusion, there are two groups of children with atopic dermatitis. One group consists of those with atopic dermatitis (allergic disease), which is characterized by early development, high IgE titers, the presence of antigen-specific IgE to allergens and a family history of atopy and which is clinically moderate or severe. Early diagnosis and treatment are important in these children, as is the prevention of progression of the disease to bronchial asthma. The other group consists of children whose dermatitis is clinically atopic in terms of its localization and morphology, who have no demonstrable allergic disease and whose management differs from that in children presenting allergic disease


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