Food allergies and intolerance

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18 Food allergies and intolerance

Greg Whelan, Patrick Allen

Case

A male aged 16 years presents complaining of abdominal bloating and diarrhoea for 1 month. This commenced following an outbreak of what was described as viral gastroenteritis in his boarding school. All the other pupils have completely recovered.

His symptoms occur soon after eating or drinking. Specific inquiry reveals that milk or milk products appear to exacerbate his symptoms of bloating and diarrhoea. He has lost approximately 2 kg weight.

Physical examination was normal.

A lactose tolerance test was positive. This was confirmed by a positive lactose breath hydrogen test.

Following a consultation with a dietician he commenced on a lactose-free diet using soy products to substitute for milk. He has remained symptom-free.

Introduction

Many patients who present with gastrointestinal symptoms—particularly abdominal pain, diarrhoea and abdominal distension—complain of food-induced symptoms and believe that they are ‘allergic to food’. In some of these individuals there is food intolerance secondary to an underlying disease such as lactose malabsorption. However, the majority of patients have a functional gastrointestinal disorder, in which the mechanism of the perceived food intolerance is obscure. Only a minority of the apparently food-intolerant individuals will subsequently be found to be truly reacting adversely to components of the food they eat and rarely will this reaction be of an immunological (allergic) nature.

Adverse food reaction can be broadly based into two categories. The first category is immunologically mediated adverse reactions to foods. These particular reactions are unrelated to any physiological effect of the food or food additive, and are mediated by immunoglobulin E (IgE) antibodies and others result from non-IgE-mediated mechanisms.

The second category is food intolerance. These reactions include any adverse physiological response to a food or food additive that is not immunologically mediated, such as lactose intolerance or pharmacologically related adverse food reactions.

The mainstay of management of food allergies and adverse reactions remains focused on avoidance of the allergenic or reactive foods. There have been recent multiple advances to various therapies that may eventually complement or even replace the main therapeutic approach, which is food avoidance.

A Clinical Approach

History and physical examination

The relationship of the gastrointestinal symptoms to meals needs to be determined. In true food allergy this commonly occurs soon after ingestion. Excessive bloating and diarrhoea suggests lactose intolerance. In functional gastrointestinal disorders, symptoms after meals are common but symptoms between meals are also frequent and often no food can be consistently blamed. The specific symptoms of irritable bowel syndrome should be sought (Ch 7). Individuals may react to the nutrients in food, such as protein, carbohydrate, fat, vitamins or minerals or to food additives. Foods that commonly cause reactions are summarised in Table 18.1.

Table 18.1 Main foods that commonly cause gastrointestinal disturbances

Food type Common examples of trigger foods
Cereal grains Wheat
Dairy products Milk, cheese
Fruit Citrus Fruit
Vegetables Onions, capsicum
Miscellaneous foods Coffee, eggs, chocolate

A physical examination is generally unhelpful, unless the patient is currently experiencing symptoms. Occasionally skin rashes or signs of asthma are detected. It may be helpful in excluding other disorders.

There are multiple approaches to elicit a history from individuals with adverse food reactions that are possibly due to an allergen.

The suggested approach is to elicit three main elements from the history:

1. symptoms associated with adverse food reaction such as nausea, bloating, vomiting, itch;
2. possible reactive or triggering foods—peanuts, for example;
3. possible contributing factors that may have exacerbated the adverse reaction such as associated with concomitant drug therapy or associated with exercise.

Note that allergic reactions to food have the potential for serious, even fatal, outcomes. Thus the highest priority is to elicit the symptoms of the allergic reaction if they can be identified.

What are the symptoms involved with the allergic reaction?

These can include the following common presentations:

• systemic symptoms—palpitations, dizziness, fainting and collapse;
• gastrointestinal symptoms—nausea, vomiting, diarrhoea and cramping abdominal pains;
• dermatological—urticaria, angio-oedema, flushing, swelling or itching a few minutes after food;
• respiratory symptoms—stridor, wheeze, cough and dyspnoea.

What was the onset of symptoms like? Was the onset acute or subacute?

How rapidly did the symptoms occur after the ingestion of the allergen? IgE allergic reactions can typically occur within minutes, whereas non-IgE (cell-mediated) reactions tend to develop more gradually over hours to days.

How severe was the allergic reaction on this occasion?

All of the symptoms experienced should be documented and their severity explored. Did the patient require hospital admission with severe cardiorespiratory symptoms? If this is the case, this is usually an acute IgE-mediated reaction.

Has this reaction occurred in the past? If so what was the severity grade then?

If the patient had anaphylaxis requiring intramuscular adrenaline and treatment in an intensive care unit, this is likely to be a severe IgE-mediated reaction. The patient’s medical records should be requested and reviewed to confirm symptoms such as wheezing, flushing, stridor and collapse as patients may not be fully aware of these events.

Identification of Food Allergens

It is important to accurately document the potential food allergens and their previous effects and reactions. Such documentation includes the following points:

• Develop a list of foods that may have caused the symptoms. Eggs, nuts and seafood are the usual suspects.
• Discuss the minimum quantity of food required to produce the symptoms.
• Explore the preparation of the relevant foods (raw, cooked, contaminated with another food additive, spices and so on).
• Explore the characteristic symptoms that the patient experiences on exposure to the relevant food.

Identification of contributing factors

The questions below are potentially less helpful in identifying the offending allergen, but they may also provide the clinician with some additional information regarding the exacerbating factors to the allergic response:

• Did the patient receive any concurrent medications at the time of the allergic reaction? It has been reported that alcohol or anti-inflammatory agents may exacerbate the allergic reaction.
• Was the patient involved in any physical exertion before the reaction? Some reactions may be severe after physical exercise.

Physical examination in the emergency department

The initial examination to a patient presenting to an emergency department is to assess the severity of the condition and includes careful assessment of:

AAirway

BBreathing

CCirculation.

To assess signs of severe anaphylaxis it is important to observe for cardiorespiratory compromise and dermatological manifestations, which include the following:

• acute respiratory complications: bronchospasm, stridor, wheeze, cyanosis;
• acute cardiovascular complications: tachycardia, hypotension, delayed capillary refill time, drowsiness;
• acute dermatological signs: angio-oedema, urticaria.

If these features are present, immediate treatment should be instituted; see the sections on management below.

The majority of food allergies present subacutely or chronically, so the preferred approach is to identify any possible manifestations of their allergy, for example dermatological symptoms, along with a detailed history as above. There are various symptoms of chronic diseases where a food allergy may be responsible; for example, atopic dermatitis has been associated in approximately 40% of infants or children with moderate to severe atopic disease.

Investigations

Appropriate investigations may be needed to exclude other relevant diseases such as coeliac disease and inflammatory bowel disease or to confirm a suspicion of lactose intolerance. This is particularly important if there is evidence of weight loss or gastrointestinal tract bleeding. The specific features of immunologically mediated adverse food reactions and food intolerance are discussed below.

Pathophysiology

True allergic reactions of the hypersensitivity type are rare. In these circumstances, the offending agent is a specific food, such as eggs, nuts, milk or seafood. Food allergy reactions may be IgE-mediated, non-IgE-mediated or both. IgE-mediated antibodies are the most widely recognised mechanism of food hypersensitivity. Atopic patients can produce IgE antibodies to specific epitopes of the food allergen, which can then bind to high-affinity receptors in the skin, gastrointestinal tract and respiratory tract. These then cause the release of inflammatory mediators including histamines, leukotrienes, prostaglandins and cytokines. These can then produce various tissues effects, including mucus production, vasodilatation, and smooth muscle contraction, thereby producing the symptoms associated with food allergen exposure. Most IgE-mediated reactions are immediate reactions, so produce effects such as acute cutaneous symptoms or anaphylaxis.

Non-IgE-mediated food allergies (mainly delayed Th2-type cell-mediated responses) are usually manifest by chronic skin or gastrointestinal complaints. The absence of reliable testing for non-IgE-mediated allergies has contributed to a poorer understanding of its pathogenesis. Those allergies that are associated with several diseases, such as eosinophilic oesophagitis, are not always due to primarily an IgE or non-IgE reaction but may be a combination of both.

Food allergens are water-soluble glycoproteins resistant to heating and proteolysis with molecular weights of 10–70 kDa. These small proteins can be absorbed across mucosal surfaces, and many are well classified such as the common peanut allergens Ara h1, Ara h2 and Ara h3. Closely related foods frequently contain allergens that cross-react immunologically but less frequently cross-react clinically. There has been recent evidence that cross-reactive allergens have been identified in certain foods and airborne pollens.

Incidence

General surveys report that as many as 30% of households consider at least one family member to have an adverse food reaction. It has been estimated that between 20% and 30% of people report food allergies in themselves or their children. However ‘true’ food allergy is present in only 6% of children and in approximately 3% of adults.

Morbidity and mortality associated with food allergies

The symptoms of adverse food reactions are typically manifest in the gastrointestinal tract, skin and respiratory tract. The majority of symptoms of food allergies are mild and include various gastrointestinal symptoms such as bloating, abdominal pains and nausea. However, there have been multiple reports of severe anaphylactic reactions and death following the ingestion of certain foods. Fatalities can result from severe laryngeal oedema, bronchospasm, hypotension or a combination of all of these signs.

Investigations for food allergies

There are several objective approaches to testing for food allergens which vary between clinicians and institutions. The following are brief descriptions of the main investigations used in an attempt identify food allergies.

Skin-prick tests are performed with fresh fruits and vegetables by inserting the test device into the relevant fruit or vegetable and then pricking the patient’s cleaned skin. This has been shown to be a more reliable method to detect allergies to fresh foods (apples, tomatoes and so on) than commercial testing with food extracts. Testing with fresh fruit and vegetables has a sensitivity of 95% and specificity of 50%. Skin testing with commercial food extracts may be more useful for sensitisation to peanuts or legumes which contain stable allergens. They are also useful to assess the systemic reactions to certain allergens, as they have been shown to be better to demonstrate systemic reactions than fresh extracts.

IgE immunoassays are in vitro tests to detect food-specific IgE, for example IgE radioallergosorbent testing. They can be useful in circumstances where IgE-mediated reactions are thought to be likely, such as in life-threatening anaphylaxis. This can provide similar information to skin-prick testing, but it is more expensive and less specific. As there are significant false positives and negatives, the test results should be considered in conjunction with a detailed clinical history. IgE immunoassays have a sensitivity of 95% and a variable specificity. Availability is limited to several major allergens: including egg, milk, fish and peanuts.

Acute management of severe food allergic reactions

If these features are present immediate treatment should be instituted with high flow oxygen, intravenous (IV) hydrocortisone, IV antihistamines, and/or intramuscular adrenaline (in cases of severe anaphylaxis with hypotension, laryngeal oedema or severe bronchospasm). The patient may need to be managed in an intensive care setting depending on the severity of their reaction and their recovery with the above management. Individuals who have been diagnosed with significant allergic reactions should be taught how to use a self-administered adrenaline injection and advised to always carry it with them.

Pharmacological management of food allergies

There have been recent developments in use of monoclonal antibodies to IgE in the management of suspected IgE-mediated food allergies. A randomised controlled trial and found that an anti-IgE antibody can confer protection against unintended peanut ingestion in those with IgE-mediated allergies in 75% of patients. This drug has been discontinued due to consensus agreements among pharmaceutical companies, but in the future anti-IgE antibodies may prove to be beneficial in those with moderate to severe food allergies.

Oral immunotherapy has been the target of several studies as it may reduce the risk of side effects that are associated with subcutaneous route of administration. A randomised controlled trial that used the sublingual administration of hazelnut extracts demonstrated effectiveness with only minor systemic side effects. A similar study administered increasing doses of food allergens to children who had wheat, apple, milk, egg and fish allergies. This resulted in an 86% success rate in those patients who completed the treatment protocol, with only minor side effects. This therapeutic approach requires further study. The benefit appears to be achieved with a regular intake of the drug. Compliance may be a problem. There is also need for long-term outcome data with these therapies.

Non-IgE-mediated food allergies are more difficult to diagnose and manage than IgE-mediated allergies for several reasons. They are cell-mediated allergies and have a slow disease course compared to IgE-mediated reactions. The established tests of skin-prick testing and serum measurements of food-specific IgE levels are less sensitive in these allergies. This dictates that the overall management is different to IgE-mediated allergies. The most widely studied non-IgE-mediated food allergy has been eosinophilic oesophagitis. This is characterised by oesophageal intraepithelial eosinophilic infiltration (Ch 2).

Several therapeutic approaches have been studied for the management of eosinophilic oesophagitis. One of these is the use of an amino-acid-based formula. Several studies have shown that this can induce clinical symptomatic and histological remission in a paediatric population with eosinophilic oesophagitis. An elemental diet is an effective treatment for eosinophilic oesophagitis in children and adolescents. The limiting factor associated with this form of therapy may be compliance. Its taste is described as unpleasant and the volume required to be consumed is large. It imposes a dramatic change that is difficult for older children.

Corticosteroids are the current mainstay of treatment in eosinophilic oesophagitis. Oral methylprednisolone was given for 4 weeks to 20 children with eosinophilic oesophagitis and resulted in a dramatic histological and clinical improvement in the vast majority of patients. However, systemic side effects of corticosteroids limit their use in this disease, particularly in a paediatric population. A different route of administration of corticosteroid, which involves ‘topical’ administration consisting of swallowed aerosolised fluticasone propionate, has been developed. A recent published randomised controlled trial performed over 3 months in paediatric patients with eosinophilic oesophagitis resulted in 50% histological remission in those who were treated with fluticasone, compared with 9% remission in placebo-treated patients. Troublesome side effects have been noted with this therapy. They include oesophageal candidiasis. Disease relapse was observed on their discontinuation.

Dietary manipulation appears to have some success in treating eosinophilic oesophagitis. When food elimination based on skin-prick testing alone proved to be non-beneficial, one study demonstrated that elimination diets based on a combination of skin-prick testing and patch testing had a success rate of 77%. In an observational study, six foods thought to be highly allergenic were removed from the diet of patients with eosinophilic oesophagitis. These included egg, soy, wheat, peanut, milk and seafood. Improvement in oesophageal eosinophilia was observed in 74% of patients. Dietary manipulation may need to be considered in the future as a form of therapy, but failure to thrive in a paediatric population may preclude the use of this management.

Food Intolerance

The non-allergenic intolerances to food are heterogeneous and can be divided into two main groups: lactose intolerance and pharmacologically-related adverse food reactions as opposed to true ‘allergic food reactions’.

Lactose intolerance

Lactose intolerance is a very common precipitant of food intolerance. Lactase is a brush border enzyme that splits the milk sugar, lactose, into glucose and galactose. Absence of this enzyme results in osmotic diarrhoea due to presence of unabsorbed lactose in the small bowel and colon. In the colon lactose is converted to hydrogen and short-chain fatty acids by the bacterial flora. There are three forms of lactase deficiency:

1. congenital lactase deficiency, which is present from birth and is very rare;
2. acquired lactase deficiency, which occurs in most non-milk-consuming populations around the world and develops in late childhood; and
3. secondary lactase deficiency, which occurs in situations where small bowel mucosal damage is present, such as postgastroenteritis and coeliac disease.

Intolerance to lactose-containing foods is a common problem. In Europe and the United States it has been estimated that the prevalence is 7–20%, and is as high as 95% in Native Americans, 75% among Africans and African Americans, and 50% in Hispanics.

Clinical symptoms of lactose intolerance include abdominal pains, diarrhoea and flatulence after ingestion of milk or milk-based products. These symptoms have been attributed to low intestinal lactase levels, which may be secondary to mucosa injury, or reduced genetic expression of the enzyme lactase-phlorizin hydrolase. Lactose intolerance can also co-exist with irritable bowel syndrome and their symptoms can be similar.

The term ‘lactose malabsorption’ is generally reserved for those patients with typical symptoms in whom the intestinal malabsorption of lactose has been confirmed by a test of absorption or malabsorption. The lactose tolerance test measures the capacity for lactose absorption after the oral administration of a 50 g test dose in adults and sequential measurement of blood glucose levels. False-negative results can be seen in diabetes, bacterial overgrowth and abnormal gastric emptying. The lactose breath hydrogen test measures lactose malabsorption, by giving the patient oral lactose and measuring breath hydrogen at serial intervals. Both false-negative and positive results can occur with this test.

A genetic test for the polymorphism associated with lactose intolerance has been developed with an acceptable sensitivity and specificity.

Management of lactose malabsorption generally takes the form of three approaches:

1. reduced dietary lactose intake. The patient should be instructed to avoid lactose and in particular milk, ice-cream and cheese, which have high concentrations of lactose, for at least 2 weeks or until the symptoms resolve. Most patients can tolerate a daily intake of 240 mL of 2% fat milk, although spreading the lactose load throughout the day may be beneficial.
2. substitution of alternative nutrient sources to maintain energy and protein intake. The patient should consult with an appropriate dietician for dietary advice to maintain an adequate lactose-free food intake.
3. administration of a commercially available enzyme substitute. This is a bacterial or yeast beta-galactosidase. It can reduce symptoms and breath-hydrogen values after ingestion of lactose-containing foods in lactose-intolerant patients.

Pharmacologically related adverse food reactions

In many individuals there is no evidence of an allergic reaction or a specific enzyme-deficiency but the gut and other organs appear to react to one or more ingredients in the food ingested. In these situations reactions to food are often delayed from between 1 hour and 48 hours after ingestion. It is likely that reactions occur to more than one food, and reactions to each constituent may exhibit a dose-response relationship with a triggering threshold that depends partly on recent intake. Thus an individual food does not necessarily produce the same reaction on each occasion. This can result in a delay in diagnosis.

Recurrent aphthous ulceration is infrequent but is characteristically found in salicylate-sensitive individuals. Upper respiratory tract symptoms such as nasal congestion, excessive mucus production, recurrent sore throats or sinusitis are common in those who react to dairy products. In some individuals these foods can precipitate asthma.

Neurological symptoms are commonly present and are sometimes bizarre including headaches, general lethargy and myalgia. Patients may describe the sensation of feeling ‘drugged’ or ‘hung-over’. When challenged by these foods they may note confusion, dizziness, paraesthesia, sweating, palpitations and flushing. Objective impairment of memory and concentration may be documented.

These reactions cannot be diagnosed accurately by any available skin or blood test.

The chemicals in the responsible foods are best identified by systematic diets and oral challenge:

• Diet diary: This can be helpful irrespective of the putative cause of the food reaction. The diary consists of a detailed record of all foods consumed and any perceived food reaction experienced. This can be useful to identify culprit foods that are potentially responsible for symptoms. It helps patients focus on the foods consumed, but it is not usually diagnostic and may be misleading, as many symptoms due to adverse food reactions are delayed or infrequent.
• Elimination diets and challenge: The responsible food chemicals are best identified by systematic elimination diets and oral challenge. Since each component compound is often present in many foods and each patient is usually sensitive to several compounds, the elimination diet must be comprehensive.

This approach can be used to determine the diagnosis as well as the treatment and prevention of adverse food reactions whether allergy or not. When this is used as a diagnostic tool, it generally requires complete avoidance of suspected foods for a given time period (usually 1–2 weeks) while monitoring for a decrease in symptoms. These diets can be difficult to follow as more foods that commonly occur in the diet are eliminated. Additional limitations of this method include possible patient or physician biases, which may limit interpretation of results and treatment and variable patient compliances. Challenges should be spaced by at least 48 hours to allow for delayed reactions. Any response to a challenge should be followed by a pause of at least three symptom-free days because patients often experience a temporary refractory period during which they are unresponsive to that particular food.

When designing an elimination diet for individuals with potential food-induced problems, it is usually wise to remove cereals, dairy products, citrus fruits, beverages and food additives. A standard exclusion diet should avoid these but be nutritionally adequate and contain meat (usually lamb), fruits (particularly pears) and vegetables. If an individual has not improved after 2 weeks on an exclusion diet, as a general rule symptoms are not due to food intolerance, and it is likely that they have a functional gastrointestinal disorder.

Thus diagnosis of food intolerance can be confirmed by the use of an elimination diet to determine whether symptoms remit and re-emerge on a subsequent challenge with suspected ‘trigger foods’ stuffs versus a placebo (preferably double-blind). This means of diagnosis is time-consuming and difficult. Compliance by poorly motivated patients is low. However, the results are dramatic and sustained in some individuals when long-term dietary modifications are undertaken based on the results of individual oral provocation results.

Summary

Education is of paramount importance to patients with food allergies. Patients should be given information to contact their local food allergy organisation and the International Food Information Council. The patient should be referred to an immunologist in cases where IgE-mediated reactions are suspected. The diagnosis and management of non-IgE-mediated allergies is more complex and should involve a gastroenterologist and an immunologist. Once a food allergy has been diagnosed, it is important that the trigger allergen is strictly avoided whether by ingestion, skin contact or inhalation.

Patients with likely IgE-mediated allergies that appear mild should be given a prescription for antihistamines to take as required. However, where there is a strong suspicion of anaphylaxis or moderate to severe symptoms the patient should receive and be educated in the use of epinephrine autoinjectors.

For lactose intolerance and pharmacologically related reactions, the main treatments which appear to be useful are food avoidance and an elimination diet respectively (see Table 18.2).

Table 18.2 Summary of the characteristics, investigations and management of the main food reactions

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Key Points

• Complaints of adverse reactions to food are common.
• Irritable bowel syndrome has many similar symptoms.
• Foods commonly associated with adverse reactions include wheat, milk, citrus fruit, eggs and chocolate.
• Some reactions are immunologically mediated (allergic), for example fish and eggs.
• Some reactions are pharmacologically related adverse food reactions, for example wheat and food additives.
• Elimination diets with challenge often need to be performed to support a diagnosis of pharmacologically related food reactions.
• True allergic reactions (e.g. IgE mediated and non-IgE mediated), while rare, can be life-threatening.

Further reading

Burks A.W., James J.M., Hiegel A., et al. Atopic dermatitis and food hypersensitivity reactions. J Pediatr. 1998;132(1):132-136.

Enrique E., Pineda F., Malek T., et al. Sublingual immunotherapy for hazelnut food allergy: a randomized, double-blind, placebo-controlled study with a standardized hazelnut extract. J Allergy Clin Immunol. 2005;116(5):1073-1079.

Jansen J.J., Kardinaal A.F., Huijbers G., et al. Prevalence of food allergy and intolerance in the adult Dutch population. J Allergy Clin Immunol. 1994;93(2):446-456.

Kagalwalla A.F., Sentongo T.A., Ritz S., et al. Effect of six-food elimination diet on clinical and histologic outcomes in eosinophilic esophagitis. Clin Gastroenterol Hepatol. 2006;4(9):1097-1102.

Kelly K.J., Lazenby A.J., Rowe P.C., et al. Eosinophilic esophagitis attributed to gastroesophageal reflux: improvement with an amino acid-based formula. Gastroenterology. 1995;109(5):1503-1512.

Konikoff M.R., Noel R.J., Blanchard C., et al. A randomized, double-blind, placebo-controlled trial of fluticasone propionate for pediatric eosinophilic esophagitis. Gastroenterology. 2006;131(5):1381-1391.

Leung D.Y., Sampson H.A., Yunginger J.W., et al. Effect of anti-IgE therapy in patients with peanut allergy. N Engl J Med. 2003;348(11):986-993.

Liacouras C.A., Spergel J.M., Ruchelli E., et al. Eosinophilic esophagitis: a 10-year experience in 381 children. Clin Gastroenterol Hepatol. 2005;3(12):1198-1206.

Markowitz J.E., Spergel J.M., Ruchelli E., et al. Elemental diet is an effective treatment for eosinophilic esophagitis in children and adolescents. Am J Gastroenterol. 2003;98(4):777-782.

Patriarca G., Nucera E., Pollastrini E., et al. Oral specific desensitization in food-allergic children. Dig Dis Sci.. 2007;52(7):1662-1672.

Rasinpera H., Savilahti E., Enattah N.S., et al. A genetic test which can be used to diagnose adult-type hypolactasia in children. Gut. 2004;53(11):1571-1576.

Sampson H.A., Anderson J.A. Summary and recommendations: classification of gastrointestinal manifestations due to immunologic reactions to foods in infants and young children. J Pediatr Gastroenterol Nutr. 2000;30(suppl):S87-S94.

Sicherer S.H., Sampson H.A. Food hypersensitivity and atopic dermatitis: pathophysiology, epidemiology, diagnosis, and management. J Allergy Clin Immunol. 1999;104(3 Pt 2):S114-S122.

Spergel J.M., Andrews T., Brown-Whitehorn T.F., et al. Treatment of eosinophilic esophagitis with specific food elimination diet directed by a combination of skin prick and patch tests. Ann Allergy Asthma Immunol. 2005;95(4):336-343.

Young E., Stoneham M.D., Petruckevitch A., et al. A population study of food intolerance. Lancet. 1994;343(8906):1127-1130.

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