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
A husband and wife (36 and 38 years of age respectively) presented to the trauma unit one night with near-identical symptoms of bright red flushing and rash in the face and chest, heart palpitations and severe headache. The husband’s face and eyes were also puffy and swollen, and he was diagnosed as having urticaria. The reactions had developed within 30 minutes of dinner at home and had worsened over the preceding hour. The attending doctor thought it must be an allergic reaction. He gave them antihistamines and observed them for 2 hours. Within an hour, the husband’s swelling had started improving, and both no longer felt heart palpitations. The flushing for both seemed slightly less severe, but their heads were still pounding. They were sent home and asked to return the next day for a follow-up with an allergy consultant who was called in to evaluate the cause of this incident.

QUESTIONS AT THIS POINT:
a. Has either experienced the reactions before?
b. Does either have underlying allergic disease, e.g., asthma, hay fever, or food allergy?
c. What food and drink were ingested?
d. Was there any associated physical exertion?
e. Were they on any medication that might have induced the reactions?
f. Were there any environmental or chemical allergens that could have triggered the reactions?

On questioning, the following became clear:
a and b. Neither had ever demonstrated similar reactions, and neither had a history of atopy.
c. Dinner had been a tuna pasta bake made with canned tuna, wheat pasta and a cheese-based sauce. They had also had mixed vegetables consisting of green beans, carrots, sweet corn and tomato wedges. They had enjoyed approximately 2 glasses of white wine each with the meal.
d. The husband had gone paragliding after work that afternoon and had reached home approximately an hour before having dinner. The wife had taken the children for a walk on the beach in the afternoon, approximately 3 hours prior to dinner. Neither had experienced any difficulties during or immediately after the exercise.
e. Both had a cold but had not taken medication for it. They had instead increased their vitamin C supplementation.
f. Their pet for the last 6 years had been a cat, and neither had allergies to cats. They could think of no unusual environmental or chemical exposures in the 24 hours before the reactions.

THOUGHT PROCESS:
The dramatic speed and severity of the reaction may indicate an IgE-mediated reaction to an allergen. It is, however, unusual for both a husband and wife to present with the same symptoms. This makes food poisoning or an intolerance reaction more likely.

Urticaria has been seen in both immunologic and non-immunological (idiosyncratic, metabolic, toxic or pharmacologic) reactions. At this point, there may be a variety of causes suspected:

a. Food poisoning (a non-allergic reaction), either bacterial or viral, most commonly from spoiled fish, e.g., salmonella contamination or Ciguatera fish poisoning. In this situation, high levels of toxin would result in reactions in all exposed individuals.
b. Scombroid fish poisoning or histamine intolerance: a non-immune mechanism with a dose-dependent response. Large amounts of histamine would lead to reactions in most exposed individuals.
c. Certain foods, such as egg white, shellfish and strawberries, have been demonstrated to contain substances that are direct liberators of histamine through a non-immunologic mechanism. The ingestion of foods that contain large amounts of histamine, either naturally or as a result of spoilage, may cause acute urticaria. Alcohol in wine is also considered a histamine liberator. Histamine intolerance is dose-dependent, and therefore lower levels of histamine would cause reactions in more-sensitive individuals only.
d. Alcoholic drinks, particularly wines, can be important triggers for hypersensitivity reactions, although an asthmatic response seems to be the more common presentation. These reactions may be mediated through the presence of sulfur dioxide or histamine, or alcohol may be a histamine liberator. Sensitivity to the sulfite additives in wines seems likely to play an important role in many of these reactions. Salicylates present in wines may also affect salicylate-sensitive individuals.
e. An IgE-mediated food hypersensitivity to the following food allergens present in the meal may be possible: wheat pasta, tuna fish, cheese and wine; a “hidden” allergen may also have been present. As fish was part of the meal, Anisakis (also known as cod-worm) would also need to be considered as a potential allergen. This is a small parasitic worm which contaminates fish. Individuals may demonstrate immune-mediated allergic reactions to either the worm, the host (fish) or both. The Anisakis allergen is deactivated by freezing and thorough cooking. But with no history of atopy, and with similar reactions in 2 individuals, an allergic, immune-mediated mechanism would be unusual.

DISCUSSION:
The initial task would be to consider whether the reaction was predominantly immune- or non-immune-mediated, and further investigations would then be carried out according to the answer.

a. b. and c. Neither husband nor wife had experienced diarrhoea as a presenting symptom, making bacterial or viral food poisoning, e.g., Salmonella, highly unlikely. A stool culture may be required to confirm such a diagnosis.

Based on the symptom complex and the food ingested, a histamine intolerance was suspected. A histamine-induced pharmacologic food reaction mimics allergic reactions and may be frequently confused with a food allergic reaction. Adverse responses to histamine include abdominal cramping, flushing, headache, palpitations and hypotension. The meal did not include foods associated with inherently high histamine content but did include tuna fish, which if spoiled may result in exceedingly high levels of histamine, causing toxicity, also known as scombroid poisoning. Ingestion of scombroid fish such as tuna, yellowtail, mackerel, herring or sardines may result in flushing, nausea, vomiting, abdominal cramps, diarrhoea, headache, palpitations, urticaria, dizzinesss and hypotension within 1-2 hours.

Both points d. and e. would be considered only if non-immune mechanisms have been ruled out.
d. A double-blind placebo-controlled food challenge (DBPCFC) would be helpful to evaluate whether the wine consumed on the evening of the reactions would trigger a histamine release. CAST or Atopy patch tests could be carried out to assess hypersensitivity to sulphur dioxide or salicylate.
e. Blood tests to check for raised serum tryptase levels and total and serum-specific IgE levels for potential food allergens would be considered only if non-immune mechanisms had been ruled out. These tests would assess possible allergy to fish, Anisakis, wheat, dairy, and wine.

The leftovers of the meal were tested for histamine levels and the marine bacteria responsible for scombroid poisoning. Positive results as well as the improvement of symptoms with administration of antihistamine confirmed the diagnosis of non-allergic histamine toxicity due to improperly handled and spoiled fish.

 

TIP for Allergy Advisor users:
If an adverse reaction to fish had been experienced, there are a couple of possible causes that should be considered apart from fish allergy. For a list of such differential diagnosis, choose the “Assessment” menu of Allergy Advisor, then “Assessment Guides/Checklists”, then “Assessment Guides”, then “Differential Diagnosis” and “Differential Diagnosis for Adverse Reactions to Fish”.


B. More information:
As with food allergies in children, true food allergy in adults can be divided into 2 general immune-mediated subgroups on the basis of the immunologic mechanisms involved: food allergen-specific IgE responses, and non-IgE-dependent immunologic responses, either of which may be immediate or delayed. IgE-dependent reactions are further classified as to symptom complexes developed in the primary target organs.1 Allergies should be differentiated from intolerances and other non-immune-mediated adverse reactions to food.

1. Prevalence
Food allergy and food intolerance are believed to be frequent medical problems; however, information from epidemiologic studies in adults is scarce. Overall, adult food allergy is less common than childhood allergy, with 1 adult being affected for every 3.6 children.1,2,3 But allergy to certain types of foods may be more prevalent in adults than in children.

The public's perception of the number of food-allergic individuals is clearly far greater than controlled studies support. In 2001, a population-based case-control study attempted to obtain epidemiological information on food allergy and intolerance in adults in Germany. Frequency estimates based on self-reported symptoms ranged from 4.9% to 33%, which considerably overestimated the prevalence of food allergies when compared to reactions confirmed by double-blind, placebo-controlled food challenges (DBPCFCs): these produced estimates between 1.4 and 2.4%. But the results may be due to the DBPCFC test not being designed to evaluate delayed reactions, to real but unsubstantiated reactions, or to other factors.1,3,4,5,6,7

More recently (2005), true food allergy in adults has been estimated at approximately 3.2% worldwide (3.7% in the United States, 3.2% in France, and 3.7% in Germany). Interestingly, there appears to be a female dominance (60%) in reported reactions to food.1,2,3,5,6,7,8

2. Natural history
No specific data are available regarding the natural history of adult food allergies. Childhood food allergy can persist into adulthood, particularly in the case of some foods. More than 80% of peanut allergies persist into adulthood. In adults younger than 30 years, a third of allergy cases present as a persistence of childhood allergy, most often peanut allergy. Childhood allergy to other foods does not persist after 30 years of age, except in very rare cases of allergy to fish or eggs.2,9,10

New food allergies can manifest for the first time at any age, and once established in adults, rarely resolve. This has been seen with sesame, wheat and fish allergies.1,2,3,11

Several factors could favour the acquisition of food allergy in adults: 2

  • Sensitisation to pollens. Betulaceae and Artemisia pollens are often involved in fruit and vegetable allergies as a result of cross-reactive panallergens.
  • Occupational sensitisation by inhalation of food proteins in food industries. Heat-resistant food proteins, e.g., egg protein, could cause 20% of occupational asthma; individuals working in a wheat mill may develop an up regulation in immune response, triggering a “food allergy” which resolves with a change in occupation .
  • Drugs. Orally administered Tacrolimus in liver transplant patients and extensive use of anti-ulcer drugs have been linked to increased risk for food sensitisation and clinical reactions.12,13
  • Sudden dietary changes, particularly for slimming.
  • Alcohol.
  • Other pre-existing allergic conditions, e.g., asthma.14

Approximately one-third of food-hypersensitive adults, with the exception of those allergic to peanut, tree nut, fish, or shellfish, may lose their clinical sensitivity if the responsible food allergen is completely eliminated from the diet for at least 1-2 years. Loss of sensitivity usually correlates with allergen avoidance, but re-introduction and repeated exposure to the same allergen may cause the sensitivity to reappear in some individuals.1,15,16,17

3. Common food allergens
Relatively few foods are responsible for the vast majority of significant food-induced allergic reactions: milk, egg, peanuts, tree nuts, fish, and shellfish. Any food can, however, provoke a reaction in adults, and possibilities should never be ruled out.18

As for atopic children, peanuts, fish, shellfish and eggs and their associated cross-reactivities have been isolated as possible causes of food-allergic reactions in adults.1 The food allergens most frequently reported in adults are, however, nuts, shellfish, fruits and vegetables. Wheat flour allergy seems to be on the increase in adults. Although an allergy to wine is possible, one should also consider non-immune-mediated reactions, with histamine and sulphur dioxide as triggers. An allergy to milk and egg is considered relatively rare in the adult population.2,3,19

There may be differences in the types of food allergens between population groups. IgE-mediated food allergy to peanut, tree nuts, fruits and vegetables in Asian individuals are not as prevalent as in adult western populations, according to studies. This may be due to differences in food preparation (affecting the allergenicity of food allergens like peanut) and regional dietary habits. In France, there has been an increase in wheat flour allergy, whereas in Australia, the growth is in fish and shellfish allergy.2,9,10,19,20

Allergy to industrially processed foods, either from new allergens, or from high concentrations of allergenic proteins in the case of isolates, should be mentioned, because these are very commonly used ingredients. Hidden allergens may also be found in processed foods and their intake should be carefully evaluated in hypersensitive adults.2

Fruit and vegetables:
Fruit and vegetables associated with pollen or latex allergy are by far the most common culprits for food hypersensitivity reactions in adults.2

The first 3 classes of fruit and vegetables related to pollen sensitisation are2,9

  • Prunoideae (Rosaceae) - hazelnut, apple, peach, apricot, pear, plum
  • Latex group - avocado, kiwi, banana, chestnut
  • Umbellifereae (Apiaceae) - celery, carrot

Families of proteins essential for the development or defence of plants include the lipid transfer proteins and profilin. These can cause clinically relevant cross-reactions among pollens, fruit and vegetables. In the case of cross-sensitisation between profilins, polysensitisation to pollens or the cumulative effects of exposure could affect the risk for clinical reaction.

Allergens found in fruits and vegetables from the Prunoideae family may cross-react with the major allergen of birch pollen (Bet v 1). These Bet v 1 homologue allergens are fragile and easily destroyed by cooking and digestion.2

A number of shared protein families result in latex allergy being frequently associated with fruit and vegetable allergy due to cross-reactivity. Approximately 20% of patients with latex allergy may later develop cross-reactivity with avocado, banana, chestnut, or buckwheat.2

Allergies to fruit and vegetables are often multiple in adults, reflecting cross-sensitisations with pollen allergens, as opposed to adult food allergies to animal allergens, which tend to be mono-allergies. By contrast, a child may suffer from multiple food allergy syndrome, with both animal and fruit and vegetable allergies.2

4. Clinical features and presentation
Clinical manifestations in adults are varied and may involve the skin, the gastrointestinal tract, and the respiratory tract, but severe anaphylaxis and oral allergy syndrome are the most frequently reported symptoms.2,18,21

Anaphylaxis:
Food anaphylaxis is not uncommon, involving 17% to 37% of patients admitted to hospital emergency units.2,22,23,24 The fatality risk is estimated at 1% in severe anaphylaxis.25,26 There have been reports of anaphylaxis after ingestion of hazelnuts, almonds and peanuts. In the United States, 90% of fatal cases of anaphylaxis are caused by peanuts and hard-shelled fruit.27 In contrast, crustaceans and molluscs were found to be the most common cause of anaphylaxis in the Asian population in Singapore.20 Lupine is emerging as a significant allergen in Europe.28,29,30,31

Food-dependent exercise-induced anaphylaxis typically affects young adults and adolescents and occurs in conjunction with significant physical exertion. The activity is usually jogging or dancing. The period between food intake and the clinical reaction, like the effort period, varies from 30 minutes to 3 hours. Importantly, ‘exercise’ may be physical labour or other physical activities such as sex. Cardiovascular symptoms can be the sole manifestation of exercise-induced food allergies, in which case death may mimic sudden cardiac death during physical exertion due to other pathologic causes. All foods are involved, with a marked predominance of wheat flour. Another presentation of this condition may be the sudden exacerbation of asthma. 2,29,30,31

The risk factors besides exercise that have been identified for severe anaphylaxis in adults are agents causing increased intestinal permeability, such as alcohol, aspirin and other non-steroidal anti-inflammatory drugs, beta-blockers, and angiotensin-converting enzyme (ACE) inhibitors. There also seems to be a possible cumulative effect in sensitised patients, e.g., the simultaneous intake of several food allergens before exercise or the ingestion of fruit or vegetable allergens added to the exercise-induced polypneic inhalation of cross-reactive pollens.2 Tacrolimus may also increase the severity of allergy and has been linked to death related to food allergy in liver transplant patients.12

Approximately 1 out of 12 patients who have suffered anaphylaxis will experience recurrence within a year, and 1 out of 50 will require hospital treatment or use adrenaline. Compliance with carrying and using adrenaline is poor in the adult population. Occasionally, patients may develop new triggers or suffer psychiatric morbidity.32

Oral Allergy Syndrome:
Oral allergy syndrome (OAS) tends to be associated with fruit and vegetable allergens. If eaten raw, fruits or vegetables from the Prunoideae or Apiaceae families induce principally buccal or pharyngeal symptoms. This is a result of cross-reactivity with the major birch pollen allergen. Some authors suggest that OAS is a mild syndrome without anaphylaxis, and others argue that the condition may progress or be associated with anaphylaxis.2,21

Urticaria:
Food allergy as a cause of chronic urticaria has rarely been recognised. However, a careful screening for food allergy with skin tests, detection of specific IgE’s, and double-blind oral challenge tests, followed by an avoidance diet in a single study, have demonstrated allergy to daily ingested foods (wheat flour, dairy products, or meat) in 4.3% of adults with chronic urticaria. Recovery after implementing the necessary dietary avoidance was observed in only 50% of these patients.33

It should be noted that flushing and urticaria due to a histamine-induced pharmacological food reaction may be frequently confused with an immunologic/food-allergic reaction.34,35

Hay fever and other respiratory symptoms:
Food allergy in adults is often associated with hay fever. Subjects suffering from hay fever and food allergy may have a significantly higher need for therapy, possibly indicating that hay fever in conjunction with food allergy tends to be clinically more severe.3

Angioedema and asthma are manifestations frequently seen in those adults allergic to pollens.2

Gastrointestinal allergic reactions:
Gastrointestinal (GI) food allergy remains, to a large extent, undiagnosed and underestimated in adults. Up to now GI allergy has been poorly defined and controversial.2,21 The difficulty in characterising GI allergy syndromes may lead to either under- or over-diagnosis, or to a general diagnosis of Irritable Bowel Syndrome being made.36

Approximately 4.2% of food-allergic adults present with chronic GI allergy, and this represents 3.2% of all intestinal disorders. Symptoms tend to be non-specific, but eosinophilic GI disorders (from delayed allergic reactions) may occur.21 Recently, one condition, eosinophilic esophagitis, has been recognised as a clinical entity, appears to be increasing in parallel with asthma and allergic rhinitis, and is seen in 46% of those with respiratory allergy, 25% of whom have a food allergy.37

Cited allergens inducing GI allergy include frequently ingested foods such as wheat flour, milk, egg and meats.21,38,39 People with birch pollen and cross-reactive food allergies have been reported to manifest oral allergy syndrome as well as gastrointestinal complaints.2,21,40

5. Diagnostic tests
Unfortunately, food allergies and intolerances are frequently self-diagnosed in the adult population. Unexplained symptoms and wrong attribution are typical in subjective health complaints. There appears to be an association between subjective food hypersensitivity and subjective health complaints, such as gastrointestinal complaints, musculoskeletal complaints, "pseudoneurology" and allergy.41 Perceived food intolerance is also a common problem, with significant nutritional consequences in the population with irritable bowel syndrome (IBS).42

A systematic approach to diagnosis should include a careful history followed by laboratory studies, elimination diets, and often food challenges to confirm a diagnosis. Many food allergens have been characterised at a molecular level, which has increased our understanding of the immunopathogenesis of food allergy and will result in a more defined and accurate method of testing (component-resolved diagnostics).18,43

Skin prick and serum tests:
As for children, a 2-step procedure of skin prick tests and laboratory tests for identification of specific IgE is required to demonstrate sensitisation. In vitro tests (i.e., the RAST/blood/serum-IgE tests) are the procedure of choice when medications would interfere with skin testing, when skin disease is so extensive as to preclude skin testing, or when skin testing could place the extremely sensitive individual at risk. In adults, specific IgE and skin tests seem to have low specificity and predictive value for diagnosing food allergy (i.e., may be negative in the face of true allergy), although specific IgE is considered more sensitive than skin tests.1,2,9,10,19

The quality of commercial food-allergen extracts varies greatly, depending on their origin, and the concentration of proteins required for extract efficacy varies greatly between different foods. It is therefore particularly important to carry out skin prick or prick-prick tests with natural foods; e.g., the use of extracts of fresh fruits and vegetables is often necessary to exclude oral allergy syndrome in cases of labile allergens.1,2,44

Food challenges:
In most situations the existence of allergy must be confirmed by standardised double-blind, placebo-controlled food challenges (DBPCFC) or elimination diets over a sufficiently long period. Patients with a convincing history of systemic anaphylaxis to a specific food should not be challenged with that food, or should be challenged in a specialised clinical setting. In adults, a blinded challenge eliminates the risk of subject bias and is more useful in convincing a patient that the food of concern does or does not provoke symptoms.1,2,9,21,45,46,47,48

A diagnosis of irritable bowel syndrome (IBS) as a result of negative skin prick tests and negative specific IgE assays, could overshadow actual gastrointestinal allergy, particularly to wheat flour, milk proteins, or meat. DBPCFC’s would be helpful in these cases.1,49

In GI allergy, the amounts of food required may be very large and reactions may be delayed, so for diagnosis a 2-step procedure is suggested, comprising a DBPCFC first, then an open test with higher doses. If results are negative, it is necessary to complete the test with a fixed, sufficient amount of food for 7 to 10 consecutive days. Endoscopy and biopsies of the gastrointestinal tract may help in differential diagnosis.1,21

An awareness of the variable manifestations of food-precipitated anaphylaxis is necessary to correctly establish the diagnosis. For example, it is necessary during food provocation tests to establish the same intensity or duration of exercise as helped trigger the initial acute episode. An elevated serum tryptase level and elevated allergen-specific IgE levels indicate an allergic reaction and confirm the particular antigen leading to anaphylaxis.20,29

6. Management and treatment
As with children, the therapeutic strategy is based on strict avoidance diets, supported by educating the patient on how to avoid ingesting the responsible allergen, how to read food labels to detect hidden food allergens, and how to be safe in eating outside the home. The patient must also know how to initiate emergency medical therapy in the case of severe reactions as a result of an unintended ingestion. Severe elimination diets may lead to malnutrition, and the services of a specialised dietician are essential. Pregnancy may require special dietary attention and intervention.1,2,18

The efficacy of avoidance diets depends, to a certain extent, on suitable labelling. The growing amount of industrially processed foods on the market has resulted in the daily ingestion of a myriad of ingredients which may precipitate food hypersensitivity reactions. It is essential that the food industry be aware of the potential problems and ensures appropriate labelling of possible allergenic components in processed foods.2

Prevention of acute attacks of food-dependent exercise-induced anaphylaxis includes avoiding trigger foods (these are individual-specific but for adults are commonly shellfish, tree nuts, legumes, fruits, vegetables, grains and diary) up to 4 hours before exercise and modification of the individual’s intensity and duration of exertion during exercise.1,2,18

Specific immunotherapy for food allergy has not been extensively evaluated, but specific immunotherapy to pollens may be efficient for cross-reactive food allergies. It has been used successfully in some cases of egg, fish, and hazelnut allergies as well as in birch pollen cross-reactive allergy. Anti-IgE treatment may be useful in the future if administered on a regular basis. Although it is not a cure, it may reduce clinical reactivity to a particular allergen (e.g., clinical reactivity to peanut was decreased after a 3-month treatment). Rather than being a definitive treatment, anti-IgE could provide transient protection while immunotherapy with recombinant major allergens is implemented.2,50

A patient with potential anaphylactic reactivity must be taught to self-administer epinephrine, and must keep an epinephrine-containing syringe and an antihistamine available on hand at all times. After self-medication for a systemic reaction, the patient should immediately seek medical attention.1

  Compiled by Gina Stear RD(SA)
Private Practising Dietitian
Food & Allergy Consulting & Testing Services (FACTS)
PO Box 565
Milnerton 7435
South Africa

C. Comments by our editors

Prof Janice M. Joneja Ph. D., RDN
Symptoms of adverse reactions to foods in adults can appear in diverse organ systems, and be triggered by a variety of different immunological and physiological processes, as the information in this review clearly demonstrates. In the end, however, regardless of the mechanism responsible for the symptoms, the most important management strategy is for the food-sensitive person to avoid the foods responsible for triggering the reaction. This is easier in theory than in practice because many of the physiological and biochemical processes responsible for the clinical signs and symptoms are poorly understood, and consequently, there are few reliable tests available to the clinician for detecting the specific foods responsible. Almost all tests for adverse reactions to food, including skin tests and blood tests for antigen-specific antibody, have an unacceptably high rate of false positive and negative results, making them unusable as a definitive diagnostic test. Ultimately, elimination and challenge must be carried out in order to identify the culprit food in any food allergy or intolerance reaction, and this can be tedious and time-consuming for all concerned. However, it is a necessary process because incorrect identification of the offending food(s) can result in a continuation of the symptoms, or more commonly, nutritional deficiency as a result of the unnecessary avoidance of too many foods. It is hoped that as science uncovers more processes involved in the etiology of food sensitivity reactions, especially at the cellular level, more dependable and accurate diagnostic tests will be developed, leading to improved management and therapeutic strategies for food allergies and intolerances.

For more information on this subject and other allergy- and intolerance-related topics, visit:
www.allallergy.net
www.allergyadvisor.com
http://users.bigpond.net.au/allergydietitian

To join a professional food allergy discussion list where this subject can be discussed further, go to http://groups.yahoo.com/group/AllergyDietitian or Subscribe: AllergyDietitian-subscribe@yahoogroups.com

Please feel free to send this newsletter out to colleagues who are not subscribed. To subscribe ornsubscribe, send an e-mail to astrid@factssa.com and put “Subscribe Educational” or “Unsubscribe Educational” as the subject.


D. References
1. Metcalfe DD. Food Allergy in Adults. Chapter 10 from Food Allergy: Adverse reactions to foods and food additives. Third Edition. 2003 Blackwell Science, USA. p36-143
2. Moneret-Vautrin DA, Morisset M. Adult Food Allergy. Curr Allergy Asthma Rep. 2005 Jan; 5(1): 80-5
3. Schafer T, Bohler E, Ruhdorfer S et al. Epidemiology of food allergy/food intolerance in adults: associations with other manifestations of atopy. Allergy. 2001 Dec; 56(12):1172-9.
4. Cohen M, Splansky G, Gallagher J et al. Epidemiologic survey and validation of adverse food reactions in adult populations [Abstract]. J Allergy Clin Immunol 1985; 75:206.
5. Bender A, Matthews D. Adverse reactions to food. Br J Nutr 1981; 46:403–407.
6. Young E, Stoneham M, Petruckevitch A et al. A population study of food intolerance. Lancet 1994; 343: 1127–1130.
7. Jansen J, Kardinaal A, Huijbers G et al. Prevalence of food allergy and intolerance in the adult Dutch population. J Allergy Clin Immunol 1994; 93:446–456.
8. Burr M, Merrett T. Food intolerance: a community survey. Br J Nutr 1983; 49:217–219.
9. Crespo JF, Rodriguez J. Food allergy in adulthood. Allergy 2003; 58:98-113.
10. Sampson HA. Update on food allergy. J Allergy Clin Immunol 2004; 113:805-20.
11. Kanny G, de Hauteclocque C, Moneret-Vautrin DA. Sesame seed and sesame seed oil contain masked allergens of growing importance. Allergy 1996, 51:952-957.
12. Prabhakaran K, Lau H, Wise B et al. Incidence of allergic symptoms in pediatric liver transplant recipients treated with tacrolimus based immunosuppression. Pediatrics 1999, 104:786-787.
13. Untersmayr E, Scholl I, Swoboda I et al. Antacid medication inhibits digestion of dietary proteins and causes food allergy: a fish allergy model in BALB/c mice. ] Allergy Clin Immunol 2003, 112:616-623.
14. Vally H, de Klerk N, Thompsom PJ. Alcoholic drinks: important triggers. J Allergy Clin Immunol 2000;105:462-7
15. Pastorello EA, Stocchi L, Pravettoni B et al. Role of the elimination diet in adults with food allergy. J Allergy Clin Immunol 1989; 84:475-483.
16. Businco L, Benincori N, Cantani A et al. Chronic diarrhoea due to cow's milk allergy: a 4 to 10-year follow-up study. Ann Allergy 1985; 55:844-847.
17. Bock SA, Atkins FM. The natural history of peanut sensi¬tivity. J Allergy Clin Immunol 1989; 83:900-904.
18. Sicherer SH, Sampson HA. Food allergy. J Allergy Clin Immunol. 2006 Feb; 117(2 Suppl Mini-Primer):S470-5.
19. Scibilia J, Pastorello EA, Zisa G et al. Wheat allergy: a double-blind, placebo-controlled study in adults. J Allergy Clin Immunol. 2006 Feb; 117(2):433-9.
20. Thong BY, Cheng YK, Leong KP et al. Anaphylaxis in adults referred to a clinical immunology/allergy centre in Singapore. Singapore Med J. 2005 Oct;46(10):529-34.
21. Moneret-Vautrin AD. Gastrointestinal allergy in adults. Eur J Gastroenterol Hepatol. 2005 Dec; 17(12):1293-7.
22. Brown A, McKinnon D, Chu K. Emergency department anaphylaxis: a review of 142 patients in a single year. / Allergy Clin Immunol 2001; 108:861-866.
23. Wilson R. Upward trend in acute anaphylaxis continued in 1998-9. BMF 2000; 321:1021-1022.
24. Pastorello E, Rivolta F, Bianchi M et al. Incidence of anaphy¬laxis in the emergency department of a general hospital in Milan. 7 Chromatol B Biomed Sci Appi 2001; 756:11-17.
25. Moneret-Vautrin DA, Kanny G, Morisset M et al. Severe food anaphylaxis: 107 cases registered in 2002 by the Allergy Vigilance Network. Allerg Immunol 2004; 36:46-51.
26. Helbling A, Hurni T, Mueller LIR et al. Incidence of anaphy¬laxis with circulatory symptoms: a study over a 3-year period comprising 940,000 inhabitants of the Swiss Canton Bern. Clin Exp Allergy 2004; 34:285-290.
27. Bock SA, Munoz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. / Allergy Clin Immunol 2001; 107:191-193.
28. Moneret-Vautrin DA, Guerin L, Kanny G, Flabbee J, Fremont S, Morisset M. Cross-allergenicity of peanut and lupine: the risk of lupine allergy in patients allergic to peanuts. J Allergy Clin Immunol 1999;104(4 Pt 1):883-8
29. Flannagan LM, Wolf BC. Sudden death associated with food and exercise. J Forensic Sci. 2004 May; 49(3):543-5.
30. Romano A, Di Fonso M, Giuffreda F et al. Diagnostic work-up for food-dependent, exercise-induced anaphylaxis. Allergy 1995, 50:817-824.
31. Kano H, Juji F, Shibuya N et al. Clinical courses of 18 cases with food-dependent exercise-induced anaphylaxis. Arerugi 2000; 49:472-478.
32. Mullins RJ. Anaphylaxis: risk factors for recurrence. Clin Exp Allergy. 2003 Aug; 33(8):1033-40.
33. Pigatto PD, Valsecchi RH. Chronic urticaria: a mystery. Allergy 2000; 55:306-308.
34. Atkins FM. Food-induced urticaria. Chapter 12 from Food Allergy: Adverse reactions to foods and food additives. Second Edition. 1997 Blackwell Science, USA. p212
35. Baldwin JL. Pharmacologic food reactions. Chapter 10 from Food Allergy: Adverse reactions to foods and food additives. Second Edition. 1997 Blackwell Science, USA. p419-423
36. Bischoff SC, Herrmann A, Manns MP. Prevalence of adverse reactions to food in patients with gastrointestinal disease. Allergy 1996; 51:811–818.
37. Croese J, Fairley SK, Masson IW et al. Clinical and endoscopic features of eosinophilic esophagitis in adults. Gastrointest Endosc 2003; 58:516-522.
38. Bengtsson U, Nilsson-Balknas U, Hanson LA, Ahlstedt S. Double blind, placebo controlled food reactions do not correlate to IgE allergy in the diagnosis of staple food related gastrointestinal symptoms. Gut 1996; 39:130–135.
39. Pfaffenbach B, Adamek RJ, Bethke B, Stolte M, Wegener M. Eosinophilic gastroenteritis in food allergy. Z Gastroenterol 1996; 34:490–493.
40. Magnusson J, Lin XP, Dahlman-Hoglund A, et al. Seasonal intestinal inflammation in patients with birch pollen allergy. J Allergy Clin Immunol 2003; 112:45-50.
41. Lind R, Arslan G, Eriksen HR et al. Subjective health complaints and modern health worries in patients with subjective food hypersensitivity. Dig Dis Sci. 2005 Jul; 50(7):1245-51.
42. Monsbakken KW, Vandvik PO, Farup PG. Perceived food intolerance in subjects with irritable bowel syndrome-- etiology, prevalence and consequences. Eur J Clin Nutr. 2006 May; 60(5):667-72.
43. Lidholm J, Ballmer-Weber BK, Mari A, Vieths S. Component-resolved diagnostics in food allergy. Curr Opin Allergy Clin Immunol 2006 Jun;6(3):234-240
44. Rosen J, Selcow J, Mendelson L et al. Skin testing with natural foods in patients suspected of having food allergies: Is it a necessity? Allergy Clin Immunol 1994; 93:1068-1070.
45. Ballmer-Weber BK, Vieths S, Luttkopf D et al. Celery allergy con¬firmed by double-blind, placebo-controlled food challenge: a clinical study in 32 subjects with a history of adverse reactions to celery root. J Allergy Clin Immunol 2000; 106:373-378.
46. Ballmer-Weber BK, Wuthrich B, Wangorsch A et al. Carrot allergy: double-blinded, placebo-controlled food challenge and identification of allergens. / Allergy Clin Immunol 2001; 108:301-307.
47. Bock SA, Sampson HA, Atkins FM, et al. Double-blind, placebo controlled food challenges as an official procedure manual. J Allergy Clin Immunol 1988; 82:986-997.
48. Kanny G, de Hauteclocque C, Moneret-Vautrin DA. Sesame seed and sesame seed oil contain masked allergens of growing importance. Allergy 1996; 51:952-957.
49. Lin XP, Magnusson J, Ahlstedt S et al. Local allergic reaction in food-hypersensitive adults despite a lack of systemic food-specific IgE. I Allergy Clin Immunol 2002; 109:879-887.
50. Leung DY, Sampson H, Yunginger W et al. Effect of anti-IgE therapy in patients with peanut allergy. N Engl J Med 2003; 348:986-993.


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.)

This newsletter with questions has been accredited for South African dietitians only. You can obtain 3 CEUs for reading this newsletter and answering the accompanying questions.
CEU Activity Reference Number: DTA06/02/026

HOW TO EARN YOUR CEUs
1. Complete your personal details below.
2. Read the newsletter and answer the questions.
3. Indicate your answers to the questions by making an “X” in the appropriate block at the end.
4. You will earn 3 CEUs if you answer more than 70% of the questions correctly. A score of less than 70% will unfortunately not earn you any CEUs.
5. Make a photocopy for your own records in case your answers do not reach us.
6. Cut and paste the area indicated below into an e-mail message and e-mail it to astrid@factssa.com no later than 30 September 2006. Answer sheets received after this date will not be processed.


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

1. True or False: In adults younger than 30 years, two thirds of the cases present as a persisting childhood allergy, most often related to peanuts.
a. True
b. False

2. The factors which could favour the acquisition of allergy in adults include:
a. Sensitisation to pollens, occupational sensitisation by inhalation of food proteins, drugs, sudden dietary changes, alcohol
b. Sensitisation to foods, occupational sensitisation by contact of food proteins, vitamins, sudden dietary changes
c. Sensitisation to pollens, occupational sensitisation by inhalation of food proteins, ingestion of leeks and butternut
d. Sensitisation to house dust mites, occupational sensitisation by inhalation of dust particles, drugs, sudden dietary changes

3. In adults, the food allergens most frequently reported are:
a. Nuts, fish, milk, fruits and vegetables
b. Nuts, shellfish, fruits and vegetables
c. Nuts, shellfish, wine, milk and eggs
d. Nuts, shellfish, wine, fruits and soya
e. Nuts, shellfish, wine, beans and vegetables

4. Latex allergy is a vector for fruit and vegetable allergy. What percentage of latex-allergic patients will develop avocado, banana, chestnut, or buckwheat allergy?
a. 15%
b. 50%
c. 26%
d. 20%
e. 32%

5. Oral allergy syndrome tends to be associated with which allergens?
a. Wheat and milk
b. Peanuts and soya
c. Fruit and vegetables
d. Meat and eggs

6. In adults, which allergic symptom tends to be clinically more severe in conjunction with a food allergy and to require higher therapy?
a. Hives
b. Hay fever
c. Eczema
d. Diarrhoea

7. True or False: The existence of allergy must be confirmed by standardised double-blind, placebo-controlled food challenges except in those with a history of anaphylaxis, in which case the challenges can be carried out only in a specialised clinical setting.
a. True
b. False

8. True or false: Prevention of acute food-dependent exercise-induced anaphylaxis includes avoiding trigger foods up to 2 hours before exercise and modification of the individual’s intensity and duration of exercise.
a. True
b. False

Cut and paste the section below into an e-mail message

Adult Food Allergy
CEU Reference number: DTA06/02/026

HPCSA number: DT
Surname as registered with the HPCSA:
Initials:
Contact number:
E-mail address:

Please make an “X” in the appropriate block for each question

1. a [ ] b [ ]   2. a [ ] b [ ] c [ ] d [ ]   3. a [ ] b [ ] c [ ] d [ ] e [ ]
4. a [ ] b [ ] c [ ] d [ ] e [ ]   5. a [ ] b [ ] c [ ] d [ ]   6. a [ ] b [ ] c [ ] d [ ]
7. a [ ] b [ ]   8. a [ ] b [ ]    



Index

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