Saudi Journal of Gastroenterology
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Year : 1998  |  Volume : 4  |  Issue : 1  |  Page : 25-29
Foods and food allergy: The prevalence of IgE antibodies specific for food allergens in Saudi patients


Department of Pathology, College of Medicine and King Khalid University Hospital Riyadh, Saudi Arabia

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Date of Submission06-Oct-1997
Date of Acceptance01-Dec-1997
 

   Abstract 

Objective: The intent of this study is to determine the prevalence and pattern of sensitivity to food allergens in Saudi patients. Subjects: The subjects included in this study were 58 patients with asthma, 47 patients with rhinitis and 112 patients with urticaria. They all gave clinical history suspecting food as causing or aggravating their symptoms. Methods: Specific IgE antibodies to different food allergens were measured in the patients serum by using the Pharmacia CAP Radioaller gosorbent (RAST) Fluoroimmunoassay (FEIA) test. Results: IgE-antibodies specific for different foods were detected in 38 (17.5%) out of 217 patients. Most positive reactions were detected in urticaria patients (9.7%) followed by asthmatic patients (5.5%) and allergic rhinitis (2.3%). Reactions to peanut (22.6%), egg white (14.5) and cow's milk (12.9%) were very prominent. Conclusion: The prevalence rate of food allergy seems to be high in Saudi patients when compared to studies from other regions. The pattern of food reactions, detected in this study, can be utilized in diagnosis of patients with suspected food allergy. Further studies will be required to obtain more information about the prevalence and incidence rates among different patient groups.

How to cite this article:
El-Rab MG. Foods and food allergy: The prevalence of IgE antibodies specific for food allergens in Saudi patients. Saudi J Gastroenterol 1998;4:25-9

How to cite this URL:
El-Rab MG. Foods and food allergy: The prevalence of IgE antibodies specific for food allergens in Saudi patients. Saudi J Gastroenterol [serial online] 1998 [cited 2014 Sep 2];4:25-9. Available from: http://www.saudijgastro.com/text.asp?1998/4/1/25/33904


The consumption of variety of foods is essential for health and survival. Most individuals can tolerate most foods most of the time. Occasionally, adverse reactions may occur which could be due to immunologic, toxic, pharmacologic, infectious, metabolic, neuropsychologic or idiosyncratic mechanisms. Of all adverse reactions, less than 29 are due to allergy or hypersensitivity [1],[2] .

Allergic reactions to foods involve abnormal immune responses and affect infants (4-8%), children (8%) and adults (1-2%) [3] . However, other reports claim that 10% of the general population, 13% of children and 7% of adults in North America, and 0.3 - 7.5% of children and 2% of adults in Europe and 10% of atopic individuals have a documented food allergy [4],[5] .

The risk of developing sensitivity to a food protein depends on age, heredity, exposure to food antigens, gastrointestinal permeability and environmental factors [6],[7] . Many foods such as corn, rice, rye, nuts, shrimp, chicken, turkey, beef, banana, potatoes and peanuts have been reported to cause adverse reactions [3] .

A wide range of symptoms have been attributed to food allergy. Most documented allergic reactions to foods occur within two hours of ingestion [3] . In infants, gastrointestinal manifestations are common and include persistent colic, vomiting, diarrhoea, blood in stools and protein-losing enteropathy [8],[9] . Eosinophilic gastroenteropathy is an unusual manifestation of food allergy in susceptible hosts [10] . Fatal anaphylaxis which may involve the gastrointestinal tract, the respiratory tract or the skin can occur in those with extreme food hypersensitivity [11] .

Generalized urticaria and angioedema may be the only symptoms of an acute systemic reaction to food [12] . Food allergy occasionally contributes to allergic asthma [13] . A relationship between food allergy and migraine headaches has also been suggested [3] . Since there is no information available on the prevalence of food allergy in Saudis, the present study was planned to determine the prevalence and pattern of IgE antibodies specific for food allergens in Saudi patients.


   Patients and methods Top


A group of 217 adult patients attending the allergy clinic at King Khalid University Hospital, Riyadh, were selected for this study. These included 58 asthmatic patients, 47 patients suffering from allergic rhinitis, and 112 patients complaining of urticaria. They all gave clinical history suspecting foods as causing or aggravating their symptoms, hence they were referred for allergy evaluation and work-up.

Blood samples were obtained from the patients and the serum separated and stored at -20°C until assayed.

The samples were tested for the presence of specific IgE antibodies to food allergens. These allergens were selected from those most frequently suspected by the patients as causing their complaints. They consisted of egg (white), egg (yolk), cow's milk, fish, meat, peanut, wheat, tomato, cacao, chicken, shrimp, yeast, banana and orange.

Specific IgE was measured by the new Pharmacia CAP system (Uppsala, Sweden), which had been shown to be very sensitive [14],[15] . The patient serum was added to the allergen of interest which was covalently coupled to immuno CAP. After washing away non-specific IgE, enzyme labelled antibodies against IgE were added to form a complex. After incubation, unbound enzyme anti-IgE was washed away and the bound complex was then incubated wtih a developing agent. Afater stopping the reaction, the fluorescence of the eluate was measured in fluorocount 96. The higher the fluorescence value, the more specific IgE was present in the specimen. The assay was caliberated against the World Health Organization (WHO) standard IgE, and values were expressed as Ku/L.


   CAP classes and interpretation Top


Values under 0.35 Ku/L were considered to be negative, those between 0.36 and 0.70 Ku/L to be borderline (Class 1) and those above 0.70 to be positive.

Values between 0.70 and 3.5 Ku/L were attributed to Class 2, values between 3.5 Ku/L to 17.5 Ku/L to Class 3, 17.5 to 50 Ku/L to Class 4 and 50 to 100 Ku/L to Class 5.


   Results Top


The frequency of IgE-mediated reactions to various food allergens in 217 patients is summarized in [Table - 1]. Out of 217 patients, a total of 38 (17.5%) showed a positive reaction. When the different patient groups were evaluated separately, 21 (18.8%) of 112 patient with urticaria showed positive reactions. In patients with asthma, 12 (20.7%) out of 58 patients showed positive reeactions while 5 (10.6%) out of 47 patients suffering from rhinitis gave positive reactions.

The distribution of the reactions to the 14 food allergens are shown in [Table - 2]a for urticaria patients, [Table - 2]b for asthma patients and [Table - 2]c for rhinitis patients.

It is noticeable that specific IgE was more frequently encountered for some of the food allergens tested than for others. [Table - 2]a, b & c show the unhomogenous distribution of the reactions. Positive reactions were more frequently encountered to egg (white), peanut, milk, fish, meat and tomato. Few reactions were observed to banana and orange. Most reactions fall in Class 1 with lesser reactions in Class 2, 3 and 4. No reactions were observed to any food allergen in Class 5.

The prevalence of different foods implicated in the IgE-mediated reactions (a total of 62 reactions) appear in [Table - 3]. The frequency of reactions to peanut was very prominent amounting to 22.6%. This was followed by egg white 14.5%, cow's milk 12.9%, wheat 11.3%, tomato 11.3% and fish 8.1%.


   Discussion Top


In the present study, the prevalence of IgE­mediated reactions to food allergens was found to be 17.5%. All Class 1 reactions (0.35 - 0.70 Ku/L) were excluded as they are considered borderline with no clinical significance. As some CAP RAST reactions, particularly classl, could result from cross-reactions, past sensitivity or possibly false positive reactions, detection of IgE antibodies should be considered as a first step in diagnosing food allergy [14] . The only conclusive evidence for confirming food allergy is by double-blind placebo-controlled food challenge [15] .

The prevalence rate of 17.5% detected in this study, is high when compared to similar studies. In North America, a prevalence of 10% was reported. This could be due to the fact that our study group were selected patients while the North American report refer to the prevalence in the general population. Moreover, awareness of the problem and hence early preventive measures could reduce the prevalence rate.

It is noticeable that more reactions were encountered in patients with urticaria. This is in agreement with previous studies which have shown that the skin constitutes the principal target organ in food allergy, being involved in about 75% of food allergy cases [16] . With regard to the other groups, there is evidence that food allergens may induce respiratory symptoms. In one study, asthma symptoms related to food was demonstrated in 8 of 140 (5.7%) patients [17] . In this study, 5.5% of asthma patients showed positive reactions.

With regard to the types of foods implicated, it is relevant to mention that food allergy shows important geographical variations. This depends primarily on nutritional habits in different populations. It is evident from this investigation that reactions to peanut 22.6%, egg white 14.5% and cow's milk 12.9% were very prominent. These were followed by wheat 11.3%, tomato 11.3% and fish 8.1%. For the purpose of comparison, 60% of allergic reactions to foods, in the United States, are caused by peanuts and eggs [18] . In this study, peanut and egg (whole) accounted for 40.3% of the reactions. In Scandinavian countries, allergy to fish has a predominant role [19] , while in the Finnish population, the foods most frequently implicated were citrus fruits, tomatoes and egg.

In conclusion, data from this study can be utilized as guidelines in the diagnosis of patients with food allergy. Furthermore, detection of food reactions is essential for patient counselling regarding diet elimination. Many patients restrict their diet without justification and this has been shown to result in serious nutritional deficiencies [20],[21] . It seems that more studies are required to investigate the different aspects of food allergy in this region. This may help to improve our understanding of this growing medical problem.

 
   References Top

1.Chandra RK, (Eds.) Nutrition and immunology. St. John's, ARTS Biomedical Publishers, 1992.  Back to cited text no. 1    
2.Esteban MM, (Eds.). Adverse reaction to foods in infancy and childhood. J Pediatr 1992;121:S1-S126.  Back to cited text no. 2    
3.Mahan LK, Escott-Stumps. Food nutrition and diet therapy. 9th (Eds.) W.B. Saunders Co., London, 1996.  Back to cited text no. 3    
4.Kajosaari M. Food allergy in Finnish children aged I to 6 years. Acta Paediatr Scand 1982;71:815-19.  Back to cited text no. 4  [PUBMED]  
5.Kardinall AFM. Epidemiology of food allergy and food intolerance in: Somoggi JC, Muller HR, Ockhuizen Th (Eds.). Food allergy and food intolerance. Nutritional aspects and developments. Basel:Karger, 1991:105-15.  Back to cited text no. 5    
6.Soothil JF, Stokes CR, Turner MW, et al. Predisposing factors in the development of reagenic allergy in infancy. Clin Allergy 1976;6:305-7.  Back to cited text no. 6    
7.Mowat AM. The regulation of immune responses to dietary antigens. Immunol Today 1987;8:93-9.  Back to cited text no. 7    
8.Bengtsson U, Rognum TP, Brandtzaeg P, et al. IgE-positive duodenal mast cells in patients with food-related diarrhoea. Int Arch Allergy AppI Immunol 1991;95:86-91.  Back to cited text no. 8    
9.Bock SA, Atkins EM. Patten of food hypersensitivity during sixteen years of double-blind, placebo controlled food challenges. J Pediatr 1990;117:561-7.  Back to cited text no. 9    
10.Katz AJ, Twarog FJ, Zeiger RS, et al. Milk-sensitive and eosinophilic gastroenteropathy: similar clinical features with contrasting mechanisms and clinical course. J Allergy Clin Immunol 1984;74:72.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Sampson HA. Fatal and near-fatal anaphylactic reactions to food in children and adolescents. N Engl J Med 1992;327:380-4.  Back to cited text no. 11    
12.Champion RH, Roberts SOB, Carpenter RG, Roger JH. Urticaria and angio-odema. A review of 554 patients. Br J Dermatol 1969;81:588-97.  Back to cited text no. 12    
13.Martin JA, Compaired JA, DE LA Hox B, et al. Bronchial asthma induced by chickpea and lentil. Allergy 1992;47:187-7.  Back to cited text no. 13    
14.Johansson SGD, Dannacus A, Lilja G. The relevance of anti­food antibodies for the diagnosis of food allergy. Ann Allergy 1984;53:665-71.  Back to cited text no. 14    
15.Bock SA, Sampson HA, Atkins FM. Double-blind placebo­controlled food challenge as an office procedure, manual. J Allergy Clin Immunol 1988;82:986-97.  Back to cited text no. 15    
16.Dieguez I, Martin-Gil D, Ochling A. A statistical study of the shock-organ in food allergy and the agreement between skin and haemagglutination test. Allergol Immunopathol 1978;6:117-26.  Back to cited text no. 16    
17.Novembre E, De Martino M and VierucciA. Foods and respiratory allergy. J Allergy Clin Immunol 1988;81::1059-65.  Back to cited text no. 17    
18.Bock SA. The natural history of food sensitivity. J Allergy Clin Immunol 1982;60:137-7.  Back to cited text no. 18    
19.Aas K. Studies on hypersensitivity to fish. A clinical study. Int Arch Allergy Appl Immunol 1966;29:346-63.  Back to cited text no. 19    
20.Lloyd-Still JD. Chronic diarrhoea of childhood and the misuse of elimination diets. J Paediatr 1979;95:10-13.  Back to cited text no. 20    
21.David TJ. Waddington E, Stanton RHJ. Nutritional hazard of elimination diets in children with atopic dermatitis. Arch Dis Child] 984;59:323-5.  Back to cited text no. 21    

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Correspondence Address:
Mohamad Osman Gad El-Rab
Associate Professor & Consultant, Allergy & Imunology, College of Medicine and King Khalid University Hospital. P.O. Box 2925, Riyadh 11461
Saudi Arabia
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PMID: 19864783

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