Food allergies and intolerances

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Chapter 10 FOOD ALLERGIES AND INTOLERANCES

KEY POINTS

• Food allergies may affect up to 6% of the population.
• Food allergies are adverse reactions to foods mediated by the immune system. Food allergies may be mediated by antibodies e.g. IgE (immediate hypersensitivity) or they may be cell mediated (delayed hypersensitivity).
• Intolerances are adverse reactions to foods that are not mediated by the immune system.
• A thorough history is the most important aspect in the evaluation of a patient with a suspected food adverse reaction.
• Allergy tests may aid in the diagnosis of a food allergy but should never be exclusively relied upon in the absence of a supportive history.
• Exclusion diets and re-challenge remain the ‘gold standard’ for the diagnosis of many clinical food allergy-related syndromes.
• Appropriate education regarding both the risk of a severe reaction and food avoidance is the most important aspect in the management of patients with food adverse reactions.

DEFINITIONS

Food adverse reaction

Any abnormal reaction that is related to the ingestion of a food.

Food allergy

An adverse reaction to food resulting from an immune-mediated response to a food protein. Food allergic reactions are usually either IgE mediated (immediate hypersensitivity e.g. urticaria) or non-IgE (cell) mediated (delayed hypersensitivity e.g. food protein enteropathy). Some allergic diseases are associated with demonstrable IgE to foods and other allergens but a causative link has not been firmly established (e.g. eosinophilic gastroenteropathy). Isolated gastrointestinal food allergies are usually either delayed or IgE-associated.

Food intolerance

Any non-immune-mediated adverse reaction to food. Intolerances are usually caused by an inherent characteristic of the patient e.g. a disaccharidase deficiency causing lactose intolerance. Intolerances may require a much larger amount of the food to cause clinical symptoms and are usually delayed in onset.

Toxic reactions

Adverse reactions to foods mediated by a toxin contained in the food e.g. food poisoning or histamine in scombroid fish. These reactions occur in all people who ingest the food and are not dependent on either immune- or non-immune-mediated susceptibility.

EPIDEMIOLOGY

Food allergy of all types may affect up to 6% of children and 4% of adults. Estimates from the USA suggest that around 4% of the general population have IgE-mediated food allergy while IgE-mediated allergy to specific foods varies from between 0.5% to around 2% of the general population, especially in children. The incidence of IgE-mediated food allergy is much higher in individuals with other atopic diseases e.g. up to one-third of children with atopic dermatitis have been reported to have concomitant food allergy. IgE-mediated food allergy is also found more frequently among asthmatic patients, but is rarely the cause of wheeze in the absence of other symptoms.

CLINICAL SYNDROMES

IgE-mediated immediate hypersensitivity

A relatively small number of foods, including cow’s milk, hen’s egg, wheat, peanut and shellfish cause the majority of IgE-mediated immediate hypersensitivity reactions. Symptoms usually occur within minutes of ingestion of the food and very rarely occur more than 2 hours following the ingestion. Symptoms involving the gastrointestinal system include abdominal pain, nausea, vomiting and diarrhoea. Immediate hypersensitivity reactions rarely involve the gastrointestinal system in the absence of other systems. The most severe form of IgE-mediated allergy is called anaphylaxis and is defined as the involvement of any two organ systems and the respiratory or cardiovascular system. Anaphylaxis is a medical emergency and can be fatal in some cases.

Food protein-induced proctocolitis

Cell-mediated (eosinophilic) hypersensitivity, usually to cow’s milk or soy, is characterised by macroscopic blood and mucus in the stool of an otherwise healthy, usually breastfed, infant. Onset is at around 2 months on average. Usually no special investigations are needed to make the diagnosis. Treatment is avoidance of the causative protein by breastfeeding mothers or, if symptoms persist or the infant is not breastfed, a hydrolysed formula may be used. This usually resolves between 1 and 2 years of age.

Food protein enteropathy

Cell-mediated (T cell) hypersensitivity, usually to cow’s milk but occasionally also grains, egg and shellfish, is characterised by chronic vomiting, diarrhoea and malabsorption. The onset is usually in infancy in formula-fed infants and failure to thrive is common. Protein loss may lead to oedema and iron deficiency may follow. Diagnosis is made through a combination of endoscopy (biopsy), allergen avoidance and re-challenge. This condition generally resolves between 1 and 2 years of age.

Food protein enterocolitis

Cell-mediated (T cell) hypersensitivity is similar to, but more severe than, food protein enteropathy. It usually begins in infancy and is most often caused by cow’s milk, but between 30% and 50% are also sensitive to soy. Chronic ingestion of the causative protein causes vomiting, bloody diarrhoea and lethargy that may lead to dehydration and acidosis. The clinical picture may mimic sepsis including an elevated blood neutrophil count. Re-exposure to the causative protein leads to a dramatic, but delayed (± 2 hours) recurrence of symptoms that may lead to shock in up to 20% of cases. The diagnosis is made through an elimination diet, re-challenge with the suspected food under medical supervision and examination of the stool for blood, white cells and eosinophils (colitis). A rise in the blood neutrophil count over 3500 cells/mL may be observed. Biopsy is usually not necessary for the diagnosis. Treatment is by avoidance of the causative food and the use of hydrolysed formula. This condition usually resolves between 2 and 3 years of age.

Eosinophilic gastroenteropathy (EoG)

A group of disorders characterised by infiltration of the gut wall by eosinophils. In contrast to food protein enteropathy and enterocolitis, eosinophilic gastroenteropathy (EoG) may affect people of any age. EoG is thought to be mediated by a combination of both IgE-mediated and non-IgE-mediated allergy to food proteins. Common symptoms include vomiting, diarrhoea, dysphagia, abdominal pain and bloating. Up to 50% of patients have a personal or family history of atopy and 75% may have eosinophilia or an elevated total IgE. The diagnosis depends on demonstrating elevated numbers of eosinophils on biopsy. Adjunctive tests such as skin prick tests and atopy patch tests (discussed below) may be useful to identify causative foods in some cases. Treatment is by a combination of restrictive diet, elemental diet and, if needed, systemic corticosteroids.

ASSESSMENT

As there are no specific diagnostic tests available for many food allergens, delayed allergic reactions and food intolerances, the reproducibility of the symptoms after ingestion of a common food is often important in establishing a causal relationship. There are a number of bedside and laboratory based investigations which, when used in conjunction with a thorough history, may help to make the diagnosis of food allergy or intolerance. The sensitivity and specificity of the tests vary significantly and one should be careful about making a diagnosis of food allergy or intolerance based exclusively on a diagnostic test in the absence of a supportive history.

History

The clinical history remains the most important diagnostic tool in the assessment of a patient with a suspected adverse reaction to a food. Information relating to the temporal relationship of the symptoms with ingestion of the food may help to differentiate immediate from delayed hypersensitivity reactions. Most IgE-mediated adverse reactions to foods occur within 2 hours following the ingestion of a food, although a very small proportion of IgE-mediated reactions may be delayed for up to 6 hours. Non-IgE mediated adverse reactions occur much later, even up to 72 hours after the ingestion of a food. Other important factors in the history include previous exposure to the suspected food, with or without a reaction, the reproducibility of the adverse reaction on re-exposure to the food, the amount of food ingested and the severity of the adverse reaction. The severity of the reaction on history may help to determine further management, e.g. anaphylaxis may require the prescription of self-injectable adrenaline (EpiPen® and EpiPen Jr®). In some cases it may be recommended that the patient keep a diet diary. This may be particularly useful in cases of suspected delayed adverse reactions where the causative food, or the definite relationship between a food and the onset of symptoms, is difficult to determine.

Tests for immediate hypersensitivity

An important aspect of the diagnosis of IgE-mediated immediate food hypersensitivity is the demonstration of IgE antibody to the offending food in the presence of a supportive history.

Skin prick tests

The most commonly performed test for food-specific IgE is the skin prick test (SPT). Various commercial food allergen extracts are available, or in some cases fresh foods, especially fruits, are used. A positive skin prick test results in a wheal 3 mm by 3 mm larger than a saline negative control. A histamine or codeine positive control is usually applied simultaneously. The sensitivity of a negative skin prick test is >95%. A positive skin prick test indicates the presence of IgE but has poor specificity. Diagnostic cut-offs of the skin prick test wheal size have been proposed for various foods, but it is prudent not to consider any skin prick test wheal size diagnostic of IgE-mediated food allergy in the absence of a supportive history. Furthermore, the size of the skin prick test wheal has not been shown to correlate with the severity of the reaction.

Specific IgE levels

Food-specific IgE is measured in kilounits per litre (kU/L) of serum. Most commercial assays have a range of 0.35–100 kU/L. The sensitivity of a negative food-specific IgE assay (<0.35 kU/L) is >95%, but the specificity of a positive test (>0.35 kU/L) is poor. Various diagnostic cut-off levels of food-specific IgE have been proposed but, like skin prick testing, one should be cautious about diagnosing immediate hypersensitivity to food based only on a specific IgE cut-off in the absence of a supportive history and when specific IgE levels have also not been shown to correlate with the severity of a reaction.

Atopy patch tests

Atopy patch testing, in which a food extract is applied to the patient’s skin for up to 72 hours, may be helpful in the diagnosis of delayed hypersensitivity reactions e.g. food protein enterocolitis. Induration occurring at the site of the patch is considered a positive result. The sensitivity of the atopy patch test is poor but the specificity is reasonable together with a supportive history. However, nonspecific irritation of the skin is common and as such these tests should be interpreted cautiously. A lack of standardised extracts has hampered the widespread use of this testing; however, commercial atopy patch tests are being developed that may improve the usefulness of this test.

Food challenges

The ‘gold standard’ for the diagnosis of food adverse reactions, immediate or delayed, is the oral food challenge. This can be done either open, single blinded or double blinded. Patients ingest incremental amounts of the suspected food and are then observed for a reaction. Food challenges are potentially risky and should be performed under medical supervision with facilities for resuscitation of the patient. Food challenges are especially important in the absence of a convincing history of a causative link between an adverse reaction and a food. They are also important to confirm that a patient has become tolerant of a food to which they were previously allergic. Protocols for the performance of food challenges often vary from clinic to clinic and are usually not standardised, however, various protocols for determining minimal reactive doses of various foods etc have been proposed.

MANAGEMENT

Treatments for the specific disorders are mentioned above. In general the management of food adverse reactions involves the avoidance of the causative food. A very important aspect of the management of food adverse reactions is the appropriate education of the patient or, in the case of children, their parents or carers. Patients should be told the estimated risk of a severe, life-threatening reaction, especially in the case of IgE-mediated food allergy. They should know how to administer emergency medications (e.g. an EpiPen®), if needed, and how to access medical care urgently. Most importantly, patients need to understand that avoidance is the mainstay of treatment. They should be educated to check for the presence of the causative food in all new foods, which may often involve thorough reading of food labels. Additional support, such as liaising with schools or child care in the case of children, is often necessary. Finally, all patients with food adverse reactions should receive regular medical review to ensure that management strategies, such as restricted diets, are still necessary and appropriate.

SUMMARY

Food allergy of all types may affect up to 6% of children and 4% of adults (Figure 10.1). The clinical syndromes induced are:

1. IgE-mediated immediate hypersensitivity. Peanut and shellfish are included in this category and may cause an anaphylactic reaction
2. Food protein-induced proctocolitis. This is a cell-mediated (eosinophilic) hypersensitivity, usually to cow’s milk or soy
3. Food protein enterocolitis is a cell-mediated (T cell) hypersensitivity similar to, but more severe than, food protein enteropathy. It is often caused by cow’s milk but between 30% and 50% of hypersensitive individuals are also sensitive to soy
4. Eosinophilic gastroenteropathy is a group of disorders characterised by infiltration of the gut wall by eosinophils. The diagnosis depends on demonstrating elevated numbers of eosinophils on biopsy.
image

FIGURE 10.1 Approach to suspected food adverse reaction.

Critical to management is a detailed clinical history. Information relating to the temporal relationship of the symptoms with ingestion of the food may help to differentiate immediate from delayed hypersensitivity reactions.

Diagnostic tests for immediate hypersensitivity include the skin prick test for food-specific IgE, specific IgE levels and the atopy patch test. However, the gold standard for the diagnosis of food adverse reactions, immediate or delayed, is the oral food challenge.

In general, management involves avoidance of the causative food. Appropriate education of the patient or, in the case of children, their parents is pivotal.

FURTHER READING

Bock SA, Sampson HA. Evaluation of food allergy. In: Leung DYM, Sampson HA, Geha RS, et al, editors. Pediatric allergy principles and practice. St Louis: Mosby; 2003:478-487.

Moneret-Vautrin AD. Gastroinestinal allergy in adults. Eur J Gastroenterol Hepatol. 2005;17:1293-1297.

Sampson HA. Update on food allergy. J Allergy Clin Immunol. 2004;113(5):805-819.

Sampson HA, Sicherer SH, Birnbaum AH. AGA technical review on the evaluation of food allergy in gastrointestinal disorders. Gastroenterology. 2001;120:1026-1040.

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