Peanut allergy is strongly associated with atopic disease trajectories, which are characterized by early-onset, persistent eczema and wheeze, but not with transient eczema or wheeze. These were among study findings recently published in the journal Clinical & Experimental Allergy.

Recognizing that understanding the risk factors for peanut allergy is essential for the development of effective preventive measures, the researchers sought to establish associations and predictors of PA, as well as the relationship between peanut allergy and severity of asthma, using data from the Manchester Asthma and Allergy Study, a population-based birth cohort study conducted in the United Kingdom. All participants in this study were recruited prenatally and were followed prospectively; they attended review clinics at 1, 3, 5, 8, and 11 years of age.

At each visit, interviewer-administered, validated questionnaires were utilized to obtain information on parentally reported symptoms, physician-diagnosed diseases, treatments received, and environmental exposures. Additional questions on food allergy and diet were embedded throughout. Skin prick tests (SPTs), along with specific immunoglobulin E (sIgE) measurements to common foods (ie, milk, eggs, and peanuts) and aero-allergens (ie, house dust mite, cat, dog, molds, grass, and birch pollens), were obtained at all time points. FLG genotyping was carried out, to determine the presence of 6 different FLG loss-of-function mutations.


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The recently published analysis explored the association between objectively confirmed peanut allergy with early-life environmental exposures, filaggrin (FLG)-loss-of-function mutations, and other atopic diseases. Following this, researchers investigated the association of peanut allergy with longitudinal trajectories of sensitization, wheeze, and allergic comorbidities. The investigation also determined the relationship between peanut allergy and asthma severity.

Peanut sensitization was defined as SPT mean wheal diameter to peanut extract of 3 mm or greater than the negative control and/or sIgE to whole peanut extract of more than 0.35 kUA/L. All children in the cohort with evidence of peanut sensitization at ages 5 and/or 8 years (SPT response of ≥3 mm or sIgE level of ≥0.2 kUA/L), or with a history of immediate reaction upon exposure, were offered an oral food challenge to confirm their peanut allergy.

A total of 959 children were included in the study. Overall, 53.6% (514 of 959) of the children were boys and 93.3% (895 of 959) of them were identified as being of White race/ethnicity. Peanut allergy was verified in 3.1% (30 of 959) of the participants who had evaluable data. Per multivariate analysis, eczema in infancy (odds ratio [OR], 4.4; 95% CI, 1.5-13.2; P =.007), egg sensitization at 3 years of age (OR, 9.7; 95% CI, 3.3-29.9; P <.001), and early-life cat ownership (OR, 3.0; 95% CI, 1.1-8.4; P =.04) were all independently associated with peanut allergy.

Per the stratified analysis in 700 participants with genetic information available, in those children who experienced early-life eczema, no difference was observed in FLG mutations between children with peanut allergy and those without peanut allergy (16.7% [3 of 18] vs 19.1% [42 of 220], respectively; P =1.00). In contrast, among children without eczema, those with peanut allergy were nearly 8 times more likely to have FLG mutations (33.3% [2 of 6] vs 5.9% [27 of 456], respectively; P =.049).

Additionally, associations were observed between peanut allergy and multiple allergic sensitization profiles that were derived with the use of machine learning, with an approximate 60-fold increase in risk among those participants who were assigned to multiple early sensitization. Moreover, peanut allergy was significantly associated with persistent wheeze (OR, 6.9; 95% CI, 2.5-18.8; P <.001), but not with any other wheeze phenotypes, as well as with trajectories of atopic disease characterized by comorbid persistent eczema and wheeze, but not with transient phenotypes. Although children with peanut allergy were more likely to have asthma, no evidence of an association between peanut allergy and asthma severity was reported.

A major limitation of the current study is the relatively small number of peanut-allergic children who were available for the analysis, which is inevitable when investigating a relatively uncommon outcome in an unselected birth cohort. Thus, these study results warrant cautious interpretation. Another study limitation was the fact that because the population was not ethnically diverse, the results are not directly transferable to other ethnic groups.

The researchers concluded that the association between peanut allergy and asthma severity warrants further investigation in larger studies. Although no link between peanut allergy and FLG genotype was demonstrated in children with eczema, among those without eczema, carriers of FLG loss-of-function mutations were more likely to have a peanut allergy.

Disclosure: Some of the study authors have declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures. 

Reference  

Kotsapas C, Nicolaou N, Haider S, et al. Early-life predictors and risk factors of peanut allergy, and it association with asthma in later life: population-based birth cohort study. Clin Exp Allergy. Published online February 2, 2022. doi:10.1111/cea.14103