|Year : 2006 | Volume
| Issue : 2 | Page : 111-114
|Profile of food allergens in urticaria patients in Hyderabad
Priya V Hari Sai, B Anuradha, VV Vijayalakshmi, Suman G Latha, KJR Murthy
Immunology Unit, 10/1/1, Bhagwan Mahavir Hospital and Research Center, Hyderabad - 500 004, India
V V Vijayalakshmi
Consultant Immunologist, 10/1/1, Bhagwan Mahavir Hospital and Research Center, A. C. Guards, Hyderbad - 500 004 (A.P.)
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Urticaria is one of the manifestations of a pattern of allergy. The associated disorders are vascular reaction and wheals. The objective of this study was to determine the prevalence of sensitivity to food allergens in Hyderabad in patients suffering from allergy. Four hundred and one patients attending the Allergy Clinic at BMMRC, with a confirmed diagnosis of bronchial asthma, rhinitis or urticaria were skin tested. Total sIgE levels were estimated by ELISA. Positivity to beans (53%) was highest, followed by mustard (41%) and cardamom (40%). Often patients having positive skin tests to food allergens which may have skin reactions to foods prove to be a problem. Foods that produce significant positive skin tests could be avoided in the diet; however, other foods that do not show skin reactions may contribute to the disease.
Keywords: Urticaria, Food allergens, IgE, Skin test
|How to cite this article:|
Hari Sai PV, Anuradha B, Vijayalakshmi V V, Latha SG, Murthy K. Profile of food allergens in urticaria patients in Hyderabad. Indian J Dermatol 2006;51:111-4
|How to cite this URL:|
Hari Sai PV, Anuradha B, Vijayalakshmi V V, Latha SG, Murthy K. Profile of food allergens in urticaria patients in Hyderabad. Indian J Dermatol [serial online] 2006 [cited 2020 Jan 26];51:111-4. Available from: http://www.e-ijd.org/text.asp?2006/51/2/111/26931
| Introduction|| |
Urticaria is a vascular reaction in the upper dermis, marked by the development of wheals on virtually any area of the body. It is caused by foods, drugs, insect stings which are identified as the most common precipitants. Rhinitis and Asthma are other atopic diseases also affected by these allergens. The patient history is one of the important evaluations about the preexisting allergies, physical stimuli exposure, ingestion of foods or drugs, stress or exertion, exposure to chemicals, new environment, animals, insects, other symptoms. Allergy to food involves the production of antibodies known as IgE and a network of interactions between various cell types and chemical mediators. This further causes the cells to release substances lymphocytes and monocytes are attracted to the site and promote an inflammatory reaction. The prevalence of food allergy in the general population ranges from 1 to 2% in adults , to 6 to 8% in children. Cow's milk, eggs, wheat, soy, peanut, and fish account for about 90% of documented food allergy in infancy and early childhood.,,, Peanut, tree nuts, seafood for 85% of severe reactions in older children and adults, . The objective of this study was to find out the prevalence of food allergy in Hyderabad.
| Materials and Methods|| |
The study comprised a total of 401 patients with confirmed diagnosis of urticaria, Rhinitis and Asthma who attended the Allergy Clinic, Mahavir Hospital and Research Center during the period January 2000-December 2002. The study excluded children below 12 years and pregnant women. The diagnosis was usually based on IgE-mediated total serum IgE levels-and confirmed by the results of intradermal skin test.
Intradermal injection of buffer saline acted as negative control and histamine phosphate as positive control. Immediate and late phase cutaneous responses were recorded at 20 min and 6-8 hours after allergen challenge. Patients who showed the skin test responses equal to or above histamine phosphate were considered as skin test positive to that particular antigen.
The total IgE levels were performed by using commercially available ELISA kit from General Biologicals Corp, Taiwan. The cut off value for IgE levels was 325 IU/ml.
| Results|| |
Of the total 401 patients, there were 180 male and 221 female patients, with a mean age group of 35.7 years. The study included 54.9% of the patients with urticaria, 22.4% with Urticaria/Rhinitis and 23% with Urticaria/Asthma.
53.1% of the patients showed positive skin test responses for beans, followed by mustard (41.1%) and cardamom (40%) [Table - 1].
The most predominant food allergen to which majority of the patients have shown positivity is beans, of which 61.9% were urticaria patients, 23.4% were with urticaria/rhinitis and 14.5% were having urticaria/asthma [Table - 2].
34.9% of the patients were positive to less than 5 food allergens with a duration of 4 years and 32% were positive to £ 10 food allergens respectively. 35.2% of the patients suffering since childhood were positive to ³ 5 food allergens [Table - 3]
52.1% of the patients suffering from urticaria had IgE values £ 325 IU/ml and 24.3% of the patients having IgE values greater than 800. [Table - 4].
46% of the patients positive to less than five food allergens and 67.4% of the patients positive to greater than twenty food allergens had IgE values £ 325 IU/ml and Only 17.5% of the patients showed IgE values ³ 800 who were allergic to 16-20 food allergens [Table - 5].
| Discussion|| |
Skin test reactivity showed that beans were the most predominant allergen in this study. The harmful proteins present in beans may be one of the reasons for its high allergic nature. The lectins present in the beans may be capable of damaging the intestinal mucosa, causing increase in intestinal permeability. The lectin proteins or haptens which enter the blood stream trigger the allergic reactions. Another high risk of being allergic to beans is due to the presence of pan allergen called profiling. This is a homologous protein found in many plants, pollens and fruits. It has been found that a person allergic to Artemisia pollen is also allergic to beans, legumes, mustard, kiwi and hazelnut. An individual who is sensitive to beans is more likely to have allergies to peas, peanuts, and lentils as they all are members of leguminaceae family. In the present study, out of the 224 patients sensitive to beans 39% were sensitive to peas 35% were sensitive to lentils, and 33% to peanuts. The prevalence rate of certain food allergies depends mainly on eating habits. Beans is also a common allergen in Spain and Brazil, whereas in Scandinavian countries the most prevalent food allergy is fish.
The second most predominant allergen in the present study was mustard. It is considered as an extremely potent allergen. Exposure to mustard is high in Indians as mustard is consumed almost everyday. Prevalence of allergy to mustard is also high in France. Allergies to other vegetable foods were attributed to mustard allergy in Spanish population. Bra j IE has been considered to be the major allergen in oriental mustard (Brassica juncea) and its antigenic determinant was found to be involved in the allergenicity.
The subsequent allergen is cardamom. It is used extensively as a domestic spice especially in India. Cardamom is also used primarily in Europe, Latin America and Middle Eastern countries. It was reported that cardamom contains terpenoid compounds. These terpenes were found to elicit contact dermatitis.
The next major allergen is cashew nut and it constantly cross reacts with pistachio nuts. Allergy to cashew nut appears to be much less common than to other tree nuts. Legumin-like protein has been identified as a major allergenic component in cashew nut. In a study it is quoted that cashew nut is life threatening due to a component of the kernel itself.
The fifth common allergen is ginger and it is the most popularly used spice in India. Salicylates are chemicals found naturally in ginger and also in many vegetables, where they act as preservatives to protect them against harmful microorganisms and rotting. Salicylate sensitive individuals tend to have adverse reactions to benzoates and tartrazine that are one of the components of Azo dyes commonly used in many food products as a preservative. Some people sensitive to these dyes suffering from allergic diseases like asthma and uriticaria should avoid them.
Some of the explanations put forth, to explain the observation that a higher number of individuals with a recent onset (43%) were positive to a large number of food allergens, include either a genetic predisposition, or a recent exposure to the same or other food allergens to which the patient is already sensitized, or due to cross- reactivity.
A large number of patients with urticaria alone in this study had normal levels of total IgE, unlike in majority of the patients suffering from Urticaria with asthma or rhinitis, suggesting an atopic etiology for asthma and rhinitis and not for urticaria. An explanation offered for this may be the heterozygocity of an IgE regulator gene, Rr that results in an increased risk for atopic disease, despite a normal total serum IgE. Urticaria patients need to be studied for their heterozygocity (Rr) to explain their normal levels of total IgE in further studies.
In the present study, majority of the patients were skin test positive to more than 5 food allergens. It has been reported that an array of foods may contain similar allergenic proteins, which might result in multiple skin test positives despite not having symptoms and allegenic conditions to all those food allergens. Interestingly, majority of the patients who were sensitive to more than 15 food allergens had IgE levels within the normal range. It is probably due to the increased skin mast cell that patients with urticaria release histamine immediately after the exposure of allergen.
The mainstay in the food allergy treatment involves avoidance of a specific food from which the patient is suffering. Furthermore, there is a need to focus more on the identification and characterization of allergenic proteins and the development of new therapeutic strategies in order to treat these disorders by means of immunotherapy.
While keeping away from a specific food there is also a need for the patient to be aware of the cross-reactions with other food allergens or aeroallergens. Further means to evade the allergenic foods is to desensitize the patient by eliminating that offending food and then reintroducing it after a certain period, which might be helpful for the patient to gain tolerance.
| Acknowledgements|| |
We thank Dr. Akbar Yazdani, Dr. Nafees Sultana and Ms. R. Eswari for the clinical and technical help rendered during the study.
| References|| |
|1.||Sveum RJ The diagnostic challenge of hives Vol. 100, No 2/ August 1996. |
|2.||Jackson WF. Food Allergy, Web site |
|3.||Public Health Guidance note, March 2002. |
|4.||Young E, Stoneham MD, Petruckevitch A, Barton J, Rona R. A population study of food intolerance. Lancet 1994;343:1127-30. [PUBMED] |
|5.||Schafer T, Bohler E, Ruhdorfer S, Weigl L, Wessner D, Heinrich J, et al . Epidemiology of food allergy/food intolerance in adults: Associations with other manifestations of atopy. Allergy 2001;56:1172-9. |
|6.||Bock SA, Munoz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. J Aller Clin Immunol 2001;107:191-3. [PUBMED] [FULLTEXT]|
|7.||Sampson HA, Albergo R. Comparison of results of skin tests, RAST and double-blind, placebo-controlled food challenges in children with atopic dermatitis. J Aller Clin Immunol 1984;74:26-33. [PUBMED] [FULLTEXT]|
|8.||Burks AW, James JM, Hiegel A, Wilson G, Wheeler JG, Jones SM, et al . Atopic dermatitis and food hypersensitivity reactions. J Pediatr 1998;132:132-6. |
|9.||Niggemann B, Sielaff B, Beyer K, Binder C, Wahn U. Outcome of double-blind, placebo-controlled food challenge tests in 107 children with atopic dermatitis. Clin Exp Aller 1999;29:91-6. [PUBMED] [FULLTEXT]|
|10.||Sicherer SH, Morrow EH, Sampson HA. Dose-response in double-blind, placebo-controlled oral food challenges in children with atopic dermatitis. J Aller Clin Immunol 2000b;105:582-6. [PUBMED] [FULLTEXT]|
|11.||Sampson HA, Food allergy. Part 1: Immunopathogenesis and clinical disorders. J Aller Clin Immunol 1999;103:717-28. |
|12.||Sicherer SH, Sampson HA. Food hypersensitivity and atopic dermatitis: Pathophysiology, epidemiology, diagnosis and management, J Aller Clin Immunol 1999;104:S114-22. [PUBMED] [FULLTEXT]|
|13.||D'Mello JP. Antinutritional factors and mycotoxins. In : D'Mello JP, editor. Farm animal metabolism and nutrition. CAB International: Wallingford, UK; 2000. p. 383-403. |
|14.||http://www.worldallergy.org/professional/allergic_diseases_centre/anaphylaxis/an aphylazissynopsis.shtml. |
|16.|| Waterhouse JC. Food allergy/Sensitivity: The Pulse Test and Other Stratgegies. CISRA's Synergy Health Newsletter, Issue 5, Vol.2(2), Summer/Fall: 1999. |
|17.||Chaud SG, de Oliveira AC, Ocheuze Trivelin PC. Nitreogen 15 abundance in protein fractions of beans fertilized with (15NH4)2SO4. Sci. agric. Piracicaba: Braz; 2002;59:4. |
|19.|| Tripathi et al. A prospective study of mustard allergy in allergic rhinitis cases. ENT and allergy Centre. Chandigarh, Mumbai, India. |
|20.||Caballero T, San-Martin MS, Padial MA, Contreras J, Cabanas R, Barranco P, et al . Clinical characteristics of patients with mustard hypersensitivity. Ann Allergy Asthma Immunol 2002;89:166-71. |
|21.||Monsalve RI, Gonzalez de la Pena MA, Menendez-Arias L, Lopez-Otin C, Villalba M, Rodriguez R. Characterization of a new oriental-mustard (Brassica juncea) allergen, Bra J IE: Detection of an allergenic epitope. Biochem J 1993;293:625-32. [PUBMED] [FULLTEXT]|
|23.|| Mobacken H, Fregert S. Allergic contact dermatitis from cardamom. Contact Dermat 1975;1(3):175-6. |
|24.||Garcia F, Moneo I, Fernandez B, Garcia-Menaya JM, Blanco J, Juste S, et al . Allergy to Anacardiaceae:description of cashew and pistachio nut allergens. J Invest Allergoil Clin Immunol 2000;10(3):173-7. |
|25.||Wang F, Robotham JM, Teuber SS, Sathe SK, Roux KH. Ana o 2, A major cashew (Anacardium occidentale L.) nut allergen of the legumin family. Int Arch Allergy Immunol 2003;132:27-9. [PUBMED] [FULLTEXT]|
|26.||Mitchell JC, Rook A. Botanical Dermatology, Plants and Plant products injurious to the skin. Greengrass: Vancouver; 1979. |
|27.||Anderson JA. The clinical spectrum of food allergy in adults. Clin Exp Allergy 1991;1:304-15. |
|28.||Borecki et al . Bivariate segregation analysis for sIgE and level 1 liability to allergy, 1985. |
|29.||Food and Agriculture Organization of the United Nations (FAO) and World Health Organization (WHO). Evaluation of Allergenicity of Genetically Modified Foods:Joint FAO/WHO Expert Consultation on Allergenicity of Foods Derived from Biotechnology. FAO: Rome; 2001. |
|30.||Cohen RW, Rosenstreich DL. Discrimination between Urticaria-prone and other allergic patients by intradermal skin testing with codeine. J Allergy Clin Immunol 1986;77:802-7. [PUBMED] [FULLTEXT]|
[Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5]
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