The Australasian Society of Clinical Immunology and Allergy

Definitions and prevalence

'Food hypersensitivity' is defined as an adverse reaction to a food protein that results from an immunologic mechanism. It is important to differentiate food hypersensitivity from 'food intolerance' as the management of these conditions is different (Box 1). Food intolerance refers to an adverse reaction to food caused by a non-immunological mechanism such as a direct pharmacologic effect of a chemical contained within food (Eg: tyramine induced nausea, emesis, headache) or metabolic disorders (Eg: lactase or disaccharidase deficiency). Food hypersensitivity is common, affecting up to 6%of children and 1.5 - 2% of adults[1][2]. The majority of food hypersensitivity reactions are caused by a small number of foods - egg, milk, peanut/tree nuts, wheat, soy, fish, shellfish. Different foods are more likely to cause allergy at different ages (Box 2).

Clinical features

Food hypersensitivity reactions may be IgE mediated ("Food Allergy") or non-IgE mediated.

IgE mediated "allergic" reactions generally occur rapidly upon ingestion of an offending food (within 30min - 1hr) and can involve a number of organ systems - skin, gastrointestinal, respiratory, cardiovascular (Box 3). Most reactions involve the skin or gastrointestinal system with various combinations of urticaria, angioedema, vomiting, diarrhoea and abdominal cramps. Severe IgE mediated reactions can lead to systemic anaphylaxis with involvement of respiratory and/or cardiovascular systems in addition to skin and gut. Such reactions may be fatal. Food allergic reactions rarely cause isolated respiratory symptoms without associated cutaneous reactions. 'Gastrointestinal anaphylaxis' may occur in infants with immediate onset of severe vomiting and diarrhoea leading to dehydration and hypotension. IgE mediated food reactions may also be associated with delayed development or exacerbation of eczema. The 'oral allergy syndrome' refers to a condition in which allergic symptoms are restricted to the oropharynx, with tingling or swelling of lips and tongue. It is most commonly seen in patients with seasonal allergic rhinitis who report symptoms following ingestion of a variety of fruits and vegetables, and is thought to reflect allergenic cross reactivity between pollens and foods (Eg: birch pollen and apple). Exercise related food reactions may occur following a combination of exercise and ingestion of a food within a given time period, while either exercise or food alone does not cause a reaction. Such exercise related food reactions are frequently severe and can result in anaphylaxis.

Non-IgE mediated hypersensitivity reactions are generally delayed with symptoms developing several hours to days after ingestion of an offending food. They present predominantly with gastrointestinal symptoms. A number of non-IgE mediated food hypersensitivity syndromes have been described (Box 4).

Diagnosis of food hypersensitivity

In most cases, patients should be referred to a medical specialist (Allergist / Clinical Immunologist) who can confirm the diagnosis of food hypersensitivity, determine if hypersensitivity to other foods is present and provide advice regarding further management. History is an important tool in the diagnosis of food allergy and hypersensitivity (Box 5). History will provide clues to the food causing a reaction and whether the reaction is likely to be IgE mediated or non-IgE mediated. Patients should avoid the implicated food until further evaluation is completed. Careful examination and appropriate investigations should be performed to exclude other causes (Box 6).

In IgE mediated food allergy, diagnosis may be confirmed by skin prick testing or allergen specific IgE (RAST) testing. Other methods of testing (Vega tests, pulse tests etc) have not been validated and are not recommended. Skin prick testing is preferred over RAST testing since it is simple, inexpensive, does not require a blood sample and provides immediate results. Results of skin prick and RAST (serum specific IgE) tests must be interpreted with caution. A positive test only demonstrates the presence of specific IgE to the food in question. It does not necessarily indicate the presence of clinical allergy. Less than 50% of individuals with a positive skin test to a food will react to that food upon formal challenge. Thus, if the history is clear, a positive skin test can confirm the diagnosis of IgE mediated food allergy. However, if the history is uncertain, the significance of a positive skin test may need to be confirmed by formal food challenge. A negative skin test on the other hand is very helpful as it almost eliminates the possibility of IgE mediated reaction to the food in question. In cases of suspected IgE mediated food allergy, food challenges must only be performed by a specialist allergist as there is a risk of serious reaction that may be life-threatening.
There are no specific diagnostic tests for non-IgE mediated food hypersensitivity. Diagnosis requires an elimination diet followed by challenge to the suspected food. Endoscopy and biopsy may be helpful particularly in cases of suspected eosinophilic colitis, food induced enteropathy and eosinophilic gastroenteritis.

Natural History of Food Allergy and Hypersenstivity

The likelihood of resolution of food allergy or hypersensitivity depends upon the food in question. Allergies to egg, milk, wheat and soy generally resolve with age. The majority (85%) of children with IgE mediated allergy to milk, egg, wheat or soy allergy will lose their allergies by 3-5 years of age. Allergies to peanut, tree nuts, fish and shellfish are generally prolonged.
Non-IgE mediated food hypersensitivities are mostly associated with cow's milk or soy and generally resolve with time. Fifty percent of non-IgE mediated food reactions resolve within 1-3 years.

Treatment of food hypersensitivity

Once a diagnosis of food allergy or food hypersensitivity is established, strict elimination of the offending food is the only treatment available. There is no cure for food allergy at the present time. Elimination of a food requires careful attention to reading ingredient labels. Patients should be educated about "hidden" sources of a food - Eg: egg in cakes and biscuits. Referral to a dietician with a particular interest in food allergy should be considered as part of the management when implementing an elimination diet in children. As most food allergies resolve with time, patients should be reviewed at 1-3 year intervals with repeat skin testing and in some cases challenged to monitor for the development of clinical tolerance. At this time, there is no role for desensitisation therapy for food allergy.

All patients with IgE mediated food allergy, particularly those with asthma, should be warned about the possibility of developing severe anaphylactic reaction and should have an appropriate action plan (which may include an adrenaline Epipen) in case of accidental ingestion. In cases of systemic anaphylaxis with generalised symptoms and involvement of respiratory or cardiovascular systems, the first line treatment is adrenaline. Delayed administration of adrenaline was a major factor associated with fatal anaphylaxis. Once adrenaline is administered, corticosteroid and antihistamines may be given and arrangements made for transfer to hospital. Antihistamines may be used for mild allergic reactions confined to the skin. Regular review of an action plan is important as patients may have accidental exposures to the food(s) concerned.

References

• Bock SA. Prospective appraisal of complaints of adverse reaction to foods in children during the first 3 years of life. Pediatr 1987;79:683-688.
  
• Young E, Stoneham MD, Petruckevitch A, et al. A population study of food intolerance. Lancet 1994;343:1127-30.
  
• Sampson HA, Adverse reactions to foods, in Allergy: Principles and Practice, E. Middleton, et al., Editors. 1993, C.V. Mosby: St Louis. p. 1661-1686.
  
• Machida H, Smith A, Gall D, et al. Allergic colitis in infancy: clinical and pathologic aspects. J Pediatr Gastroenterol and Nutrit 1994;19:22-26.
  
• Kuitunen P, Visakorpi J, Savilahti E, et al. Malabsorption syndrome with cow's milk intolerance: clinical findings and course in 54 cases. Arch Dis Child 1975;50:351-356.
  
• Lee C, Changchien C, Chen P, et al. Eosinophilic gastroenteritis: 10 years experience. Am J Gastroenterol 1993;88:70-74.
  
• Kelly KJ, Lazenby AJ, Rowe PC, et al. Eosinophilic oesophagitis attributed to gastrooesophageal reflux: improvement with an amino acid based formula. Gastroenterol 1995;109:1503-1512.

© ASCIA 2010

The Australasian Society of Clinical Immunology and Allergy (ASCIA) is the peak professional body of Clinical Immunologists and Allergists in Australia and New Zealand.

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Disclaimer

ASCIA Education Resources (AER) information is reviewed by ASCIA members and represents the available published literature at the time of review. Information contained in this document is not intended to replace professional medical advice and any questions regarding a medical diagnosis or treatment should be directed to a medical practitioner.

Content last updated January 2010