The allergen-specificity of early peanut consumption and the impact on the development of allergic disease in the LEAP Study Cohort (original) (raw)
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Early consumption of peanuts in infancy is associated with a low prevalence of peanut allergy
Background: Despite guidelines recommending avoidance of peanuts during infancy in the United Kingdom (UK), Australia, and, until recently, North America, peanut allergy (PA) continues to increase in these countries. Objective: We sought to determine the prevalence of PA among Israeli and UK Jewish children and evaluate the relationship of PA to infant and maternal peanut consumption. Methods: A clinically validated questionnaire determined the prevalence of PA among Jewish schoolchildren (5171 in the UK and 5615 in Israel). A second validated questionnaire assessed peanut consumption and weaning in Jewish infants (77 in the UK and 99 in Israel).
Acta Clinica Belgica, 2016
Peanut allergy shows distinct clinical patterns that can be predicted by component resolved diagnosis. However data about peanut sensitization profiles in populations with a broad agestratification are scarce. Methods Sera of 89 peanut allergic patients (age 1-70 years), 21 infants (< 1y) with atopic dermatitis (AD) sensitized to peanut, 24 age matched peanut tolerant individuals with positive sIgE to peanut and 15 healthy individuals were tested for sIgE reactivity to rAra h 1, rAra h 2, rAra h 3, rAra h 8, rAra h 9 and rBet v 1 (FEIA ImmunoCAP, Thermo Fisher Scientific). Results In infants with AD, Ara h 1, Ara h 2 and Ara h 3 enabled to explain 14/21 (67%) of peanut sensitizations. No sensitization to Ara h 8 or Bet v 1 was observed. Patients with generalized reactions were more frequently sensitized to Ara h 1, Ara h 2 and Ara h 3 compared to patients with an oral allergy syndrome (OAS) and peanut tolerant patients. Sensitization to Ara h 8 was significantly more observed in patients with an OAS. Ara h 2 showed to be the best marker to distinguish patients with generalized reactions from patients with an OAS and/or peanut sensitized patients but tolerating the legume. Conclusion Faber et al., 4 Sensitization to Ara h 1, Ara h 2 and Ara h 3 can have early onset and is predominantly associated with a more severe outcome. Ara h 2 is the best marker of a generalized peanut allergy.
The Journal of allergy and clinical immunology, 2015
The purpose of this brief communication is to highlight emerging evidence to existing guidelines regarding potential benefits of supporting early, rather than delayed, peanut introduction during the period of complementary food introduction in infants. This document should be considered as interim guidance based on consensus among the following organizations: American Academy of Allergy, Asthma & Immunology, American Academy of Pediatrics, American College of Allergy, Asthma & Immunology, Australasian Society of Clinical Immunology and Allergy, Canadian Society of Allergy and Clinical Immunology, European Academy of Allergy and Clinical Immunology, Israel Association of Allergy and Clinical Immunology, Japanese Society for Allergology, Society for Pediatric Dermatology, and World Allergy Organization. More formal guidelines regarding early-life, complementary feeding practices and the risk of allergy development will follow in the next year from the National Institute of Allergy and...
Environmental peanut exposure increases the risk of peanut sensitization in high risk children
Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2018
High household peanut consumption is associated with the development of peanut allergy, especially when peanut allergic cases are compared against atopic controls; thus environmental peanut exposure (EPE) may be a risk factor for peanut sensitization and allergy. In this study we explored the relationship between EPE and school-age peanut sensitization in a population based cohort. Maternal bed-dust was collected postnatally and EPE was quantified using a polyclonal peanut ELISA. Peanut sensitization was assessed by specific IgE to peanut extract and sIgE to peanut protein component allergens Ara h 1, 2 or 3 ≥0.35kU/L (primary peanut sensitization). Initial nested case control analysis was performed comparing peanut sensitized cases against high-risk controls (matched for parental atopy) (n=411) using a conditional regression analysis. This was followed by whole cohort analysis (n=1878) comparing EPE against peanut sIgE sensitization at ages 4 and 8 years using Generalized Estimatin...
Journal of Allergy and Clinical Immunology, 2015
Background: There are no prospectively collected data available on the natural history of peanut allergy in early childhood. Previous studies of predictors of tolerance development have been biased by failure to challenge high-risk children when IgE antibody levels are high, therefore potentially introducing bias to persistent allergy. Objectives: We sought to describe the natural history of peanut allergy between 1 and 4 years of age and develop thresholds for skin prick test (SPT) results and specific IgE (sIgE) levels measured at age 1 and 4 years that have 95% positive predictive value (PPV) or negative predictive value for the persistence or resolution of peanut allergy. Methods: One-year-old infants with challenge-confirmed peanut allergy (n 5 156) from the population-based, longitudinal HealthNuts Study (n 5 5276) were followed up at 4 years of age with repeat oral food challenges, SPTs, and sIgE measurements (n 5 103). Challenges were undertaken in all peanut-sensitized children at 1 and 4 years of age, irrespective of risk profile. Results: Peanut allergy resolved in 22% (95% CI, 14% to 31%) of children by age 4 years. Decreasing wheal size predicted tolerance, and increasing wheal size was associated with persistence. Thresholds for SPT responses and sIgE levels at age 1 year with a 95% PPV for persistent peanut allergy are an SPT-induced response of 13 mm or greater and an sIgE level of 5.0 kU/L or greater. Thresholds for SPT and sIgE results at age 4 years with a 95% PPV for persistent peanut allergy are an SPT response of 8 mm or greater and an sIgE level of 2.1 kU/L or greater. Ara h 2, tree nut, and house dust mite sensitization; coexisting food allergies; eczema; and asthma were not predictive of persistent peanut allergy. Conclusion: These thresholds are the first to be generated from a unique data set in which all participants underwent oral food challenges at both diagnosis and follow-up, irrespective of SPT and sIgE results. (J Allergy Clin Immunol 2015;nnn:nnn-nnn.)
Rising prevalence of allergy to peanut in children: Data from 2 sequential cohorts
Journal of Allergy and Clinical Immunology, 2002
Background: Allergy to peanut is common. However, it is not known whether the prevalence of sensitization and clinical allergy to peanut is increasing. Objective: We sought to determine any change in the prevalence of peanut sensitization and reactivity in early childhood in 2 sequential cohorts in the same geographic area 6 years apart. Methods: Of 2878 children born between September 1, 1994, and August 31, 1996, living on the Isle of Wight, 1273 completed questionnaires, and 1246 had skin prick tests at the age of 3 to 4 years. Those with positive skin prick test responses to peanut were subjected to oral peanut challenges, unless there was a history of immediate systemic reaction. These data were compared with information on sensitization and clinical allergy to peanut available from a previous cohort born in 1989 in the same geographic area. Results: There was a 2-fold increase in reported peanut allergy (0.5% [6/1218] to 1.0% [13/1273]), but the difference was nonsignificant (P = .2). Peanut sensitization increased 3-fold, with 41 (3.3%) of 1246 children sensitized in 1994 to 1996 compared with 11 (1.1%) of 981 sensitized 6 years ago (P = .001). Of 41 sensitized children in the current study, 10 reported a convincing clinical reaction to peanut, and 8 had positive oral challenge results, giving an overall estimate of peanut allergy of 1.5% (18/1246). Conclusions: Sensitization to peanut had increased between 1989 and 1994 to 1996. There was a strong but statistically nonsignificant trend for increase in reported peanut allergy. (J Allergy Clin Immunol 2002;110:784-9.)
Peanut sensitization in a group of allergic Egyptian children
Allergy, Asthma & Clinical Immunology, 2011
Background: There are no published data on peanut sensitization in Egypt and the problem of peanut allergy seems underestimated. We sought to screen for peanut sensitization in a group of atopic Egyptian children in relation to their phenotypic manifestations.
Household peanut consumption as a risk factor for the development of peanut allergy
Journal of Allergy and Clinical Immunology, 2009
Background: Most children with peanut allergy (PA) react on first known oral exposure to peanut. Recent data suggest cutaneous exposure as a route of sensitization. Objectives: This study aimed to establish the relevant route of peanut exposure in the development of allergy. Methods: Questionnaires were administered to children with PA and to high-risk controls (with egg allergy) and controls without allergy. Questionnaires were completed before subjects were aware of their PA status, avoiding recall bias. Questionnaires recorded maternal peanut consumption during pregnancy, breast-feeding, and the first year of life. Peanut consumption was determined among all household members, allowing quantification of environmental household exposure (household peanut). Results: Median weekly household peanut in the 133 PA cases was significantly elevated (18.8 g) compared with 150 controls without allergy (6.9 g) and 160 high-risk controls (1.9 g). There were no differences in infant peanut consumption between groups. Differences in maternal peanut consumption during pregnancy (and lactation) were significant but become nonsignificant after adjusting for household peanut. A doseresponse relationship was observed between environmental (nonoral) peanut exposure and the development of PA, which was strongest for peanut butter. Early oral exposure to peanut in infants with high environmental peanut exposure may have had a protective effect against the development of PA. Conclusions: High levels of environmental exposure to peanut during infancy appear to promote sensitization, whereas low levels may be protective in atopic children. No effect of maternal peanut consumption during pregnancy or lactation is observed, supporting the hypothesis that peanut sensitization occurs as a result of environmental exposure.
Pediatric Allergy and Immunology, 2016
Background: The aim of this study was to explore the natural history of peanut allergy in childhood in two birth cohorts from the same geographical region in the South of England. Methods: The FAIR birth cohort was established on the Isle of Wight (UK) between 2001-2002 (n = 969). Children were followed up prospectively, skin prick tested (SPT) to peanut allergens at 1, 2, 3 and 10 years and food challenges performed. The Isle of Wight (IOW) Birth cohort was established in 1989 (n = 1456). SPTs were performed at 1, 2, 4 and 10 years. Peanut allergy was based on positive SPT and a good clinical history. Results: In the FAIR cohort, the prevalence of sensitization to peanut was 0.4%, 2.0%, 2.0% and 2.4% at 1,2,3 and 10 years respectively. At 10 years of age, 12/828 (1.5%) children were diagnosed with peanut allergy. One child (8%) outgrew her peanut allergy between 3 and 10 years and two children (15%) presented with new onset peanut allergy. Over the first ten years of life, 13/934 (1.4%) children were diagnosed with peanut allergy. In the IOW cohort, 6/1034 (0.58%) were diagnosed with peanut allergy at 10 years. We found no significant differences between the FAIR and the IOW birth cohort for any of the time points studied. 3 Conclusion: Peanut allergy appears to be stable over the first ten years of life in our cohorts. There was no significant difference in peanut sensitization or clinical peanut allergy between 1989 and 2001.