About the Author: This article was written by Christophe Dupont, Paris, France
The information in this article is correct at date of publication: 2007
Opinions expressed by the author are not necessarily those of the publisher or editorial staff.
Epidemiological studies suggest that nearly 4% of people in western countries are afflicted with food allergies, a prevalence much higher than appreciated in the past. In addition, in the past five years the prevalence of peanut allergy has doubled in American children aged less than five years. The increased understanding of the immunopathogenesis of many allergic disorders has contributed to novel diagnostic and immunotherapeutic approaches. Many food allergens have been characterised at the molecular level. The management of food allergies consists of educating patients on how to avoid relevant allergens, to recognise the early symptoms of an allergic reaction in case of accidental ingestion, and to initiate the appropriate emergency therapy. Recent successful clinical trials of immunotherapy and anti-IgE treatments in some patients with severe allergy (e.g. peanut) might herald a real hope for the treatment of patients with food allergy.
Adverse food reactions (food hypersensitivities) include any abnormal reaction resulting from the ingestion of a food and might be the result of food intolerances (non-allergic food hypersensitivities) or food hypersensitivity/allergy (food allergy). Food intolerances (non-allergic food hypersensitivities) are adverse responses caused by some unique physiologic characteristic of the host, such as metabolic disorders (eg, lactase deficiency). Food hypersensitivities/ allergies are adverse immunologic reactions that might be due to IgE- or non–IgE-mediated immune mechanisms
2.
The prevalence of food hypersensitivities is greatest in the first years of life, affecting about 6% of infants below three years of age and decreasing over the first decade. Virtually all infants who have cows` milk allergy have it in the first year of life, with clinical tolerance developing in about 80% by their 5th birthday. About 60% of infants with cows` milk allergy experience IgE-mediated reactions, and about 25% of these infants retain their sensitivity into the second decade of life, with 35% going on to have other food allergies.
Despite the enormous diversity of the human diet, relatively few foods account for the majority of food allergies: milk, egg, and peanut in children, peanut, tree nuts, fish, and shellfish in adults
1.
Regional dietary habits and methods of food preparation clearly play a role in the prevalence of specific food allergies. The consumption of peanuts is essentially the same in China and in the United States, but there is virtually no peanut allergy in China, where peanuts are eaten predominantly boiled or fried, whereas Americans eat peanuts almost exclusively dry-roasted
Table 1. Food hypersensitivity disorders
2.
IgE mediated
|
Gastrointestinal
Cutaneous
Respiratory
Generalised
|
Oral allergy syndrome, gastrointestinal anaphylaxis
Urticaria, angioedema, morbilliform rashes and flushing
Acute rhinoconjunctivitis, bronchospasm (wheezing)
Anaphylactic shock |
Mixed IgE and cell mediated
|
Gastrointestinal
Cutaneous
Respiratory
|
Allergic eosinophilic esophagitis, allergic eosinophilic gastroenteritis
Atopic dermatitis
Asthma |
Cell mediated
|
| Gastrointestinal |
Food protein–induced enterocolitis, food protein–induced proctocolitis,
food protein–induced enteropathy syndromes, celiac disease |
Cutaneous
Respiratory |
Contact dermatitis, dermatitis herpetiformis
Food-induced pulmonary hemosiderosis (Heiner syndrome) |
Diagnosis
For IgE-mediated disorders, skin prick tests provide a rapid method to screen patients for sensitivity to specific foods. Allergens eliciting a wheal of at least 3mm larger than that produced by the negative control are considered positive, indicating the possibility that the patient has symptomatic reactivity to the specific food. Strongly positive results (e.g. median wheal diameter >8-10 mm) indicate a greater likelihood of clinical reactivity. In children aged less than two years, skin prick tests to milk, egg or peanuts with wheal diameters of 8mm or larger are reportedly more than 95% predictive of reactivity.
The use of the atopy patch test in addition to skin prick tests for the diagnosis of non–IgE-
mediated food allergy has been examined by a number of investigators, primarily in patients with atopic dermatitis and allergic eosinophilic esophagitis. The atopy patch test shows promise in identifying foods that might be eliciting non IgE-mediated reactions, and standardised reagents or methods of application are currently being developed
4.
RASTs and similar qualitative in vitro assays provide suggestive evidence of IgE-mediated food allergy, but these assays are giving way to quantitative measurements of food-specific IgE antibodies (e.g. CAP System FEIA, Phadia), which have been shown to be more predictive of symptomatic IgE-mediated food allergy
3.
Other standard laboratory studies may be useful when evaluating patients with gastrointestinal hypersensitivities. About 1 in 2 patients with allergic eosinophilic esophagitis (AEE) and allergic eosinophilic gastroenteritis (AEG) have peripheral eosinophilia, and patients with severe AEG might have anaemia, blood in the stool, and decreased serum protein, albumin, and IgG levels (with preservation of IgA and IgM levels). Endoscopy and biopsy are the most definitive approaches for diagnosing many of the gastrointestinal hypersensitivities. Greater than 10 to 20 eosinophils per 40X high-power field in the esophagus is diagnostic of AEE
5. The gold standard for the diagnosis of food allergies remains the double-blind, placebo-controlled food challenge (DBPCFC), as outlined by a number of reviews, and efforts to standardise challenge materials are underway. The clinical history, skin test or RAST results, or both, indicate which foods should be evaluated. Open or single-blind food challenges are often used to screen foods unlikely to provoke food-induced allergic reactions. To increase the likelihood of a non-equivocal food challenge result, suspect foods should be eliminated for at least 14 days before challenge and longer in some non IgE mediated gastrointestinal disorders (e.g. AEE and AEG). Many young children with AEE and AEG have multiple food allergies, and consequently, it is necessary to start them on an elemental formula (i.e. Neocate) for 4 to 6 weeks before initiating the challenges.
Therapeutic optionsOnce the diagnosis of food hypersensitivity is established, the only proven therapy remains elimination of the offending allergen, although as indicated below, promising therapeutic modalities are on the horizon.
In children with cows` milk allergy, the diet relies on hydrolysates and in some situations an amino acid based formula (i.e. Neocate) is necessary. Antihistamines might partially relieve symptoms of oral allergy syndrome. Novel forms of immunotherapy are being explored for the treatment of IgE-mediated food allergy. A pilot trial indicates the potential role of sublingual immunotherapy with cows` milk allergy
6. Some success with anti-IgE therapy has been shown in patients with peanut allergy
7
Prevention Meta-analyses of published studies suggest a beneficial role for breastfeeding in the prevention of atopic disease during the first 3 to 6 months of life in high-risk infants.
Currently, there is no conclusive evidence that the manipulation of the mother`s diet during pregnancy or whilst breastfeeding further contributes to prevention. Delaying the introduction of allergenic foods in the infant`s diet probably restrains the development of food allergy. Extensively hydrolysed casein-based formula or partially hydrolysed whey formula might be useful in the prevention of some atopic diseases and food allergy when used as weaning formulas or as a supplement to breastfeeding in high-risk infants.
References 1. Sicherer SH, Munoz-Furlong A, Sampson HA. Prevalence of peanut and tree nut allergy in the United States determined by means of a random digit dial telephone survey: a 5-year follow-up study. J Allergy Clin Immunol 2003;112:1203-7.
2. Sampson HA. Update on food allergy. J Allergy Clin Immunol. 2004;113:805-19.
3. Garcia-Ara C, Boyano-Martinez T, Diaz-Pena JM, et al. Levels in the diagnosis of immediate hypersensitivity to cows` milk protein in the infant. J Allergy Clin Immunol 2001;107:185-90.
4. Kalach N, MD, Soulaines P, de Boissieu D, et al. A pilot study of the usefulness and safety of a ready-to-use atopy patch test (APT) (Diallertest®) versus a comparator (Finn Chamber®) during cow’s milk allergy in children. J Allergy Clin Immunol 2005;116:1321-6.
5. Rothenberg ME. Eosinophilic gastrointestinal disorders (EGID). J Allergy Clin Immunol. 2004;113:11-28.
6. De Boissieu D, Dupont C. Sublingual immunotherapy for cow milk protein allergy: a preliminary report. Allergy 2006;61:1238-9.
7. Leung DYM, Sampson HA, Yunginger JW, et al. Effect of anti-IgE therapy in patients with peanut allergy. N Engl J Med 2003;348:986-93.
