Patterns of tree nut sensitisation and allergy in the first 6 years of life in a population-based cohort.
INTRODUCTION: Longitudinal population-based data regarding tree nut allergy are limited. OBJECTIVES: To determine population prevalence of tree nut allergy at age 6 years, and explore the relationship between egg and peanut allergy at age 1 year and development of tree nut allergy at age 6 years. METHODS: A population-based sample of 5,276 children were recruited at age one and followed up at age 6 years. At age 1 allergy to egg and peanut were determined by oral food challenge and parents reported their child's history of reaction to tree nuts. Challenge-confirmed tree nut allergy was assessed at age 6. RESULTS: At age 1, prevalence of parent-reported tree nut allergy was 0.1% (95% CI 0.04-0.2). Only 18.5% of infants had consumed tree nuts in the first year of life. At age 6, challenge-confirmed tree nut allergy prevalence was 3.3% (95%CI 2.8-4.0), with cashew the most common (2.7%, 95% CI 2.2-3.3). Of children with peanut allergy only at age 1, 27% (95%CI 16.1-39.7) were tree nut allergic at age 6, compared with 14% (95%CI 10.4-17.9) of those with egg allergy only and 37% (95%CI 27.2-47.4) of those with both peanut and egg allergy. CONCLUSIONS: Tree nut allergy is uncommon in the first year of life, likely due to limited tree nut consumption. At age 6 years, tree nut allergy prevalence is similar to peanut allergy prevalence. Over a third of children with both peanut and egg allergy in infancy have tree nut allergy at age 6. Understanding how to prevent tree nut allergy should be an urgent priority for future research.
Quantitative Risk Reduction Through Peanut Immunotherapy: Safety Benefits of an Increased Threshold in Europe.
BACKGROUND: The clinical relevance of increasing an allergic individual's peanut sensitivity threshold by immunotherapy, i.e., eliciting dose (ED) to 300 or 1000 mg peanut protein, has not been previously characterized in a European population. In this study, we quantify the clinical benefits of an increased threshold of reaction following immunotherapy for the peanut-allergic individual. METHODS: Quantitative risk assessments incorporated numerous inputs to predict the risk of an allergic reaction after exposure to residual peanut protein in packaged foods. The three primary inputs for the risk assessment were the peanut-allergic individual's clinical threshold value, the amount of food consumed per eating occasion of selected packaged foods and the concentration of peanut protein in the consumed product. Individual risk reductions were calculated for both children and adolescents-adults. RESULTS: Using available consumption and packaged food contamination data, children reaching an ED of 300 mg (if initial ED ≤ 100 mg) or 1,000 mg (if initial ED 300 mg) achieved >99.99% risk reduction. Adolescents-adults also achieved >99.99% risk reduction in all cases but one. Adolescents-adults who reached an ED of 300 mg (if initial ED ≤ 100 mg) achieved 99.3-99.9% risk reduction when consuming ice cream. CONCLUSIONS: It is concluded that an increase in threshold following immunotherapy which achieves an eliciting dose of 300 or 1000 mg peanut protein is clinically relevant for the European peanut-allergic population. Benefits of an increased threshold include a significant reduction in risk due to traces of peanut protein.
Development and Evaluation of a Real-Time PCR Multiplex Assay for the Detection of Allergenic Peanut Using Chloroplast DNA Markers.
Peanut is one of the most commonly consumed allergy-causing foods in the United States. Prevention of accidental consumption by allergic individuals is assisted by methods that effectively identify the presence of peanut in food, even at trace levels. This study presents a multiplex real-time polymerase chain reaction (PCR) assay that uses chloroplast markers (matK, rpl16, and trnH-psbA) to specifically detect peanut in three types of foods: baked goods, chocolate, and tomato sauces. Food matrices were spiked with raw peanut at concentrations ranging from 0.1 to 105 ppm. The assay was evaluated with respect to linear range and reaction efficiency. High reaction efficiencies were generally obtained across 6-7 orders of magnitude. Limits of detection were between 0.1 and 1 ppm, and reaction efficiencies were mostly within the preferred range of 100 ± 10%. Our results indicate that real-time PCR assays using chloroplast markers can be a valuable tool for peanut detection.
Dietary Supplementation with Non‐Digestible Oligosaccharides Reduces Allergic Symptoms and Supports Low Dose Oral Immunotherapy in a Peanut Allergy Mouse Model.
SCOPE: A major downside of oral immunotherapy (OIT) for food allergy is the risk of severe side-effects. Non-digestible short- and long-chain fructo-oligosaccharides (scFOS/lcFOS), reduced allergy development in murine models. We therefor hypothesized that scFOS/lcFOS can also support the efficacy of OIT in a peanut allergy model. METHODS AND RESULTS: After sensitization to peanut extract (PE) using cholera toxin, C3H/HeOuJ mice were fed a 1% scFOS/lcFOS or control diet and received OIT (1.5 or 15 mg PE). Hereafter, mice were exposed to PE via different routes to determine the safety and efficacy of treatment in clinical outcomes, PE-specific antibody production and numbers of various immune cells. scFOS/lcFOS increased short-chain fatty acid levels in the caecum and reduced the acute allergic skin response and drop in body temperature after PE exposure. Interestingly, 15 mg and 1.5 mg OIT with scFOS/lcFOS induced protection against anaphylaxis, whereas 1.5 mg OIT alone did not. OIT, with or without scFOS/lcFOS, induced PE-specific IgG and IgA levels and increased CD103+ dendritic cells in the mesenteric lymph nodes. CONCLUSIONS: scFOS/lcFOS and scFOS/lcFOS combined with a low dose OIT are able to protect against a peanut-allergic anaphylactic response.
Allergy and Asthma: Food Allergies.
Food allergies are immune-mediated allergic adverse reactions that occur after exposure to specific foods. The most commonly recognized food allergies are immunoglobulin E (IgE)-mediated reactions (eg, urticaria, angioedema, anaphylaxis) that result from exposure to milk, egg, peanut, tree nuts, shellfish, fish, wheat, or soy. However, other foods can cause food allergies. Oral allergy syndrome is a common but underrecognized condition characterized by transient oropharyngeal symptoms that result from ingestion of uncooked fruits or vegetables. Non-IgE-mediated food allergies manifest with more delayed symptoms than IgE-mediated food allergies, and predominately cause gastrointestinal symptoms. Food allergies often are overreported because they may be confused with food intolerances or nonimmunologic adverse food reactions (eg, lactose intolerance, food poisoning, caffeine intolerance). Food allergies are diagnosed using IgE skin tests, IgE serum tests, or oral food challenge tests. These allergies are best managed by avoidance of the food or foods related to the allergy because they require ingestion rather than contact to precipitate symptoms. Injectable epinephrine should be prescribed for patients at risk of anaphylaxis. Careful food label reading and food preparation, awareness, and education are keys to prevention.
Jug r 6 is the allergenic vicilin present in walnut responsible for IgE cross-reactivities to other tree nuts and seeds.
Walnuts are ranked high in the list of the culprit foods inducing severe allergic reactions. Jug r 2 has been identified as a major allergen in common walnut by cDNA cloning from a somatic cell line. So far, studies were performed on the allergenic activity of recombinant Jug r 2, yet there is still no evidence about the physicochemical characteristics of the natural allergen. Therefore, we aimed to purify and deeply characterize natural Jug r 2 and to assess IgE cross-reactivity among vicilins from different tree nuts. Extensive mass spectrometry analysis of the obtained purified vicilin allowed identification of the protein sequence that displayed only 44% identity to Jug r 2. The newly identified vicilin (Jug r 6) was recognized by IgE of 26% in walnut allergic patients' sera tested. In contrast to Jug r 2, Jug r 6 displayed a remarkable level of cross-reactivity when tested with homologues from hazelnut, sesame and pistachio. It is the first report showing the necessity of proteomic studies to improve allergy component resolved diagnosis.
Simultaneous detection of eight species of tree nut in foods using two tetraplex polymerase chain reaction assays.
Tree nuts comprise a category of food allergens that must be included in the food labels in several countries. We developed a polymerase chain reaction (PCR) method using eight specific primer pairs to detect eight representative tree nuts (almond, Brazil nut, cashew, hazelnut, macadamia nut, pecan, pistachio, and walnut) under the same experimental conditions. The specificity of the eight primer pairs was confirmed by PCR testing against a variety of plant and animal samples. The detection limit of the method ranged from 1 fg to 1 pg DNA of individual tree nuts. The method detected tree nut DNA in processed and unprocessed food. In addition, the primer pairs could be combined into two sets of tetraplex PCR system. The developed method is specific, sensitive, and efficient, making it useful for detecting trace amounts of eight species of tree nut in foods.
Retrospective definition of reaction risk in Italian children with peanut, hazelnut and walnut allergy through component-resolved diagnosis.
BACKGROUND: Serum IgE evaluation of peanut, hazelnut and walnut allergens through the use of component-resolved diagnosis (CRD) can be more accurate than IgE against whole food to associate with severe or mild reactions. OBJECTIVES: The aim of the study was to retrospectively define the level of reaction risk in children with peanut, hazelnut and walnut sensitization through the use of CRD. METHODS: 34 patients [n=22 males, 65%; median age eight years, interquartile range (IQR) 5.0-11.0 years] with a reported history of reactions to peanut and/or hazelnut and/or walnut had their serum analyzed for specific IgE (s-IgE) by ImmunoCAP® and ISAC® microarray technique. RESULTS: In children with previous reactions to peanut, the positivity of Arah1 and Arah2 s-IgE was associated with a history of anaphylaxis to such food, while the positivity of Arah8 s-IgE were associated with mild reactions. Regarding hazelnut, the presence of positive Cora9 and, particularly, Cora14 s-IgE was associated with a history of anaphylaxis, while positive Cora1.0401 s-IgE were associated with mild reactions. Concerning walnut, the presence of positive Jug r 1, Jug r 2, Jug r 3 s-IgE was associated with a history of anaphylaxis to such food. ImmmunoCAP® proved to be more useful in retrospectively defining the risk of hazelnut anaphylaxis, because of the possibility of measuring Cor a14 s-IgE. CONCLUSIONS: Our data show that the use of CRD in patients with allergy to peanut, hazelnut and walnut could allow for greater accuracy in retrospectively defining the risk of anaphylactic reaction to such foods.
Asian children living in Australia have a different profile of allergy and anaphylaxis than Australian‐born children: a State‐wide survey.
BACKGROUND: Asian children born in Australia have higher rates of eczema and nut allergy than non-Asian children. However, it is not known whether this country of birth differential exists for other allergies or anaphylaxis risk. OBJECTIVE: We investigated the influence of maternal and child's country of birth on the prevalence of parent-reported eczema, asthma, food allergy, and being diagnosed by a doctor as being "at risk of anaphylaxis". METHODS: We assessed the relationship between mother and child country of birth and allergies using the 2010 School Entrant Health Questionnaire, completed for 57,005 5-year old children (85.8% response rate) in Victoria, Australia. Analyses were conducted using logistic regression with results presented as odds ratios (OR) with 95% confidence intervals (CIs). RESULTS: Children born in Australia to Asian-born mothers were more likely to have parent-reported food allergy (OR 2.33, 95%CI 1.96-2.77) and eczema (OR 2.04, 95%CI 1.73-2.41), but not more likely to have asthma (OR 0.87, 95% CI 0.74-1.02) than non-Asian children. By contrast, children born in Asia who subsequently migrated to Australia had a lower risk of food allergy (OR 0.33, 95%CI 0.20-0.55), eczema (OR 0.37, 95%CI 0.24-0.57) and asthma (OR 0.29, 95% CI 0.21-0.40). Patterns of anaphylaxis risk differed depending on the trigger. Compared with Australian-born non-Asian children, Australian-born Asian children were more likely to be diagnosed as being at risk of both food-induced and non-food induced anaphylaxis. For children born in Asia, risk was lower for anaphylaxis to milk, peanut and tree nuts compared to non-Asian children, but higher for soy, wheat and non-food triggers. CONCLUSIONS & CLINICAL RELEVANCE: Patterns of allergy/anaphylaxis risk and their triggers differed according to both ethnicity and country of birth, suggesting a gene-environment factor is in play. The difference in patterns for asthma compared with other atopic diseases is surprising and warrants further exploration.
Peanut Allergy: Changes in Dogma and Past, Present, and Future Directions.
The prevalence of food allergy in the pediatric population, specifically to peanuts, has been rising. Accidental exposure to peanuts in a person who is allergic may have life-threatening consequences. Previous recommendations regarding peanut allergy included a delay in introduction of peanut to infants. However, more recent studies have provided sufficient contrary evidence supporting early introduction of peanuts for prevention of peanut allergy. Therefore, prompt evaluation by a specialist should be considered in infants at high risk of developing peanut allergy. Current treatment is strict avoidance of the allergen; however, future therapies are being sought, including oral immunotherapy, sublingual immunotherapy, and epicutaneous immunotherapy.