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. 2024 Oct;79(10):2775-2786.
doi: 10.1111/all.16193. Epub 2024 Jun 18.

Biomarkers of peanut allergy in children over time

Affiliations

Biomarkers of peanut allergy in children over time

Ru-Xin Foong et al. Allergy. 2024 Oct.

Abstract

Background: Various biomarkers are used to define peanut allergy (PA). We aimed to observe changes in PA resolution and persistence over time comparing biomarkers in PA and peanut sensitised but tolerant (PS) children in a population-based cohort.

Methods: Participants were recruited from the EAT and EAT-On studies, conducted across England and Wales, and were exclusively breastfeed babies recruited at 3 months old and followed up until 7-12 years old. Clinical characteristics, skin prick test (SPT), sIgE to peanut and peanut components and mast cell activation tests (MAT) were assessed at 12 months, 36 months and 7-12 years. PA status was determined at the 7-12 year time point.

Results: The prevalence of PA was 2.1% at 7-12 years. Between 3 and 7-12 year, two children developed PA and one outgrew PA. PA children had larger SPT, higher peanut-sIgE, Ara h 2-sIgE and MAT (all p < .001) compared to PS children from 12 months onwards. SPT, peanut-sIgE, Ara h 2-sIgE and MAT between children with persistent PA, new PA, outgrown PA and PS were statistically significant from 12 months onwards (p < .001). Those with persistent PA had SPT, peanut-sIgE and Ara h 2-sIgE that increased over time and MAT which was highest at 36 months. New PA children had increased SPT and peanut-sIgE from 36 months to 7-12 years, but MAT remained low. PS children had low biomarkers across time.

Conclusions: In this cohort, few children outgrow or develop new PA between 36 months and 7-12 years. Children with persistent PA have raised SPT, peanut-sIgE, Ara h 2-sIgE and MAT evident from infancy that consistently increase over time.

Keywords: biomarkers; food allergy; mast cell activation test; peanut allergy; tolerance.

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Conflict of interest statement

GdT reports grants from National Institute of Allergy and Infectious Diseases (NIAID, NIH), Food Allergy & Research Education (FARE), MRC & Asthma UK Centre, UK Department of Health through NIHR, Action Medical Research and National Peanut Board. Scientific Advisory Board member Aimmune. Investigator on pharma‐sponsored allergy studies (Aimmune, and DBV Technologies). Scientific advisor to Aimmune, DBV and Novartis. RvR consults for HAL Allergy BV, Citeq BV, Angany Inc, Reacta Healthcare, Mission MightyMe and has equity in Angany Inc. SR reports grants from National Institute of Allergy and Infectious Diseases (NIAID, NIH) to cover parts of a research salary. HAB reports grants from National Institute of Allergy and Infectious Diseases (NIAID, NIH), and speaker fees from DBV Technologies, outside of the submitted work. CF is Chief Investigator of the UK National Institute for Health Research‐funded TREAT. (ISRCTN15837754) and SOFTER (Clinicaltrials.gov: NCT03270566) trials as well as the UK‐Irish Atopic eczema Systemic Therapy Register (A‐STAR; ISRCTN11210918) and a Principle Investigator in the European Union (EU) Horizon 2020‐funded BIOMAP Consortium (http://www.biomap‐imi.eu/). He also leads the EU Trans‐Foods consortium and directs the Global Atopic Dermatitis Atlas (www.atopicdermatitisatlas.org). His department has received funding from Sanofi‐Genzyme and Pfizer for skin microbiome work. He has also received compensation from the British Journal of Dermatology (reviewer and Section Editor) and EuroGuiDerm (guidelines lead). GL reports grants from National Institute of Allergy and Infectious Diseases (NIAID, NIH), other from Food Allergy & Research Education (FARE), other from MRC & Asthma UK Centre, other from UK Department of Health through NIHR, other from National Peanut Board (NPB), other from The Davis Foundation, during the conduct of the study; shareholder in DBV Technologies, and Mighty Mission Me, personal fees from Novartis, personal fees from Sanofi‐Genyzme, personal fees from Regeneron, personal fees from ALK‐Abello, personal fees from Lurie Children's Hospital, outside the submitted work. AFS reports grants from Medical Research Council (MR/M008517/1; MC/PC/18052; MR/T032081/1), Food Allergy Research and Education (FARE), the Immune Tolerance Network/National Institute of Allergy and Infectious Diseases (NIAID, NIH), Asthma UK (AUK‐BC‐2015‐01), BBSRC, Rosetrees Trust and the NIHR through the Biomedical Research Centre (BRC) award to Guy's and St Thomas' NHS Foundation Trust, during the conduct of the study; personal fees from Thermo Scientific, Nestle, Novartis, Allergy Therapeutics, Buhlmann, IgGenix, as well as research support from Buhlmann, IgGenix and Thermo Fisher Scientific through a collaboration agreement with King's College London. All the other authors have nothing to disclose.

Figures

FIGURE 1
FIGURE 1
Changes in peanut SPT across time in (A) persistent PA, (B) new PA, (C) outgrown PA, (D) Peanut sensitised but never allergic (NA). The grey lines represent individual patients and dark blue line represents the median SPT at each of the time points.
FIGURE 2
FIGURE 2
Changes in individual peanut‐specific IgE across time in (A) persistent peanut allergy, (B) new peanut allergy, (C) outgrown peanut allergy, (D) peanut sensitised but never allergic (NA). The grey lines represent individual patients, and the dark blue line represents the median specific IgE at each of the time points. IgE levels are represented on a log 10 scale.
FIGURE 3
FIGURE 3
Changes in individual Ara h 2‐specific IgE across time in (A) persistent peanut allergy, (B) new peanut allergy, (C) outgrown peanut allergy, (D) peanut sensitised but never allergic (NA). The grey lines represent individual patients and he dark blue line represents the median sIgE to Ara h 2 at each of the time points. sIgE levels are represented on a log 10 scale.
FIGURE 4
FIGURE 4
Changes in individual mast cell activation across time in (A) persistent peanut allergy, (B) new peanut allergy, (C) outgrown peanut allergy, (D) peanut sensitized but never allergic. The grey lines represent individual patients and the dark blue line represents the median % CD63+ LAD2 cells at each of the time points.

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