This issue was sponsored by Abbott Laboratories S.A (PTY) LTD All Abbott products are lactose and gluten free Tel: +27 (0)11 8582054

 

Contents A. Case study B. More information C. Editors' comments D. References E. CEU questions

Index

A. Case study

An 8-year-old boy was referred to the gastroenterologist from the hematologist. He had a 2-year history of severe iron deficiency anemia. The anemia had persisted despite previous oral iron supplementation as well as intravenous iron being administered on 2 prior occasions. He also presented with hypoalbuminaemia, abdominal pain, poor appetite, nausea and vomiting (2-3 times a week). According to his parents, these symptoms had progressively worsened over the past 2-3 years, and he had demonstrated severe failure to thrive, with no growth in either weight or length.

His early medical history showed that he was born at full term and weighing 3.1 kg. As a young child, he had had gastro-esophageal reflux that had been unresponsive to conventional treatment. Although he had no family history of allergies, he did suffer from asthma and had experienced clinical reactions to ingestion of soya (severe vomiting resulting in dehydration). He also had eczema (the cause of which had never been established), which seemed to have improved slightly with age, and he was allergic to feathers.

The first step was to establish the cause of his persistent anemia and failure to thrive.

WHAT SHOULD BE CONSIDERED AT THIS STAGE?
Iron deficiency anemia can arise from:
a. Inadequate iron intake secondary to a poor diet, as in a vegetarian regime with insufficient heme iron.
b. Inadequate absorption resulting from diarrhea, intestinal disease, atrophic gastritis or drug interference (e.g., antacids, cholestyramine, Zantac, tetracycline).
c. Inadequate iron utilization secondary to chronic gastrointestinal disturbances.
d. Increased excretion because of hemorrhage from injury, or chronic blood loss from a bleeding ulcer, bleeding hemorrhoids, oesophageal varices, regional enteritis, ulcerative colitis or other malignant disease.
e. Increased iron requirements for growth of blood volume, relevant both in infancy and adolescence.
f. Defective release of iron from iron stores into the plasma, or defective iron utilization owing to a chronic inflammation disorder.

DISCUSSION
a. Assessment of his diet showed that he was eating a relatively large variety of foods, although he consumed very little red meat (approximately twice a month). He also tried to avoid soya-containing foods because of his previous reactions.
b. On assessment, he had normal stools and no diarrhea; according to himself and his parents, he had no visible blood in his stools. A stool sample, however, identified occult blood. At this stage, he was on no medications that might have inhibited iron absorption. As a young child, he had been treated with antacids and Zantac for gastro-esophageal reflux, although this treatment had stopped by the age of approximately 4 years, as no improvement was noted.
c,d.&f. When he vomited, there was no blood. A gastroscopy and colonoscopy would be necessary to rule out gastrointestinal disorders and other chronic conditions.
e. He was not going through his adolescent growth spurt and in fact demonstrated slight stunting.

Various conditions possibly contributing to his overall clinical picture needed to be ruled out:
a. Celiac disease
b. Inflammatory bowel disease
c. Food allergy
d. Parasitic infestation

WHAT CAN BE DONE?
a. Celiac disease screening tests, including endomysial and gliadin antibody tests, were negative.
b. A gastroscope and colonoscope showed a normal colon. No obstructions, ulcers or masses were found. Inflammation and significant eosinophilic infiltration of the esophagus (25 eosinophills per high-power field) was observed. Mild eosinophilic infiltration was present in the gastric antrum and duodenum.
c. Total IgE levels were very high, and he demonstrated an IgE-mediated allergy to peanuts, mixed nuts and egg. In order to rule out non-IgE mediated reactions, an elimination diet of suspected allergenic foods was suggested. He demonstrated improvement of symptoms with the removal of milk, egg, wheat, fish, and shellfish, as well as of maize and rye, which his mother had suspected. (Soya, peanuts and tree nuts were already excluded because of previous findings). Symptoms returned with the re-introduction of maize, wheat, rye, milk, egg and shellfish. He seemed to tolerate fish.
d. A stool sample ruled out a parasitic infection.

Eosinophilic gastroenteropathy was diagnosed, presenting with malabsorption in response to allergen exposure.

He was placed on oral steroids and an allergen restriction diet and underwent a trial of an age-appropriate elemental formula, which initially provided approximately 75% of his nutritional requirements. His growth parameters improved dramatically, the first change in 2-3 years. As symptoms improved, the elemental formula was reduced and the amount and variety of regular foods were expanded. His parents also noted significant improvement in cognition and energy levels.

DISCUSSION:
This case illustrates both how insidious and how serious adverse reactions to food can be. A clinician’s view of this field must be at the same time broad and precise in order to insure that proper diagnosis and treatment give patients the best chance for a normal and healthy life. This is especially true for conditions that do not involve anaphylaxis and therefore the risk of life. Typically neglected or misdiagnosed, “low-level” reactions can have a huge impact on well-being and achievement.

Eosinophilic esophagitis (EE) and eosinophilic gastroenteritis (EG) are rare diseases of unknown etiology, characterized by patchy or diffuse eosinophilic infiltration, inflammation of the esophagus and/or gastrointestinal tract wall, and various gastrointestinal manifestations (e.g., persistent and non-responsive gastro-esophageal reflux, vomiting, nausea, abdominal pain, diarrhea, failure to thrive, strictures, dysphagia and food impaction). EE is diagnosed by identifying more than 20 eosinophils per high-power field on examination of esophageal biopsy specimens. Barium radiography may be useful for detecting obvious signs of EE, including rings and strictures.

Although extreme elevations in serum IgE may correlate with the severity of the disease, typical allergy tests are not effective for diagnosis. But skin prick and atopy patch testing may help identify culprit foods in most cases. The allergic reaction involved seems to be non-IgE-mediated, although both IgE and non-IgE mechanisms may play a role. In EE, a multi-step allergy process may occur, starting with an atopic skin response: eczema and even concomitant asthma can prime the esophagus on further allergen exposure.

Therapy involves the use of oral corticosteroids, appropriate dietary elimination once food allergens have been identified, and inclusion of an age-appropriate, nutritionally complete elemental formula. The combination should result in resolution of perceptible symptoms as well as the underlying esophageal and/or intestinal inflammation. Unfortunately, although inclusion of an elemental formula seems to be preferable both for the short and the long term, compliance is usually difficult. Moreover, symptomatic relapse after one course of corticosteroids is common, and many patients require repeated courses of treatment. The long-term prognosis is largely unknown.

The foods most commonly identified as being involved include milk, eggs, nuts, beef, wheat, fish, shellfish, corn, and soy; however, almost all foods may conceivably be implicated. Because allergy tests are often unable to determine the causative foods, complete elimination of foods is often required, to be replaced by an exclusive elemental formula for 1 to 3 months to heal the mucosa. A repeat endoscopy with biopsy is then often necessary.

This case study has been adapted with permission from Ms. Lauren Ponting (RD) and Dr. Michelle Zuckerman (MD): our thanks for the opportunity to learn from their experience.

TIP for Allergy Advisor users: Under “Assessment”, you will find “Definitions & Glossary” which includes the Classification of Adverse Reactions to Food 1995 as well as the Nomenclature for Allergy 2001. This section also includes descriptions of the differences between the various types of adverse reactions.

B. More information:
Adverse reactions to food have been self-reported by up to 25% of people at some point in their lives. The true incidence of actual adverse reactions to food is probably far lower. The highest prevalence is observed during infancy and early childhood. A wide spectrum of adverse reactions may occur after ingestion of or other exposure to food. Such reactions are generally classified on the basis of the underlying pathophysiologic changes that produced the reaction, e.g., food allergy, food intolerance, pharmacologic reactions, food poisoning and toxic reactions. The extensive range of various possible adverse reactions and the difficulty of assessing many of them (due, for example, to delayed reactions and intolerances) complicates identification of a true reaction. But the pathogenesis is, of course, relevant to the management of patients with adverse reactions to food.¹

Food reactions can first of all be divided into true reactions to food and psychosomatic or psychological reactions. In the latter, individuals believe they are sensitive to a food and react, but the reaction is not reliably reproducible.

Generally, true adverse food reactions are due to toxic or pathogenic mechanisms; another basic division is between immunological and non-immunological mechanisms.

A. Toxic
Toxic reactions to foods include bacterial food poisoning and heavy metal poisoning.

Toxic reactions may result from the presence of natural toxins in foods: e.g., the alkaloid solanine in green potatoes or the hemagglutinins in uncooked kidney beans. Toxic reactions may also result from food’s contamination by chemicals or microbial pathogens, the latter of which kind of incident is commonly called food poisoning.²

Bacterial contamination of food usually originates during handling. Symptoms may occur immediately after ingestion of the contaminated food, as with Staphylococcus exotoxin and Escherichia coli enterotoxin. There may also be a delay before the onset of the reaction, as with Salmonella or E. Coli. In many cases, an adverse reaction may be mistakenly attributed to a gastrointestinal virus. But if many individuals at a given site develop symptoms, this points to a common food source as the cause.¹

Heavy metals commonly implicated in food poisoning include lead, tin, copper, zinc, aluminum and mercury.

B. Immune-mediated reactions – Food allergy
Immunological reactions to foods need to be separated from non-immunological reactions to foods, although the clinical presentation may be very similar.¹

Food allergy can be defined as an immune-mediated response to foods or food additives. Simplistically, food allergy can be a consequence of enhanced food antigen entry into the intestinal mucosa, of an abnormal reaction to antigen presentation to lymphocytes, or of an uncontrolled inflammatory reaction of the gut or other organs. There are at least two hypotheses, which are not mutually exclusive, for the etiology of allergic responses³:

1. Food proteins in the GIT meet antigen-presenting cells in the mucosal wall, which results either in tolerance or in T cell activation toward that food protein (an allergen). Sensitized T cells or specific IgE may migrate from the site of sensitization to the affected organ.
2. Food allergens penetrating the GI epithelium may enter into the blood circulation and so may be transported to other effector organs.

The allergic immune response can be divided into 4 phases:

1. Presentation of the allergen
2. The sensitization phase (the asymptomatic development of “memory” for the food)
3. The effector phase, which has an acute and a facultative late-phase reaction
4. The chronic phase, which may be the result of repetitive late-phase reactions

The disease is preceded by a sensitization phase without symptoms. At this time, specific IgE is raised against a specific food protein that appears “foreign” to the body. Sensitization is most likely to occur by the oral route in infants and young children; in older children and adults, sensitization has been known to occur via the airways.³ It has been postulated, however, that even in infants and young children, sensitization may occur through the lungs or even the skin (skin contact with creams, foods, etc.).

An allergen challenge of sensitized individuals results in an immune response, either through antibodies (IgE) or cellular mechanisms such as those involving basophils; or the response can be mixed, triggering a number of effects, including tissue inflammation. The sites of allergen sensitization, allergen uptake and subsequent inflammatory reactions may vary, and the factors determining the selection of target organs (gut, lung, skin, etc.) are unknown. Immediate reactions occurring within seconds to minutes may be followed by late-phase reactions occurring within 2-48 hours after initial allergen exposure. Finally, these reactions may be characterized by cellular infiltration with granulocytes (basophils and eosinophils) and lymphocytes (Th2 cells).³

To summarise, then, the development of food allergy is usually a multi-step process, requiring repetitive challenges with a particular food antigen. The initial exposure results in sensitisation, whereas the second may produce an immediate reaction. But there are exceptions, and reactions may occur after more than two exposures. Several factors are relevant to the development of food allergy, including genetic polymorphisms, environmental conditions, mucosal barrier function, mucosal immune function, the type and dose of food allergen, the route of allergen administration, and the age of the subject (onset may occur late in life).³

Immunological reactions can be IgE mediated, non-IgE mediated or mixed.^1,4,5,6

1. IgE-mediated reactions (an IgE antibody response mounted by the body)
IgE-mediated reactions are often referred to as classic food hypersensitivity or immediate, type I food allergy. The time from ingestion of or exposure to the food to symptom onset is usually rapid (within minutes); small amounts of food may elicit severe reactions; and reactions will usually continue to occur with re-exposure. Commonly, manifestations occur in the gastrointestinal tract, skin and respiratory system.¹

Typically, either a failure to develop an oral tolerance or a breakdown in such tolerance results in excessive production of food-specific IgE antibodies. The allergen binds with the sensitized IgE antibody on mast cells (specialized granular cells in the intestines, skin and respiratory tract) or basophils (similar cells in the blood). This results in release of mediators (histamine, eosinophilic chemotactic factor, bradykinin, etc.) and manifestation of certain clinical symptoms.^5,7

For this type of reaction to occur, the body must have been exposed to the antigen previously, ‘priming’ the system with production of antigen-specific IgE. Subsequent exposure in the sensitized host can lead to immediate hypersensitivity reactions in the target organs.⁸

A simple, step-by-step sequence of the events generating antibody (IgE)-mediated immunity is as follows^5,7,8:

Skin prick testing and RAST tests that measure the presence of IgE specifically directed to an allergen are helpful in diagnosis of this type of adverse reaction.

2. Non-IgE-mediated reactions (a cellular response, thought to be directed by basophils mounted by the body)
Non-IgE-mediated immunological reactions to foods are often referred to as Type IV (cell-mediated) hypersensitivity and tend to be gastrointestinal; however, cutaneous and pulmonary reactions may also occur. The onset of clinical symptoms seems to be delayed for a number of hours (24-48) after the ingestion of or exposure to a culprit food, and activation requires larger doses of the allergen (but exceptions may occur due to individual variation).

Non-IgE-mediated reactions can be divided into 2 groups:

1. Delayed allergy reactions, which are still typically allergy-like and include delayed cow’s milk allergy and delayed soy allergy. These reactions are cell-mediated, typically through basophils, and can be diagnosed with relative accuracy using atopy patch testing.
2. Other reactions mediated by various putative immune complexes, IgA or other cells: food-induced enteropathy, enterocolitis and colitis; and malabsorption syndromes such as celiac disease and dermatitis herpetiformis. In these cases, a correlation between food ingestion and the reaction may be less obvious, particularly with gastrointestinal reactions.¹

The immune mechanisms of non-IgE-mediated food allergies are not well understood. Although this type of immune response does contribute to certain adverse food reactions such as enterocolitis, significant supportive evidence of a specific cell-mediated hypersensitivity disorder is still lacking.⁵ In non-IgE hypersensitivity reactions, T lymphocyte cells interact directly with the specific antigen.⁷ They recognize antigens bound to foreign cells and cause lysis. The sensitized T-cells can also release lymphokines, which activate non-sensitized cells to destroy antigens.² The strongest evidence of this type of reaction comes from the identification of food-specific T-cells in atopic dermatitis in children, and in some types of contact dermatitis in adults.^2,8 Contact allergy to food is a delayed (Type IV) hypersensitivity, often seen in food handlers.⁶ Atopic dermatitis may in fact represent a paradigm of both an IgE- (type I) and a T-cell- (type IV) mediated reaction.⁶

Skin prick testing and serum-specific IgE tests are not helpful in diagnosis of these types of adverse reactions.⁸

3. Mixed IgE and cell-mediated reactions
In some instances, both mechanisms are involved for the same food, or one mechanism may occur for one food and the other for another food.

C. Non-immune-mediated reactions – Food intolerance
Food intolerance is a general term describing an abnormal, atypical physiological response to an ingested food or food additive. This reaction has not been proven to be immunological in nature and may be caused by many factors; pharmacological properties of the food (histamine in scromboid fish poisoning, caffeine in coffee, tyramine in aged cheeses); host characteristics such as metabolic or enzymatic disorders (lactase deficiency); or idiosyncratic responses (to monosodium glutamate, sulphites, tartrazine).^5,6 In contrast to food allergy, non-immune mediated reactions can cause symptoms even after a single food exposure.³

Unfortunately, the clinical presentation of reactions due to non-immunological mechanisms may mimic immunological reactions.¹ Like the term ‘food allergy’, ‘food intolerance’ has been overused and applied incorrectly to all adverse reactions to foods.

1. Enzyme-related reactions
Enzymatic food reactions are caused by the ingestion of normal dietary amounts of foods by individuals hyper-susceptible to such reactions because of an enzyme deficiency as a result of medications, disease states, malnutrition, pancreatic insufficiency or inborn errors of metabolism (e.g., lactose intolerance or galactosemia).¹

Partial or total deficiency of one or more enzymes in the digestive tract may result in symptoms of malabsorption when foods containing certain components are consumed.² Lactose intolerance is the most common type of reaction and occurs in individuals with deficiency of the enzyme lactase. A low level or the absence of this enzyme results in fermentation of lactose into lactic acid, which causes an osmotic effect in the gastrointestinal tract, leading to symptoms of malabsorption and diarrhea. Other enzyme deficiencies include diasaccharidase deficiency (of sucrase-isomaltase, glucose-galactose), galactosemia, phenylketonuria and deficiency of the enzyme required to break down alcohol.¹

2. Pharmacological reactions
Pharmacological adverse food reactions occur due to the ingestion of foods with pharmacologically active substances, such as vasoactive amines, and produce a wide variety of clinical manifestations, mostly affecting the gastrointestinal and central nervous systems. Patients may present with flushing, sweating, nausea, dizziness, swelling of the face and tongue, respiratory distress and shock.¹

Major vasoactive amines include tyramine, tryptamine, phenylethylamine, dopamine, norepinephrine, serotonin and histamine.^1,2

Histamine may occur naturally in foods such as strawberries, tomatoes and spinach. It can also be produced by bacteria that decarboxylate histidine, leading to high histamine content in certain foods, particularly fish such as tuna, mackerel, bluefish, herring, sardines, anchovies and, in some countries, smoked fish and cheese. Ingestion and perhaps even inhalation of these foods can lead to immediate anaphylactic reactions (within an hour after ingestion). In a condition referred to as scromboid fish poisoning, patients may present with flushing, sweating, nausea, vomiting, diarrhea, headache, palpitations, dizziness, and occasionally swelling of the face and tongue, respiratory distress and shock.¹

People taking monoamine oxidase (MAO) inhibitor antidepressant drugs should avoid high intakes of vasoactive amines, particularly tyramine, as they suppress the activity of the enzyme monoamine oxidase, which deactivates and therefore prevents a build-up of vasoactive amines.²

Caffeine (found in coffee, tea, chocolate, cola drinks and caffeine-containing analgesics) can cause palpitations, sweating, shaking and anxiety.²

Monosodium glutamate (MSG), commonly used as a flavor-enhancer, can cause flushing, headache and abdominal symptoms and may even, in large amounts, mimic the features of myocardial infarction. These effects have been described as Chinese restaurant syndrome because they can be triggered by consuming Chinese food with a high MSG content.²

Note: The same substances may cause varying reactions depending on the individual: e.g., alcohol may result in adverse events as a result of either an enzyme deficiency or a pharmacological effect. Similarly, some individuals react to histamine as a result of a breakdown-enzyme deficiency, whereas all individuals will react to high levels of this substance as a result of a pharmacological mechanism.

3. Undefined mechanisms
These are often confused with allergic reactions because they can result in similar acute symptoms such as vomiting, diarrhea and rashes, but no immune mechanism – or any other well-known mechanism – is involved. They may result from direct activation of mast cells, causing the release of histamine and other mediators, but in most instances no cause has been established as yet. Reactions to the preservative sodium benzoate are a case in point. The symptoms can be severe, and even hypotension and anaphylactic reactions can occur. To cause a reaction, significant amounts of the offending food may be needed, and the severity of symptoms is more likely to be related to the amount ingested. Foods that commonly provoke this type of response are shellfish and strawberries. Food additives, including benzoates, salicylates, sulphites and tartrazine, may also provoke these reactions.¹

In addition, there are conditions not related consistently to food ingestion, such as irritable bowel syndrome and inflammatory bowel disease, symptoms of which also may mimic reactions to food. As mentioned previously, adult patients and individuals with psychological disorders often mistakenly attribute their reactions to foods.¹

In any event, correct diagnosis of the various conditions is important, as patients’ incorrect opinions as to whether a clinical condition is due to food ingestion can have serious health consequences.

C. Comments by our editors

Prof Janice M. Joneja Ph. D., RDN In spite of recent advances in our knowledge of adverse responses to foods, most of the immunological and physiological reactions responsible for such reactions are still incompletely understood. When the specific etiological mechanism of a reaction is unknown, tests are not available for diagnosis. In many instances, when a clear diagnostic tool is lacking, and especially when symptoms are not immediately apparent, the condition is too readily termed “idiosyncratic” or “psychosomatic” and the patient is dismissed without the help they require and deserve. Eosinophilic gastroenteritis and eosinophilic esophagitis are examples of conditions involving adverse reactions to foods that until recently were frequently overlooked. Because eosinophilia in these conditions is not triggered by IgE antibodies, tests such as skin tests and RAST designed for the detection of allergen-specific IgE are negative; the tests that are positive in such situations are almost invariably due to a co-existing IgE-mediated food allergy. As a result, until recent research revealed its importance, the role of food in eosinophilic gastroenteritis and eosinophilic esophagitis was not recognized and therefore largely ignored. I have counseled several patients, both children and adults, with diagnosed eosinophilia, where all tests for IgE-mediated allergy were negative, but who nevertheless responded well when specific foods were eliminated. The culprit foods in each case were identified by careful elimination and challenge1. It is also important to remember that even when an adverse reaction to food is due to IgE-mediated allergy, more than 50% of the foods that test positive in skin tests and RAST do not elicit symptoms when the food is eaten. Research has yet to reveal the complete mechanism responsible for the development of symptoms even when IgE-antibodies are present. Undoubtedly, we shall see the development of more definitive, hopefully non-invasive tests for identification of both IgE and non-IgE-mediated adverse reactions to foods in the future as their precise etiological mechanisms are revealed by careful research. In the meantime our only reliable tool for determining and avoiding the culprit food is elimination and challenge. But primarily, it is important that practitioners recognize the many different presentations of adverse reactions to foods! Reference: Joneja, J.M.Vickerstaff. Dealing with Food Allergies: A Practical Guide to Detecting Culprit Foods and Eating a Healthy, Enjoyable Diet Bull Publishing Company, Boulder, Colorado. 2003

Dr. Harris Steinman M.B.Ch.B. Prof. Joneja sums up the current situation very well. Because of the difficulty with making a diagnosis, there has been a plethora of controversial tests released on the market - some based on pseudoscience and others pure scams. It is important to save your clients needless costs from utilizing these tests, or from bizarre or nutrient deficient diets as a consequence of the results. These tests have either not been substantiated in proper studies or shown to not have any predictive capacity at all. They include the Vega test (or BEST test), ALCAT test, hair test, kinesiology and IgG analysis. Although a number of studies have confirmed that IgG does increase during the antigen processing phase, it has to date not been shown to have good predictive value, i.e., the values may be very high yet no clinical allergy has or will occur.

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D. References
1. Chapman JA, Bernstein IL, Lee RE et al. Food Allergy: a practice parameter. Ann Allergy Asthma Immunol. March 2006; 96: S1-S68
2. Thomas B Ed in conjunction with the B ritish Dietetic Association. Food allergy and intolerance. Chapter 4.34 in Manual of dietetic practice. p 598-612 Blackwell Science Publishing, Oxford. 2001
3. Metcalfe DD, Sampson HA, Simon RA. Immune mechanisms in food-induced disease. Chapter 2 from Food Allergy: Adverse reactions to foods and food additives. Third Edition. p 14-37 Blackwell Science, USA 2003
4. Lee LA, Burks AW. Food allergies: prevalence, molecular characterization, and treatment/ prevention strategies. Annu. Rev. Nutr. 2006; 26: 539-65
5. Scurlock AM, Lee LA, Burks AW. Food allergy in children. Immunol Allergy Clin N Am. 2005; 25: 369-388
6. Frieri M, Kettelhut B. Food hypersensitivity and adverse reactions. A practical guide for diagnosis and management. p 220 Marcel Dekker Inc, USA 1999
7. Hubbard WS. Medical nutrition therapy for food allergy and food intolerance. Chapter 41 in Krause’s Food, nutrition and diet therapy. Mahan LK, Escott-Stump S. 10th Edition; p 914-915. WB Saunders Co. USA 2000.
8. Spergel JM, Pawlowski NA. Review. Food allergy. Mechanisms, diagnosis, and management in children. Pediatr Vlin North Am. 2002; 49: 73-96

E. CPD Questions (For South African dietitians only. Australian dietitians: where you have relevant learning goals, CEU hours related to this resource can be included in your APD log.)

PLEASE ANSWER ALL THE QUESTIONS
(There is only one correct answer per question.)

1. True or false: Adverse food reactions are generally due to immunological pathogenic mechanisms only.
a. True
b. False

2. True or false: The onset of reactions caused by infections such as Salmonella or E. Coli may be delayed after eating the contaminated food.
a. True
b. False

3. The development of food allergy is a single-step process requiring only one challenge with a particular food antigen.
a. True
b. False

4. True or false: The sensitization phase, which precedes allergic disease, is asymptomatic.
a. True
b. False

5. In IgE-mediated reactions, which cells with sensitized IgE antibodies do the allergens bind to?
a. Red blood cells and mast cells
b. Red blood cells and platelets
c. Mast cells and basophils
d. Mast cells and platelets

6. True or false: Non-IgE-mediated immunological reactions to foods tend to be predominantly pulmonary.
a. True
b. False

7. With Type IV food hypersensitivity, how soon after the ingestion of or exposure to a suspected food do clinical symptoms seem to appear?
a. 1-24 hours
b. 24-48 hours
c. 1-2 hours
d. 0-1 hours

8. True or false: Lactose intolerance is the least common type of enzymatic metabolic food reactions
a. True
b. False

9. Scombroid fish poisoning occurs due to high levels of which vasoactive amine?
a. Histamine
b. Tyramine
c. Dopamine
d. Serotonin

10. True or false: Chinese restaurant syndrome occurs after consuming Chinese food with a high tartrazine content.
a. True
b. False

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Adverse reactions to food
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This issue was sponsored by Abbott Laboratories S.A (PTY) LTD All Abbott products are lactose and gluten free Tel: 011-8582054