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What Has Food and Dust Got To Do With Atopic Dermatitis?
BULLETIN FOR MEDICAL PRACTITIONERS
Dr Chan Yuin Chew
Associate Consultant Dermatologist, National Skin Centre
The role of exogenous allergens like food and aeroallergens in the pathogenesis of atopic dermatitis has always been a controversial one. There are several reasons why so much confusion and controversy exist:
a. Atopic dermatitis is a clinical diagnosis. There are no confirmatory investigations. As such, it is likely to be a very heterogeneous disease.
b. The pathogenesis of atopic dermatitis is complex, multifactorial and not completely understood.
c. A positive allergy test result may not be clinically relevant. In other words, an individual may not show any signs or symptoms of allergy to a particular food or aeroallergen even though he may test positive to that substance based on the test protocol.
Most dermatologists are not convinced that these exogenous allergens influence the course of atopic dermatitis. Some believe that atopic dermatitis is a genetic disease and these environmental factors have no role. Some argue that the skin prick test and specific IgE screen for IgE-mediated reactions, but atopic dermatitis is a predominantly T cell mediated disease. Even among those who concede that these allergens may play a part, the greatest difficulty is proving that the food or aeroallergen actually makes the eczema worse. In other words, an individual with atopic dermatitis may have a coincidental food allergy, but the latter may not necessarily aggravate the eczema.
I. Food allergy
Clinical and experimental data
There are many experimental and clinical studies showing that atopic dermatitis in a subset of patients is aggravated by food allergy. Food allergen-specific T cells have been cloned from skin lesions of patients with atopic dermatitis.1 After in vitro stimulation with casein, patients with milk allergy and atopic dermatitis had significantly more CLA+ T cells than controls with milk-induced enterocolitis, allergic eosinophilic gastroenteritis, or nonatopic healthy controls.2
Clinical data have to fulfill Koch’s postulates of causality; that the introduction of food allergens worsens atopic dermatitis and their removal leads to an improvement of atopic dermatitis. In a classical clinical experiment which would not have been allowed in today’s society, a child with atopic dermatitis and wheat allergy was hospitalised when his skin was clear.3 His left arm and leg were covered with bandage and he was fed 2 wheat crackers. As expected, this resulted in itch and scratching within 2 hours. On the following day, eczema was seen on the open skin, but the bandaged skin remained clear. A double-blind randomised controlled trial involving children less than 3 years of age with atopic dermatitis and proven egg allergy showed a significant improvement in eczema in the group randomised to a 4-week egg exclusion diet as compared to the group which did not have any dietary restrictions.4 Studies have shown that increased severity of atopic dermatitis and younger age correlated directly with presence of food allergy.5 Approximately 35-40% of children with moderate to severe atopic dermatitis have IgE-mediated food allergies.
In Singapore, the common causes of food allergies include hen’s egg, cow’s milk, shellfish, peanut, soy, wheat and bird’s nest. In contrast to findings from studies done in Western countries, fish is a very uncommon cause of food allergy in the local population.
Diagnosis
History is notoriously inaccurate. Studies have shown that in children with moderate to severe atopic dermatitis, only 35-40% of parental historical accounts were accurate. Dietary diaries may be more useful as they provide prospective information. History is most useful for early IgE-mediated reactions, which may manifest as perioral itch, swelling or burning sensation within minutes of food ingestion.
Investigations
The double blind placebo controlled food challenge is the "gold standard" test for food allergy. However, it requires preparation of suspected food allergens and placebo in capsule formulation and observation of the patient in a hospital setting. It is not a practical test for most clinicians. Practical investigations include the skin prick test (SPT) and specific IgE test (RAST).
The SPT and RAST for IgE-mediated food allergy are tests of exposure and possibly sensitization. However they are not always indications of clinical relevance. The positive predictive value of the SPT is less than 50%, which means that out of 100 positive skin prick test reactions, less than 50 are clinically relevant. However, its negative predictive value is more than 95%. Hence a patient with a negative test is very unlikely to have an IgE-mediated allergy.
In general, the RAST correlates well with the SPT. The SPT is cheaper, more versatile and more physiological. The RAST is expensive and the food allergen panel is more limited. However the RAST has the advantages of being a simple blood test that does not require a patch of diseasefree skin for testing and there is no need to stop antihistamines prior to the test.
The atopy patch test (APT) has been used in Europe recently as a screening tool for food allergies. The methodology is similar to the patch test for allergic contact dermatitis. Fresh foods like cow’s milk, whisked hen’s egg and soy milk are occluded with aluminium chambers for 48 hours and the test is read at 72 hour. The presence of erythematous papules and/or vesicles is taken as a positive reaction. Several studies have shown that the combination of APT and SPT or RAST enhances the positive predictive value and is more specific than the individual tests.6,7
Management
For most patients with atopic dermatitis, proper skin care and topical treatment are sufficient for good control of the disease. However, for young children with moderate to severe atopic dermatitis who do not respond well, an elimination diet for 2-4 weeks based on history and correlation with screening tests like SPT, RAST and APT may be considered. An elimination diet should be supervised by a dietician to ensure that it is nutritionally adequate and all "hidden" sources of the food item have been eliminated. If symptoms improve with the elimination diet, an open food challenge can be done for up to 1 week; this should not be done if the previous reaction is an anaphylactic one. If symptoms recur, the food item should be excluded from the diet. The duration of exclusion may be lifelong for peanuts, tree nuts and shellfish. For milk and egg, these can be re-introduced cautiously after the age of 3 years as children tend to outgrow allergies to such food.
The website www.foodallergy.org contains a lot of helpful information on food allergy.
II. Aeroallergens
Clinical and experimental data
IgE to house dust mite has been shown to be more prevalent in patients with moderate to severe atopic dermatitis (95%) than in patients with asthma (42%) or in healthy controls (17%).8 Application of dust mite, animal dander and mold by patch test on uninvolved skin has been shown to cause dermatitis in 30-50% of atopic dermatitis patients.9 In contrast, patients with respiratory allergy and healthy volunteers rarely have positive atopy patch tests. In addition, T cells that selectively respond to dust mite have been isolated from skin lesions of patients with atopic dermatitis.
There is clinical data to show that atopic dermatitis improves with avoidance of aeroallergens. In a double blind randomised controlled trial of active treatment against house dust mite (using Gore-tex bedcover, benzyltannate spray, high-filtration vacuum cleaner) versus placebo in 24 adults and 24 children with atopic dermatitis, significant improvement of atopic dermatitis in the treatment group was present at 6 months.10 In a study involving 2201 East German schoolchildren (aged 5 to 14 years) with atopic dermatitis, the degree of sensitisation to aeroallergens, especially house dust mite and cat dander, was directly associated with severity of atopic dermatitis.11
Management
In children with severe atopic dermatitis who do not respond well to topical treatment or those with concurrent asthma and/or allergic rhinitis, APT, SPT or RAST screening for aeroallergens can be considered. The most frequent culprit among the aeroallergens is house dust mite and avoidance measures include dust mite proof encasings, avoiding carpets and soft toys, washing of bed sheets and soft toys every fortnight.
Conclusion
Atopic dermatitis is a heterogeneous disease with a complex pathogenesis. For the management of this disease, the medical practitioner should always emphasize on skin care and topical treatment first. Food and aeroallergens may aggravate the disease in a small subset of patients. Children younger than 3 years of age with moderate to severe atopic dermatitis are likely to have a higher risk of food allergies. It is worthwhile screening for aeroallergens in atopic dermatitis patients with concurrent asthma or allergic rhinitis. Avoidance of allergens in these patients may improve atopic dermatitis, but does not cure the disease. The medical practitioner should not just treat test results; clinical relevance of the test results must be sought.
References
- Van Reijsen FC, Felius A, Wauters EA, Bruijnzeel-Koomen CA, Koppelman SJ. T-cell reactivity for a peanut-derived epitope in the skin of a young infant with atopic dermatitis. J Allergy Clin Immunol. 1998 Feb; 101(2 Pt 1):207-9.
- Abernathy-Carver KJ, Sampson HA, Picker LJ, Leung DY. Milk-induced eczema is associated with the expansion of T cells expressing cutaneous lymphocyte antigen. J Clin Invest. 1995 Feb; 95(2):913-8.
- Engman. Med Clin N Am 1936.
- Lever R, MacDonald C, Waugh P, Aitchison T. Randomised controlled trial of advice on an egg exclusion diet in young children with atopic eczema and sensitivity to eggs. Pediatr Allergy Immunol. 1998 Feb; 9(1):13-9.
- Guillet G, Guillet MH. Natural history of sensitisations in atopic dermatitis. A 3-year follow-up in 250 children: food allergy and high risk of respiratory symptoms. Arch Dermatol. 1992 Feb; 128(2):187-92.
- Roehr CC, Reibel S, Ziegert M, Sommerfeld C, Wahn U, Niggemann B. Atopy patch tests, together with determination of specific IgE levels, reduce the need for oral food challenges in children with atopic dermatitis. J Allergy Clin Immunol. 2001; 107(3):548-53.
- Niggemann B. Evolving role of the atopy patch test in the diagnosis of food allergy. Curr Opin Allergy Clin Immunol. 2002; 2(3):253-6.
- Scalabrin DM, Bavbek S, Perzanowski MS, Wilson BB, Platts-Mills TA, Wheatley LM. Use of specific IgE in assessing the relevance of fungal and dust mite allergens to atopic dermatitis: a comparison with asthmatic and nonasthmatic control subjects. J Allergy Clin Immunol. 1999; 104(6):1273-9.
- Allergic Skin Disease: A Multidisciplinary Approach, Leung and Greaves (eds) 2000.
- Tan BB, Weald D, Strickland I, Friedmann PS. Double-blind controlled trial of effect of housedust-mite allergen avoidance on atopic dermatitis. Lancet. 1996 Jan 6;347(8993):15-8.
- Schafer T, Heinrich J, Wjst M, Adam H, Ring J, Wichmann HE. Association between severity of atopic eczema and degree of sensitization to aeroallergens in schoolchildren. J Allergy Clin Immunol 1999; 104(6):1280-4.
DEDICATED TO EXCELLENCE IN DERMATOLOGY
By National Skin Centre (Singapore)
Copyright (C) 1995 - National Skin Centre (Singapore )
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