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Prevalence of sensitization to food allergens, reported adverse reaction to foods, food avoidance, and food hypersensitivity among teenagers.

Pereira, B., C. Venter, J. Grundy, C.B. Clayton, S.H. Arshad, T. Dean, 2005. Prevalence of sensitization to food allergens, reported adverse reaction to foods, food avoidance, and food hypersensitivity among teenagers. J Allergy Clin Immunol. 116:884-892.

Background: There is a paucity of information on food hypersensitivity (FHS) among teenagers. Objectives: We sought to investigate the sensitization rates, perception of FHS, food avoidance, and FHS assessed by means of food challenges among teenagers. Methods: This cohort study recruited 757 eleven-year-olds and 775 fifteen-year-olds in the United Kingdom. Sensitization rates, reported rates of FHS, and rates of food avoidance were measured. The prevalence of FHS was established by using food challenges. Results: The prevalence of reported FHS among the 11- and 15-year-old cohorts was 11.6% (90/775) and 12.4% (94/757), respectively. One hundred twenty-two (15.7%) and 142 (18.7%) of the 11- and 15-year-olds reported they were avoiding some food. The rates of sensitization to the food allergens were 5.1% (36/699) and 4.9% (32/649) for the 11- and 15-year-olds, respectively. FHS was confirmed in 8 (1.0%) 11-year-old children and 8 (1.0%) 15-year-old children by means of open food challenge and in 1 (0.1%) 11-year-old and 4 (0.5%) 15-year-olds by means of double-blind, placebo-controlled food challenge. The prevalence of FHS, as confirmed by using open food challenges and positive skin prick test responses  plus a history of adverse reactions, was 18 (2.3%) of 775 in the 11-year-old cohort and 17 (2.3%) of 757 in the 15-year-old cohort. Conclusions: The rate of reported FHS was significantly more than sensitization to the predetermined allergens (odds ratio, 2.17; 95% CI, 1.47-3.18; P <.001 in the 11-year-olds; odds ratio, 2.73; 95% CI, 1.81-4.13; P < .001 in the 15-year-olds). By means of objective assessment, 2.3% of both 11- and 15-year-old children had FHS, with the majority showing immediate reactions.

 

A framework for measuring costs to society of IgE-mediated food allergy.

Miles, S., R. Fordham, C. Mills, E. Valovirta, M. Mugford, 2005. A framework for measuring costs to society of IgE-mediated food allergy. Allergy. 60:996–1003.

Both immunoglobulin E (IgE)-mediated food allergy and food intolerance can lead to many changes in personal behaviour and health care resource use which have important economic consequences. These costs will impact directly, indirectly and intangibly on both individuals and society in general. It is important to measure the cost of illness (COI) of food allergy as a first step in developing and evaluating measures to reduce and control the burden of illness. This paper outlines a framework for assessing COI of food allergy from different viewpoints. It offers a structure for identifying the different cost impacts on allergic and nonallergic consumers, food producers and society as a whole, and for scoping, measurement and valuation of relevant costs. Within this structure, the existing literature is reviewed. This review illustrates the lack of information and clear methodology for assessing costs of food allergy. The paper concludes that there is a need for a more structured research programme to generate data essential for future evaluations of procedures and technologies for the diagnosis, treatment and management of food allergy.

A 50 kDa Maize γ-Zein has marked cross-reactivity with the almond major protein.

Lee, S.-H., M. Benmoussa, S.K. Sathe, K.H. Roux, S.S. Teuber, B.R. Hamaker, 2005. A 50 kDa Maize γ-Zein has marked cross-reactivity with the almond major protein. J Agric Food Chem. 53:7965-7970.

Cross-reactivity of antibodies against almond major protein (AMP, a legumin), the major almond allergen, with cereal proteins may cause problems in detecting almond contaminants in cereal products when antibody-based assays are used. Rabbit polyclonal IgG antiserum produced against AMP was used to test cross-reactivity with protein extracts from maize, a cereal commonly found in breakfast and snack foods. Gradient SDS-PAGE followed by Western blotting was performed, and two cross-reactive proteins were detected by chemiluminescence. A fraction of maize proteins purified by elution from an IgG anti-AMP affinity column followed by electrophoreseis and immunoblotting showed a high degree of cross-reactivity with a minor 50 kDa protein of maize, as well as low cross-reactivity with the 27 kDa γ-zein. The 50 kDa cross-reactive protein was identified as the 50 kDa γ-zein by immunoreaction with anti-50 kDa γ-zein antiserum. Notably, the 50 kDa maize γ-zein also reacted with IgE from pooled human sera from patients with self-reported severe almond allergies. The high immunoreactivity of the 50 kDa γ-zein should be considered in maize quality improvement programs, and such notable cross-reactivity is of relevance in the design of antibody-based assays for almond allergen detection.

The natural history of tree nut allergy.

Fleischer, D.M., M.K. Conover-Walker, E.C. Matsui, R.A. Wood, 2005. The natural history of tree nut allergy. J Allergy Clin Immunol. 116:1087-1093.

Background: Although 20% of children outgrow peanut allergy, the natural history of tree nut (TN) allergy has not been well studied. Objective: The goals of the study were to estimate the proportion of children who outgrow TN allergy and examine predictors of outgrowing it. Methods: Patients with TN allergy, defined as a history of reaction on ingestion and evidence of TN-specific IgE (TN-IgE) or positive TN-specific IgE level but no history of ingestion, were evaluated. If all current TN-IgE levels were less than 10 kilounits of antibody (kUA)/L, double-blind, placebo-controlled food challenges were offered. Patients who had undergone open TN challenges as part of routine clinical care were also included. Results: Two hundred seventy-eight patients with TN allergy were identified. One hundred one (36%) had a history of acute reactions, 12 (12%) of whom had reactions to multiple TNs and 73 (63%) of whom had a history of moderate-to-severe reactions. Nine of 20 patients who had previously reacted to a TN passed challenges, so that 9 (8.9%; 95% CI, 4% to 16%) of 101 patients with a history of prior TN reactions outgrew TN allergy. Fourteen of 19 who had never ingested TNs but had detectable TN-specific IgE levels passed challenges. One hundred sixty-one did not meet the challenge criteria, and 78 met the criteria but declined challenges. Looking at specific TN-IgE cutoffs, 58% with TN-IgE levels of 5 kUA/L or less and 63% with TN-IgE levels of 2 kUA/L or less passed challenges. Conclusions: Approximately 9% of patients outgrow TN allergy, including some who had prior severe reactions. Although ideal cutoffs for challenge cannot be firmly recommended on the basis of these data, patients aged 4 years or older with all TN-IgE levels of 5 kUA/L or less should be considered for challenge.

Hazelnut allergy: evidence that hazelnut can directly elicit specific IgE antibody response via activating type 2 cytokines in mice.

Birmingham, N., V. Gangur, S. Samineni, L. Navuluri, C. Kelly, 2005. Hazelnut allergy: evidence that hazelnut can directly elicit specific IgE antibody response via activating type 2 cytokines in mice. Int Arch Allergy Immunol. 137:295–302.

Background: Hazelnut is one of the major tree nuts that causes potentially fatal food allergy, with underlying mechanisms that are unclear at present. One suggestion is that hazelnut allergy results from immune crossreactivity of IgE antibodies produced against certain aeroallergens. We tested the  hypothesis that hazelnut is intrinsically capable of eliciting an allergic response using a mouse model. Methods: Groups of mice were injected intraperitoneally with hazelnut/filbert protein extract with or without alum as an adjuvant, and hazelnut-specific antibody (IgE, IgG1) responses were examined using optimized enzyme-linked immunosorbent assay. Hazelnut-specific type 2 and type 1 cytokine responses were evaluated by ex vivo antigen-mediated activation of spleen cells. Results: Hazelnut elicited robust IgE and IgG1 antibody responses. Timecourse and dose-response analyses further provided evidence for memory type 2-dependent antibody responses to hazelnuts. Hazelnut-specific IgE response in two strains of mice with different MHC haplotypes and IgE response to hazelnut without the use of alum adjuvant asserted that hazelnut is intrinsically an allergenic food. The type 2 cytokine analyses revealed that hazelnut sensitization results from activation of IL-4 and IL-5, thus providing a mechanistic basis for hazelnut-specific IgE response. Conclusion: Our data argue that hazelnut – a widely consumed food – is intrinsically an allergenic food capable of directly eliciting hazelnut-binding specific IgE antibodies via activation of type 2 cytokines in mice.

Plant food allergies: a suggested approach to allergen-resolved diagnosis in the clinical practice by identifying easily available sensitization markers.

Riccardo Asero, 2005. Plant food allergies: a suggested approach to allergen-resolved diagnosis in the clinical practice by identifying easily available sensitization markers. Int Arch Allergy Immunol. 138:1–11.

Background: Molecular biology techniques have led to the identification of a number of allergens in vegetable foods, but due to the lack of purified food proteins for routine diagnostic use, the detection of sensitizing allergens remains a nearly impossible task in most clinical settings. The allergen-resolved diagnosis of food allergy is essential because each plant-derived food may contain a number of different allergens showing different physical/chemical characteristics that strongly influence the clinical expression of allergy; moreover, many allergens may cross-react with homologue proteins present in botanically unrelated vegetable foods. Objective: Through a review of the available literature, this study aimed to detect ‘markers’ of sensitization to specific plant food allergens that are easily accessible in the clinical practice. Results: There are several ‘markers’ of sensitization to different allergenic proteins in vegetable foods that can be helpful in the clinical practice. Specific algorithms for patients allergic to Rosaceae and to tree nuts were built. Conclusion: Clinical allergologists lacking the assistance of an advanced molecular biology lab may take advantage of some specific clinical data as well as of some ‘markers’ in the difficult task of correctly diagnosing patients with plant food allergy and to provide them the best preventive advice.

Food allergy—accurately identifying clinical reactivity

Sampson H.A., 2005. Food allergy—accurately identifying clinical reactivity. Allergy. 60 (Suppl.79):19-24.

Up to 25% of adults believe that they or their children are afflicted with a food allergy. However, the actual prevalence of food allergy is much lower: approximately 6-8% of children suffer from food allergy during their first 3 years of life, and many children then develop clinical tolerance. Food allergy encompasses a whole spectrum of disorders, with symptoms that may be cutaneous, gastrointestinal or respiratory in nature. Food disorders also differ according to the extent that they are immunoglobulin E (IgE)-mediated. Skin-prick testing is often used to identify food sensitization, although double-blind, placebo-controlled food challenge (DBPCFC) tests remain the gold standard for diagnosis. Recent evidence suggests that quantitative IgE measurements can predict the outcome of DBPCFC tests and can replace about half of all oral food challenges. When an extensive medical history is obtained in combination with IgE quantification, even fewer patients may require formal food challenges. It has also become possible to map the IgE-binding regions of many major food allergens. This may help to identify children with persistent food allergy, as opposed to those who may develop clinical tolerance. In future, microarray technology may enable physicians to screen patients for a large number of food proteins and epitopes, using just a few drops of blood.

Impact of γ -irradiation and thermal processing on the antigenicity of almond, cashew nut and walnut proteins.

Su, M., M. Venkatachalam, S.S. Teuber, K.H. Roux, S.K. Sathe, 2004. Impact of γ -irradiation and thermal processing on the antigenicity of almond, cashew nut and walnut proteins. J Sci Food Agric. 84:1119–1125.

Whole unprocessed almonds, cashew nuts and walnuts were each subjected to γ -irradiation (1, 5, 10 and 25 kGy) followed by heat processing including autoclaving (121°C, 15 psi for 15 and 30min), dry roasting (138 and 160°C for 30min each, 168 and 177°C for 12 min each), blanching (100°C for 5 and 10 min), oil roasting (191°C, 1min) and microwave heating (500W for 1 and 3 min). Rabbit polyclonal antibodies were raised against each major protein isolated from defatted, but not subjected to γ -irradiation and/or any thermal processing, almond, cashew nut and walnut flours. Immunoreactivity of almond, cashew nut and walnut proteins soluble in borate saline buffer, normalised to 1mg protein ml−1 for all samples, was determined by inhibition enzyme-linked immunosorbent assay (ELISA) and Western blotting. ELISAs and Western blotting experiments indicated that almond, cashew nut and walnut proteins exposed to γ -irradiation alone or followed by various thermal treatments remained antigenically stable.

A novel approach for the detection of potentially hazardous pepsin stable hazelnut proteins as contaminants in chocolate-based food.

 Akkerdaas, J.H., M. Wensing, A.C. Knulst, O. Stephan, S.L. Hefle, R.C. Aalberse, R. van Ree, 2004. A novel approach for the detection of potentially hazardous pepsin stable hazelnut proteins as contaminants in chocolate-based food. J. Agric. Food Chem.  52:7726−7731.

Contamination of food products with pepsin resistant allergens is generally believed to be a serious threat to patients with severe food allergy. A sandwich type enzyme-linked immunosorbent assay (ELISA) was developed to measure pepsin resistant hazelnut protein in food products. Capturing and detecting rabbit antibodies were raised against pepsin-digested hazelnut and untreated hazelnut protein, respectively. The assay showed a detection limit of 0.7 ng/mL hazelnut protein or <1 microg hazelnut in 1 g food matrix and a maximum of 0.034% cross-reactivity (peanut). Chocolate samples spiked with 0.5-100 microg hazelnut/g chocolate showed a mean recovery of 97.3%. In 9/12 food products labeled “may contain nuts”, hazelnut was detected between 1.2 and 417 microg hazelnut/g food. It can be concluded that the application of antibodies directed to pepsin-digested food extracts in ELISA can facilitate specific detection of stable proteins that have the highest potential of inducing severe food anaphylaxis.

Anaphylaxis: can we tell who is at risk of a fatal reaction?

Pumphrey, R., 2004. Anaphylaxis: can we tell who is at risk of a fatal reaction? Curr Opin Allergy Clin Immunol.  4:285–290.

Purpose of review: Anaphylaxis is frightening and patients commonly fear their next reaction will be fatal. This review looks at the characteristics of fatal reactions to find if a fatal recurrence is predictable. Recent findings: Most publications on fatal anaphylaxis are case reports that do not help predict risks. Most epidemiological studies focus on non-fatal reactions. The UK fatal anaphylaxis register demonstrates that over two-thirds of those dying from sting reactions and over four-fifths dying from drug anaphylaxis had no previous indication of their allergy, whereas those dying from food allergy had usually had previous reactions but these were typically not severe. Recent reports of anaphylaxis epidemiology based on diagnostic coding or attendance for treatment may be biased by differences in health service resource utilization according to the cause and course of the reaction. Summary: Most fatal anaphylactic reactions are unpredictable. The appropriate management after recovery from a severe reaction may be protective against a fatal recurrence. An accurate identification of the cause and effective avoidance is a crucial part of this management, together with effective treatment of asthma for those with food allergy, immunotherapy for sting allergy, the avoidance of drugs that potentiate anaphylaxis, and effective training in self-treatment.