Search

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 and 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 of 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 10 years of life, 13 of 934 (1.4%) children were diagnosed with peanut allergy. In the IOW cohort, 6 of 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., Conclusion: Peanut allergy appears to be stable over the first 10 years of life in our cohorts. There was no significant difference in peanut sensitization or clinical peanut allergy between 1989 and 2001., (© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background: Prevalence, incidence and natural history of food hypersensitivity (FHS) and its trends in an unselected cohort of older children are unclear., Methods: A birth cohort born on the Isle of Wight (UK) between 2001 and 2002 was followed up prospectively. Children were clinically examined and skin prick tested at set times and invited for food challenges when indicated. At 10 years of age, children were also invited for a blood test., Results: A total of 969 children were recruited at 12 weeks of pregnancy, and 92.9%, 88.5%, 91.6% and 85.3% were assessed at 1, 2, 3 and 10 years. Prevalence of sensitization to any allergen over 10 years was 186 of 969 (19.2%; 95% CI: 16.84-21.8) and 108 of 969 (11.2%; 95% CI: 9.31-13.29) children were sensitized to at least one predefined food allergen. Excluding wheat (due to cross-reactivity with pollen), 40 of 969 (4.1%; 95% CI: 3.19-5.32) children were sensitized to a predefined food allergen. Using food challenges and/or a good clinical history, the cumulative incidence of food hypersensitivity (FHS) in the first decade of life was 64 of 947 (6.8%, 95% CI: 5.2-8.4), while the prevalence of FHS at 10 years was 30 of 827 (3.6%, 95% CI: 2.54-5.15). The vast majority, 25 of 827 (3.0%, 95% CI: 1.8-4.2), suffered from IgE-mediated food allergy, while 5 of 827 (0.6%, 95% CI: 0.07-1.3) had non-IgE-mediated food allergy/food intolerance., Conclusions: By the age of 10 years, 6.8% of children suffered from FHS based on food challenges and a good clinical history. There was a large discrepancy between reported and diagnosed FHS., (© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background: Patients often report adverse reactions to wheat. Interpretation of sensitization to wheat pollen and flour with/without sensitization to grass pollen is a clinical problem., Aim: We set out to determine the prevalence of wheat allergy in a birth cohort (10/11 year olds) and investigate the usefulness of performing skin prick tests (SPT), specific IgE tests and component resolved diagnostics to wheat pollen and flour., Methods: The Food Allergy and Intolerance Research (FAIR) birth cohort included babies born on the Isle of Wight (UK) between September 2001-August 2002 (n = 969). Children were followed up at 1, 2, 3 and 10/11 years. 588 children had SPTs to wheat pollen and grass during the 10 year follow-up. 294 children underwent further SPT to wheat flour and 246 had specific IgE testing to wheat and grass., Results: Eight children underwent oral food challenges (OFC). We diagnosed 0.48 % (4/827; 95 % CI 0-1 %) children with wheat allergy based on OFC. 16.3 % (96/588) were sensitized to grass pollen, 13.4 % (79/588) to wheat pollen; 78 % (75/96) sensitized to both. Only one child was sensitized to wheat flour and wheat pollen, but not grass pollen. For specific IgE, 15.0 % (37/246) and 36.2 % (89/246) were sensitized to wheat and grass pollen, with 40.5 % (36/89) sensitized to both. Of the 37 children sensitized to wheat, 3 (8.1 %) were sensitized to omega 5 gliadin, 1 (2.7 %) to wheat lipid transfer protein and 1 to wheat gliadin., Conclusion: Clinicians should be aware of the high level of cross-sensitization when performing tests to wheat and grass pollen i.e. sensitisation to wheat specific IgE and wheat pollen SPT should be assessed in the presence of grass pollen SPT and/or specific IgE.

Objective: To determine the prevalence of sensitisation to peanuts and tree nuts in all children born during one year in one geographical area., Design: Birth cohort study with structured review at ages 1, 2, and 4 years., Setting: All children born on the Isle of Wight between January 1989 and February 1990., Subjects: Of 1456 children originally included, 1218 were reviewed at age 4 years. Of these, 1981 had skin prick tests., Main Outcome Measures: Positive skin test results, clinical atopic disease, and risk factors for the development of atopy., Results: 15 of 1218 (1.2%) children were sensitised to peanuts or tree nuts (13 to peanuts). Six had had allergic reactions to peanuts (0.5% of the population), one to hazelnuts, and one to cashew nuts; three had had anaphylactic reactions. Seven children had positive skin test results or detectable IgE to peanuts without clinical symptoms. Two children who reacted to peanut in infancy had lost their sensitivity by 4 years. Family history of atopy, allergy to egg (odds ratio 9.9, 95% confidence interval 2.1 to 47.9, and eczema (7.3, 2.1 to 26.1) were important predictors for peanut allergy., Conclusions: IgE mediated allergy to peanuts is common in early childhood. In many the allergy persists but a minority may develop tolerance.

House dust mites are believed to be major triggers for allergic disease in atopic individuals. As part of a programme controlling dietary and aero-allergen exposure in high-risk infants, an acaricidal foam and powder (Acarosan) was applied to bedroom and main living room carpets, as well as upholstered furniture, on four occasions in the first year of life. Dust was assayed for mite antigen (Der p1) and these results compared with the semi-quantitative assay of guanine content (Acarex Test). After nine months mean Der p1 levels had decreased by 70% in the treatment group. Proportionally, the greatest fall occurred in those items that had the highest initial mite antigen content. The Acarex score does show a correlation with Der p1 levels, but cannot replace antigen assay when accurate data is required. A chemical acaricide may help reduce house dust mite antigen levels, but is not by itself sufficient to reduce levels below that considered critical for sensitisation.