International Journal of Nutrition and Food Sciences
Volume 5, Issue 4, July 2016, Pages: 234-240

 Review Article

The Progress of Food Allergy Concept, Classifications and Diagnosis

Kamal-Alahmad1, 2, 4, Sameh A. Korma1, 3, 5, Tao Zhang1, 3, Jinfang Zhang1, 3

1School of Food Science and Technology, Jiangnan University, Wuxi, Jiangsu, China

2Laboratory of Food Enzymology and Food Chemistry, Jiangnan University, Wuxi, Jiangsu, China

3State Key Laboratory of Food Science and Technology, Synergetic Innovation Centers of Food Safety and Nutrition, School of Food Science and Technology, Jiangnan University, Wuxi, Jiangsu, China

4Department of Food Science and Technology, Faculty of Agriculture, University of Alfurat, Deir Ezzor, Syria

5Department of Food Science, Faculty of Agriculture, Zagazig University, Zagazig, Egypt

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To cite this article:

Kamal-Alahmad, Sameh A. Korma, Tao Zhang, Jinfang Zhang. The Progress of Food Allergy Concept, Classifications and Diagnosis. International Journal of Nutrition and Food Sciences. Vol. 5, No. 4, 2016, pp. 234-240. doi: 10.11648/j.ijnfs.20160504.11

Received: May 9, 2016; Accepted: May 21, 2016; Published: June 4, 2016

Abstract: Food allergies, defined as an immune response to food proteins, affect as many as 8% of young children and 5% of adults in most countries, and their prevalence appears to be rising like all allergic diseases, In addition to well-recognized urticaria and anaphylaxis triggered by IgE antibody-mediated immune responses. Food allergy is a rapidly growing public health concern because of its increasing prevalence and life-threatening potential. Food allergic reaction can be further subdivided into IgE mediated and non IgE mediated. The diagnosis of food allergy is made from the history, supported by investigations and by responses to avoidance of specific food triggers. So in this work we want to introduce some concepts in food allergy such as classification of allergic and diagnosis of food triggers and finally how to manage this problem and minimize the prevalence of food allergy.

Keywords: Allergy, IgE, Diagnosis, Application in Food Industries

1. Introduction

Food allergy is defined as an immunological reaction resulting from consumption or other contact with food. It only affects susceptible people who are sensitive, or sensitized to the specific food allergen, which would otherwise normally be well tolerated by the rest of the population [1]. Food hypersensitivity symptoms only appear, or are ‘elicited’, when you consume or have contact with the food to which you are sensitized [2]. Typical symptoms of IgE-mediated food allergy can be subjective symptoms such as purities or itching [3]. Food-allergic reactions can be triggered by consuming even very small amounts of food in the range of 10–100 mg [4]. The most common food allergies in the United States are milk, egg, peanut, soy, wheat, tree nuts, fish and shellfish. The individual food allergy does vary by culture and population [5]. The type of food allergies can even vary across regions of Northern Europe. In Russia, Estonia, and Lithuania; citrus fruits, apple, hazelnut, strawberry, fish, tomato, egg, and milk were common self-reported allergy. But, in Sweden and Denmark; tree nuts, apple, pear, kiwi, stone fruits, and carrot were the most common self-reported food allergy [6] For reasons that are not yet clear, 90% of hypersensitivity reactions are attributable to only eight major types of food: milk, eggs, shellfish (particularly crustaceans), peanuts, soybeans, tree nuts, and wheat [8]. [9]. Allergic responses to milk, soybeans, eggs, and wheat are typically transient and restricted to childhood; while peanuts, tree nuts, and shellfish are more likely to induce life-long anaphylactic hyperreactivity [7] [10].

2. Classification

Food intolerance refers to an adverse physiologic response to a food and may be due to inherent properties of the food (i.e. toxic contaminant, pharmacologic active component) or to characteristics of the host (i.e. metabolic disorders, idiosyncratic responses, psychological disorder) [11-12].

Food-induced anaphylaxis is a serious allergic reaction that is rapid in onset and can cause death. 10 IgE-mediated food-induced anaphylaxis involves systemic mediator release from sensitized mast cells and basophils. In patients with food-dependent, exercise-induced anaphylaxis, whether a reaction occurs depends on the amount of time between food consumption and exercise, usually within 2 hours not included under food intolerance reactions, the reason being that they do not depend on individual susceptibility [14].

2.1. Mixed IgE-and Non– IgE-Mediated or Non– IgE Mediated Food Allergy

Diagnosing mixed IgE- and non–IgE-mediated or non–IgE mediated food allergies is more challenging than diagnosing IgE mediated food allergy. The approach begins with the clinical history. A clear cause and effect between food ingestion and symptoms might not be clear because the symptoms of these types of food allergy are typically chronic versus immediate but on toxic effects. Non that are immune whereas non immune [15]. Intradermal tests, total serum IgE measure, and atopy patch tests were not recommended for use in diagnosing food allergy in the NIAID-sponsored guidelines and in the Diagnosis and Rationale for Action against Cow’s Milk Allergy guidelines sponsored by the World Allergy Organization mediated react. [16-17]. the guidelines for specific immunotherapies for IgE mediated food allergies face several specific issues. [18]

2.2. Diagnosis of IgE-Mediated Food Allergy

The diagnosis of IgE-mediated food allergy, Allergen-specific IgE can be detected by SPTs or immunoassays of serums IgE levels. These tests identify foods that might provoke IgE-mediated reactions, but neither can be considered diagnostic of food allergy and must be combined with the history. [47-48] Serums IgE levels can be measured by using immunoassays (Immuno CAP, Immunlite), which provide reliable and reproducible measurements, although results can take hours to days. SPTs are quick and simple to perform. The SPT wheal size is correlated with the likelihood of clinical allergy,[49-50] and 95% positive predictive thresholds (wheal size above which there is a >95% chance of clinical allergy) have been described for the common allergens. [51-52].

3. Epidemiology

The most common food allergens in the pediatric population include cow’s milk, eggs, peanuts, tree nuts, soy, wheat, fish, and shellfish, whereas peanuts, tree nuts, fish, and shellfish predominate in adults in the United States (US). [19-20-21]. The prevalence of sensitization to the specific food allergens varies based on the age and characteristics of the population, but studies incorporating diagnostic food challenges currently estimate that the prevalence of cow’s milk allergy in infants is 2.5%, egg hypersensitivity prevalence in young children is 1.6% and peanut allergy is estimated to be between 0.8 and 1.5% in young children in US and England. [22-23].

Most infants with non-IgE mediated cow’s milk allergy "outgrow" their sensitivity by the third year of life, but about 10- 25% of infant with IgE mediated cow’s milk allergy retain their sensitivity and about 50% develop sensitivity to other foods. [24-25] most children with egg allergy are also likely to develop egg tolerance by late childhood, with the exception of patients with an egg IgE greater than 50 kU L, who are unlikely to develop egg tolerance. [26] Peanut, sesame seeds and tree nuts allergies are more persistent with a chance of becoming tolerant is about 20% for peanut and sesame seeds and about 10% for tree nuts. [27-28]. There has been a significant increase in the incidence of food allergies including a rise of Emergency Department visits for food allergic reactions. [29-30], moreover peanut allergy prevalence in children in US and England doubled in the last few years in identical telephone surveys. [31-32]. the reasons for the increase in food allergy prevalence are not known, but, the short period of time over which the increase occurred, suggests that environmental factors are more likely to be relevant than genetic factors as part of the hygiene hypothesis. [33-34]. the introduction of food later in the infant diet has been postulated to play a role in the increase of food allergy [35]. As food allergy is more common in infants [36], higher permeability of the intestinal mucosa in infants and early exposure to allergenic antigens have been proposed as a possible cause of sensitization in infant. However, it has been shown that the gastrointestinal mucosa reaches its maturity in terms of permeability at day 2-3 of life and the increased permeability observed in some children with food allergy is a consequence rather than a cause of the allergic inflammation [36-37-38].

4. Microbiota Regulation of Tolerance and Allergy

Alterations in the microbiota have now been implicated in the pathogenesis of AD, asthma, and food allergy. [39] Intestinal microbiota influences the network of the immune system and result in impaired regulatory functions and TH2 skewing. While germ-free (GF) conditions are almost impossible in human studies, limiting the types of analysis that can be performed, a role for commensal microbiota in promoting oral tolerance has been clearly defined by using gnotobiotic mice, in which reconstitution of GF mice with well-characterized communities of microbiota or defined bacteria has been performed. Numbers of CD41Foxp31 Treg cells are reduced in antibiotic-treated mice or GF mice, [40-41] which exhibit a prides position toward allergic sensitization. [41-42] Administration of defined commensal microbiota, such as Clostridia species and Bactericides fragilis, or short-chain fatty acids (microbiota-derived products) to GF mice induced Treg cells [40, 43-44] and reduced allergic sensitization, [40] supporting the notion that intestinal commensal microbiota promote Treg cells and limit allergic responses to foods. Il4raF709 mice carrying a gain-of-function mutation in IL-4 receptor a-chain, which are susceptible to allergic sensitization and anaphylaxis, [45-46] exhibit an altered gut Microbiota signature from that seen in control mice.

5. Studies of OIT for Peanut and Tree Nut Allergies

It is important to develop therapeutics that target the causes of peanut and tree nut allergies. Fewer patients have natural tolerance to these allergens than to other food allergens; most children who are allergic to peanuts remain allergic as

Teenagers and adults and have more severe reactions. [53]. Peanuts and tree nuts are responsible for most food-induced anaphylactic reactions among children. [54]. However, subcutaneous immunotherapy for peanut allergy has many side effects. [55]. OIT for peanut allergy has only recently been investigated, and there have been no studies for tree nut allergy. The first studies of OIT for peanut allergy were uncontrolled and performed in the United States [56-57] and Europe, [58-59] and these studies showed promising results. A systematic review of OIT for peanut allergy by Sheikhet [60] discussed findings from these studies and 3 abstract articles. Most recently, 1 controlled study was performed in the United States and another uncontrolled one in Europe. [61-62] the details of all uncontrolled and controlled studies are summarized in Table 1. [56-58-59-61-62].

OIT and sublingual immunotherapy seem to be the most promising approaches for treating food allergies. OIT was initially described decades ago in case reports and small uncontrolled trials. The first controlled studies reported high levels of efficacy, but the safety and side effects of the therapy were debated. [64-65]. several studies have been conducted since, but it has been difficult to compare their results because different protocols and allergens were used. [63].

Table 1. Characteristics of OIT and peanut allergy.

Year publish 2009 2009 2010 2011
Countries Europe united states Europe Europe
Type immunotherapy OAT OAT OAT OAT
Randomized controlled trial NO NO NO NO
NO. of patients 4 39 23 22
Ages of patients 9-13 1-9 3-14 4-18
Exclusion criteria not given severe life Anaphylaxis unstable asthma major immuno deficiency

Characteristics of OIT and sublingual immunotherapy for peanut allergy [56-58-59-61-62]

6. Diagnosis

The importance of a thorough clinical history of the patient, taking in as many relevant details as possible, cannot be over emphasized. In the case of IgE mediated food allergy, the acute onset of the response is normally a useful indicator of the diagnosis. The clinical history will normally indicate the causative food (s) allowing for more defined investigation. The detection of allergen-specific IgE is also a useful laboratory test to help confirm diagnosis and identify the triggering food. This may be done either by looking for specific IgE in a blood sample or by using the skin prick test. The skin prick test involves placing a small drop of allergen solution on the skin and gently breaking the skin below the drop. The allergen in the solution will make contact with any IgE bound to mast cells in the skin. If the IgE is specific for the allergen, the bound IgE will be cross-linked by the allergen causing mast cell degranulation, histamine release and a wheal and flare reaction. [66]. In general, the history can be more helpful in IgE-mediated disorders, because these reactions occur so soon after food ingestion and because multiple target organs are affected. History is harder for food-protein induced enterocolitis, where symptoms occur hours later or days later in eosinophilic esophagitis. What is the time frame for the reaction? Immediate hypersensitivity reactions generally occur rapidly, often within minutes and virtually always within 2½hours. [67]. Mixed and T-cell mediated reactions have a characteristically delayed onset. Therefore patients with FPIEC begin to have symptoms later than 1 ½ hours after ingestion Additional clinical history elements can be helpful.

7. Diagnosis in Laboratory

Immediate hypersensitivity skin tests (prick skin tests) examine for the presence of food protein specific IgE. In general, skin tests have positive predictive accuracies of about 50%; but their negative predictive values are in excess of 95%. [68]. the larger the size of wheal on skin test, the more likely a patient will react to the food [68-69].

An alternative method to detect food protein specific IgE is by in vitro methods, (FEIA-CAP or "RAST test"). Some investigators may prefer to use in vitro testing when there is persistent dermatographism (rare), severe eczema, or when families are reluctant either to discontinue H1 blockers. Similar to prick skin tests, a "cut-off" value can be developed for predicting 95% [70-71] or even 50% predictive values [72] on food challenges (Table 1). However, similar to prick skin test, the predictive values changes for the food, age of the patient or the history of previous reaction. Predictive values can only be developed for milk, egg, peanut, tree nuts, sesame seed and fish. 95% predictive values cannot be developed for soy and wheat. The younger patients have a lower "cut-off" value for 95% predictive value, while no previous exposure to the food or clear history has a higher predictive value (Table 1). For non-IgE-mediated disorders, fewer laboratory diagnostic tools exist. Atopy patch test have been used for eosinophilic esophagitis, food protein induced enterocolitis and atopic dermatitis. [73-74] Compared to prick skin test, atopy patch test is more specific, but less sensitive. [75-76-77]. the negative predictive value is close to 90% except for milk, where it is close to 60%. Therefore, atopy patch test can be provide guidance but not absolute for dietary advice for nonIgE mediated food allergy. Eosinophils in the blood or stool may point to an ongoing enteropathy, but these findings are certainly nonspecific. Serum levels of allergen-specific IgG are not helpful. Endoscopy followed by examination of biopsy specimens are the most important tools in non-IgE-mediated disorders and critical for the diagnosis of eosinophilic esophagitis. Challenges are needed to identify specific food triggers in all cases. There are no tests that indicate the severity or what patients are at high risk for severe allergic reaction or anaphylaxis. However, recent work by Vadas and colleagues examining patients with experienced fatal and nonfatal peanut-induced anaphylaxis compared to normal controls, patients with food allergy and patients with mild peanut reactions. The patients with peanut anaphylaxis had elevated factor (PAF) and decreased PAF acetyl hydrolase suggesting failure of PAF acetyl hydrolase to inactivate PAF contributes to anaphylaxis. [78].

8. Application of Existing Therapies to Food Allergy

The global suppression of immune responses is a common therapeutic strategy applied to inflammatory diseases, such as allergic asthma, autoimmune diseases, or post-transplantation. For allergic asthma, glucocorticoids have become a mainstay, and yet they are generally considered ineffective for food allergy. Work with a murine model of food allergy examined the potential effects of rapamycin in altering food-induced allergic responses. [79] Perhaps not surprisingly, given its potent abilities to suppress T-cell responses, rapamycin was able to diminish the generation of food allergy associated pathology when administered during the sensitization window. In addition, treatment of fully sensitized mice was also sufficient to reduce the severity of diarrhea, symptoms, and core body temperature decreases seen on antigen challenge. Interestingly, the immediate responses to passive immunization with antigen-specific IgE or in cultured mast cells were unaffected, but instead, the IL-9–mediated survival of mast cells was diminished. Increasing evidence from animal models has supported the critical role for mast cells and the IL-9 pathway in the severity of food-induced allergic responses, [80-81] including the beneficial effects of mast cell stabilization in IL-9 transgenic mice with systemic cromolyn sodium treatment. [81] Interestingly, several case reports have shown therapeutic benefit from oral cromolyn sodium treatment for food dependent exercise-induced anaphylaxis [82] and, taken together, the results suggest that existing therapies that limit mast cell numbers or enhance mast cell stability might be clinically effective for food allergy.

Similarly, recent work has demonstrated the potential efficacy of the tyrosine kinase inhibitor compound sunitinib malate (Sutent; Pfizer, New York, NY) [83] in food allergy models. Several receptor systems, including that of the stem cell factor receptor, which is highly expressed on mast cells, and has been successfully used in the treatment of renal carcinoma and resistant gastrointestinal tumors. [84]. although high doses were used, the findings demonstrated a clear diminishment of oral antigen–triggered anaphylactic responses in mice previously sensitized to ovalbumin. Importantly, inhibition of passively immunized mice, as well as primed in vitro mast cells, was shown, suggesting that the efficacy of this approach lies with inhibition of the immediate mast cell response to antigen.

9. Conclusion

Food allergy is of increasing importance to public health, with a growing emphasis on provision of accurate, reliable allergen information for foods and urgent need for capable analytical tools to support and assure food industry risk management programs, allergen labeling and claims, and regulatory authority monitoring and control.

Increased understanding for the pathogenesis of both IgE and non-IgE mediated reactions have been done with the use of new techniques and murine models. These advances are creating the opportunities for novel therapies for food allergy. There is still a need to validate the methods for the use of new diagnostic tools and to evaluate their use in the management of food allergic disorders. More information is required to clarify precipitating factors.


  1. Gi Boyce, J. A. (2010) Guidelines for the diagnosis and management of food allergy in the United States.J Allergy Clin Immunol, (2010) 126 (suppl), S1–58.
  2. Taylor, S. L. and Hefl e, S. L. Food allergies and other food sensitivities. J Food Technol, (2010) 55, 68–83
  3. Cianferoni, A. and Spergel, J. Food allergy: review, classification and diagnosis. Allergol Int. (2009), 58, 457–466.
  4. Hourihane, J. O’B. and Knulst, A. C. Thresholds of allergenic proteins in food. Tox Appl Pharmacol, (2005) 207, S152–S156.
  5. Antonella Cianferoni Food Allergy: Review, Classification and Diagnosis, Allergology International 2009 Vol 58.
  6. Eriksson NE, Moller C, Self-reported food hypersensitivity in Sweden, Denmark, J Investig Allergol Clin Immunol 2004; 14: 70-9.
  7. Cath ryn R. Nagler Introduction to Special Issue on Food Allergy, Semin Immunopathol (2012) 34: 615–616.
  8. Montserrat Fernández-Rivas, Ricardo Asero Risk Management for Food Allergy, 2014, Pages 25-43.
  9. Ja¨rvinen KM. Food-induced anaphylaxis. Curr Opin Allergy Clin Immunol 2011; 11: 255-61.
  10. Wu TC, Tsai TC, Huang CF, Chang FY, Lin CC, Huang IF, et al. Prevalence of food allergy in Taiwan: a questionnaire-based survey. Intern Med. J. 2012; 42: 1310-5.
  11. Sampson HA. Food allergy. Part 2: diagnosis and management. J Allergy Clin Immunol 1999; 103: 981-9.
  12. Lee LA, Burks AW. Food allergies: prevalence, molecular characterization, and treatment prevention strategies. Annu Rev Nutr2006; 26: 539-65.
  13. Anderson. J. A. The establishment of common language concerning adverse reaction to food. J. allergy clin. Immuno. 1988.78. 140-143.
  14. Sampson HA, Mu~noz-Furlong A, Bock SA, Schmitt C, Bass R, Chowdhury BA, et al. Symposium on the definition and management of anaphylaxis: summary report. J Allergy Clin Immunol 2005; 115: 584-91.
  15. Sackeyfio A, Senthinathan A, Kandaswamy P, Barry PW, Shaw B, Baker M. Diagnosis and assessment of food allergy in children and young people: summary of NICE guidance. BMJ 2011; 342: d747.
  16. Boyce JA, Assa’ad A, Burks AW, Jones SM, Sampson HA, Wood RA, et al. Guidelines for the diagnosis and management of food allergy in the United States: report of the NIAID-sponsored expert panel. J Allergy Clin Immunol 2010; 126 (suppl): S1-58.
  17. Fiocchi A, Brozek J, Schnemann H, Bahna SL, von Berg A, Beyer K, et al. World Allergy Organization (WAO) Diagnosis and Rationale for Action against Cow’s Milk Allergy (DRACMA) Guidelines. Pediatr Allergy Immunol 2010; 21 (suppl 21): 1-125.
  18. European Medicines Agency committee for medical products for human use (CHMP). Guideline on the clinical development of products for specific immunotherapy for the treatment of allergic diseases/Doc. Ref. CHMP/EWP/18504/2006/ date for coming into effect June 1st, 2009. Available at: http://www.emea.europa. eu. Accessed March 2, 2012.
  19. Venter C, Pereira B, Grundy J et al. Incidence of parentally reported and clinically diagnosed food hypersensitivity in the first year of life. J Allergy Clin Immunol 2006; 117: 1118-24 .
  20. Venter C, Pereira B, Grundy J, Clayton CB, Arshad SH, Dean T. Prevalence of sensitization reported and objectively assessed food hypersensitivity amongst six-year-old children: a population-based study. Pediatr Allergy Immunol 2006; 17: 356-63.
  21. Sicherer SH, Munoz-Furlong A, Sampson HA. Prevalence of seafood allergy in the United States determined by a random telephone survey. J Allergy Clin Immunol 2004; 114: 159-65.
  22. Schrander JJ, van den Bogart JP, Forget PP, Schrander Stumpel CT, Kuijten RH, Kester AD. Cow’s milk protein intolerance in infants under 1 year of age: a prospective epidemiological study. Eur J Pediatr 1993; 152: 640-4.
  23. Eggesbo M, Botten G, Halvorsen R, Magnus P. The prevalence of allergy to egg: a population-based study in young children. Allergy 2001; 56: 403-11.
  24. Host A, Halken S, Jacobsen HP, Christensen AE, Herskind AM, Plesner K. Clinical course of cow’s milk protein allergyintolerance and atopic diseases in childhood. Pediatr Allergy Immunol 2002; 13 (Suppl 15): 23-8.
  25. Saarinen KM, Pelkonen AS, Makela MJ, Savilahti E. Clinical course and prognosis of cow’s milk allergy are dependent on milk-specific IgE status. J Allergy Clin Immunol 2005; 116: 869-75.
  26. Savage JH, Matsui EC, Skripak JM, Wood RA. The natural history of egg allergy. J Allergy Clin Immunol 2007; 120: 1413-7.
  27. Agne PS, Bidat E, Agne PS, Rance F, Paty E. Sesame seed allergy in children. Eur Ann Allergy Clin Immunol 2004; 36: 300-5.
  28. Fleischer DM, Conover-Walker MK, Matsui EC, Wood RA. The natural history of tree nut allergy. J Allergy Clin Immunol 2005; 116: 1087-93.
  29. Poulos LM, Waters AM, Correll PK, Loblay RH, Marks GB. Trends in hospitalizations for anaphylaxis, angioedema, and urticaria in Australia, 1993-1994 to 2004-2005. J Allergy Clin Immunol 2007; 120: 878-84.
  30. Sheikh A, Alves B. Hospital admissions for acute anaphylaxis: time trend study. BMJ 2000; 320: 1441.
  31. Grundy J, Matthews S, Bateman B, Dean T, Arshad SH. Rising prevalence of allergy to peanut in children: Data from 2 sequential cohorts. J Allergy Clin Immunol 2002; 110: 784-9.
  32. Sicherer SH, Munoz-Furlong A, Burks AW, Sampson HA. Prevalence of peanut and tree nut allergy in the US determined by a random digit dial telephone survey. J Allergy Clin Immunol 1999; 103: 559-62.
  33. Bach JF. The effect of infections on susceptibility to autoimmune and allergic diseases. N Engl J Med 2002; 347: 911-20.
  34. Schaub B, Lauener R, von Mutius E. The many faces of the hygiene hypothesis. J Allergy Clin Immunol 2006; 117: 969-77; quiz 978.
  35. Du Toit G, Katz Y, Sasieni P et al. Early consumption of peanuts in infancy is associated with a low prevalence of peanut allergy. J Allergy Clin Immunol 2008; 122: 984-91.
  36. Chehade M, Mayer L. Oral tolerance and its relation to food hypersensitivities. J Allergy Clin Immunol 2005; 115: 3-12; quiz 13.
  37. Heyman M. Symposium on ‘dietary influences on mucosal immunity’. How dietary antigens access the mucosal immune system. Proc Nutr Soc 2001; 60: 419-26.
  38. Mowat AM. Anatomical basis of tolerance and immunity to intestinal antigens. Nat Rev Immunol 2003; 3: 331-41.
  39. Marrs t. bruce kd. is there an association between microbial exposure and food allergy. pediatr allergy immune. 2013; 24: 311-20.
  40. Atarashi. k shima.t imaoka. A induction of colonic regulatory t cells by indigenous clostridium species. Science 2011; 331: 337-41.
  41. Russell. Sl gold. mj woldarska. M early life antibiotic driven changes Microbiota enhance susceptibility to allergy asthma. EMBO rep. 2012; 13: 440-7.
  42. Basher. Me Anderson. C. toll-like receptor for signaling by intestinal microbes influence susceptibility to food allergy j. immunol. 2004; 172: 6978-87.
  43. Geuking. Mb cahenzli. J intestinal bacteria colonization induces mutualistic regulatory t cells responses. immunity 2011; 34: 794-806.
  44. Mazmanian. Sk round. jL amicrobial symbiosis factor prevents intestinal inflammatory disease. nature 2008; 453: 620-5.
  45. Mathias. Cb hobson ca Lawson g IgE-mediated systemic anaphylaxis impaired tolerance to food antigens in mice with enhanced IL 4 receptor signaling. j allergy clinical immunal. 2011; 127: 795-805.
  46. Noval rivas m. hobson sa. Garcia lloret m. a microbiota signature associated with experimental food allergy promotes allergic sensitization and anaphylaxis. j allergy clinical immunol. 2013; 131: 201-12.
  47. Boyce JA, Assa’ad A, Burks AW, Jones SM, Sampson HA, Wood RA, et al. Guidelines for the diagnosis and management of food allergy in the United States: report of the NIAID-sponsored expert panel. J Allergy Clin Immunol 2010; 126 (suppl): S1-58.
  48. Fiocchi A, Brozek J, Schnemann H, Bahna SL, von Berg A, Beyer K, et al. World Allergy Organization (WAO) Diagnosis and Rationale for Action against Cow’s Milk Allergy (DRACMA) Guidelines. Pediatr Allergy Immunol 2010; 21 (suppl 21): 1-125.
  49. Knight AK, Shreffler WG, Sampson HA, Sicherer SH, Noone S, Mofidi S, et al. Skin prick test to egg white provides additional diagnostic utility to serum egg white-specific IgE antibody concentration in children. J Allergy Clin Immunol 2006; 117: 842-7.
  50. Sicherer SH, Sampson HA. 9. Food allergy. J Allergy Clin Immunol 2006; 117 (suppl Mini-Primer): S470-5.
  51. Sampson HA. Utility of food-specific IgE concentrations in predicting symptomatic food allergy. J Allergy Clin Immunol 2001; 107: 891-6.
  52. Roberts G, Lack G. Diagnosing peanut allergy with skin prick and specific IgE testing. J Allergy Clin Immunol 2005; 115: 1291-6.
  53. Teuber SS, Beyer K. Peanut, tree nut and seed allergies. Curr Opin Allergy Clin Immunol 2004; 4: 201-3.
  54. Hompes S, Kohli A, Nemat K, Scherer K, Lange L, Rueff F, et al. Provoking allergens and treatment of anaphylaxis in children and adolescents—data from the anaphylaxis registry of German-speaking countries. Pediatr Allergy Immunol 2011; 22: 568-74.
  55. Nelson HS, Lahr J, Rule R, Bock A, Leung D. Treatment of anaphylactic sensitivity to peanuts by immunotherapy with injections of aqueous peanut extract. J Allergy Clin Immunol 1997; 99: 744-51.
  56. Jones SM, Pons L, Roberts JL, Scurlock AM, Perry TT, Kulis M, et al. Clinical efficacy and immune regulation with peanut oral immunotherapy. J Allergy Clin Immunol 2009; 124: 292-300.
  57. Hofmann AM, Scurlock AM, Jones SM, Palmer KP, Lokhnygina Y, Steele PH, et al. Safety of a peanut oral immunotherapy protocol in children with peanut allergy. J Allergy Clin Immunol 2009; 124: 286-91.
  58. Blumchen K, Ulbricht H, Staden U, Dobberstein K, Beschorner J, de Oliveira LC, et al. Oral peanut immunotherapy in children with peanut anaphylaxis. J Allergy Clin Immunol 2010; 126: 83-91.
  59. Clark AT, Islam S, King Y, Deighton J, Anagnostou K, Ewan PW. Successful oral tolerance induction in severe peanut allergy. Allergy 2009; 64: 1218-20.
  60. Sheikh A, Nurmatov U, Venderbosch I, Bischoff E. Oral immunotherapy for the treatment of peanut allergy: systematic review of six case series studies. Prim Care Respir J 2012; 21: 41-9.
  61. Varshney P, Jones SM, Scurlock AM, Perry TT, Kemper A, Steele P, et al. A randomized controlled study of peanut oral immunotherapy: clinical desensitization and modulation of the allergic response. J Allergy Clin Immunol 2011; 127: 654-60.
  62. Anagnostou K, Clark A, King Y, Islam S, Deighton J, Ewan P. Efficacy and safety of high-dose peanut oral immunotherapy with factors predicting outcome. Clin Exp Allergy 2011; 41: 1273-81.
  63. Beyer K, Wahn U. Oral immunotherapy for food allergy in children. Curr Opin Allergy Clin Immunol 2008; 8: 553-6.
  64. Calvani M, Giorgio V, Miceli SS. Specific oral tolerance induction for food. A systematic review. Eur Ann Allergy Clin Immunol 2010; 42: 11-9.
  65. Fisher HR, Du TG, Lack G. Specific oral tolerance induction in food allergic children: is oral desensitisation more effective than allergen avoidance. Meta-analysis of published RCTs. Arch Dis Child 2011; 96: 259-64.
  66. E. A. Miles, University of Southampton, UK. Adverse immune reactions to foods. Wood head Publishing Limited, 2013.
  67. Spergel JM, Beausoleil JL, Fiedler JM, Ginsberg J, Wagner K, Pawlowski NA. Correlation of initial food reactions to observed reactions on challenges. Ann Allergy Asthma Immunol 2004; 92: 217-24.
  68. Eigenmann PA, Sampson HA. Interpreting skin prick tests in the evaluation of food allergy in children. Pediatr Allergy Immunol 1998; 9: 186-91.
  69. Spergel JM, Beausoleil JL, Fiedler JM, Ginsberg J, Wagner K, Pawlowski NA. Correlation of initial food reactions to observed reactions on challenges. Ann Allergy Asthma Immunol 2004; 92: 217-24.
  70. Celik-Bilgili S, Mehl A, Verstege A et al. The predictive value of specific immunoglobulin E levels in serum for the outcome of oral food challenges. Clin Exp Allergy 2005; 35: 268-73.
  71. Sampson HA. Utility of food-specific IgE concentrations in predicting symptomatic food allergy. J Allergy Clin Immunol 2001; 107: 891-6.
  72. Perry TT, Matsui EC, Kay Conover-Walker M, Wood RA. The relationship of allergen-specific IgE levels and oral food challenge outcome. J Allergy Clin Immunol 2004; 114: 144-9.
  73. Fogg MI, Brown-Whitehorn TA, Pawlowski NA, Spergel JM. Atopy patch test for the diagnosis of food proteininduced enterocolitis syndrome. Pediatr Allergy Immunol 2006; 17: 351-5.
  74. Spergel JM, Beausoleil JL, Mascarenhas M, Liacouras CA. The use of skin pricks tests and patch tests to identify causative foods in eosinophilic esophagitis. J Allergy Clin Immunol 2002; 109: 363-8.
  75. Heine RG, Verstege A, Mehl A, Staden U, Rolinck Werninghaus C, Niggemann B. Proposal for a standardized interpretation of the atopy patch test in children with atopic dermatitis and suspected food allergy. Pediatr Allergy Immunol 2006; 17: 213-7.
  76. Spergel JM, Brown-Whitehorn T, Beausoleil JL, Shuker M, Liacouras CA. Predictive values for skin prick test and atopy patch test for eosinophilic esophagitis. J Allergy Clin Immunol 2007; 119: 509-11.
  77. Niggemann B. Atopy Patch Test (APT)―its role in diagnosis of food allergy in atopic dermatitis. Indian J Pediatr 2002; 69: 57-9.
  78. Vadas P, Gold M, Perelman B et al. Platelet-activating factor, PAF acetylhydrolase, and severe anaphylaxis. N Engl J Med 2008; 358: 28-35.
  79. Yamaki k. yoshino s. preventive and therapeutic effects of rapamycin, mammalian target of rapamycin inhibitor, on food allergy in mice. allergy 2012; 67: 1259-70.
  80. Osterfeld h. finkelman fd. Hogan sp. Differential roles for the IL-9/IL-9 receptor alpha- chain pathway in systemic and oral antigen – induced anaphylaxis. J allergy clinc immunol. 2010; 125: 469-76.
  81. Forbes ee. Brandt eb. Cohen e. al. IL-9-and mast cell mediated intestinal permeability predisposes to oral antigen hypersensitivity. J exp med 2008; 205: 897-913.
  82. Sugimura t. tananari y. ozaky y. ito s. yoshimoto y. effect of oral sodium cromoglycate in 2 children with food dependent exercise induced anaphylaxis (FDEIA). clin pediatr (phila) 2009; 48: 945-50.
  83. Yamaki k. yoshino s. tyrosine kinase inhibitor sunitinib relieves systemic and oral antigen induced anaphylaxis in mice. Allergy 2012; 67: 114-22.
  84. Motzer rj. Hoosen s. Christensen jg. Sunitinib malate for the treatment of solid tumours: Is view of current clinical data. Expert opin investing drug. 2006; 15: 553-61.

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