Clinical Factors Associated With Peanut Allergy in a High-Risk Infant Cohort

This study examined factors associated with the development of peanut allergy in high risk infants.

The study included 511 infants aged 3–15 months from the prospective, observational Consortium for Food Allergy Research (CoFAR2) study, who were at high risk of peanut allergy because of moderate-to-severe atopic dermatitis (39.5%), egg or milk allergy (17.8%) or both (42.7%). Infants with known peanut allergy or peanut-specific IgE >5 kU/L at the time of enrollment were excluded.

Participants were assessed for peanut allergy at enrollment, 6 months, 12 months, and annually thereafter based on history of reactions, skin prick testing (SPT), peanut IgE results, and oral challenges if clinically indicated. A prediction model was developed by stepwise multiple logistic regression and validated with a subset of the data.

Among the 511 infants (67.5% male, 82% with moderate-to-severe atopic dermatitis, median age 9.9 months and median length of follow-up 7.3 years), 40.1% developed peanut allergy and 10.6% outgrew their peanut allergy. Factors associated with developing peanut allergy (P < .05) included: moderate-severe atopic dermatitis; larger egg and peanut SPT; greater egg, milk and peanut IgE levels; greater peanut component (Ara h1, h2 and h3) levels; greater peanut IgG and IgG₄; peanut consumption >2 times per week in pregnancy; younger age; non-white race; lack of breastfeeding; and increased peanut consumption during lactation. The final model included age at enrollment, peanut-specific IgE level, peanut Ara h2, and breastfeeding status and predicted 79.4% of peanut allergy in the development data set and 74.8% of peanut allergy in the validation data set (sensitivity 66.1% and specificity 80.6%).

Among infants at high risk of peanut allergy because of moderate-severe atopic dermatitis and/or egg or milk allergy, peanut allergy development may be predicted by younger age, greater peanut IgE and Ara h2 levels, and lack of breastfeeding.

In addition to infants with moderate-severe atopic dermatitis and egg allergy previously reported to have a high risk of peanut allergy, this cohort also included infants with milk allergy. These high-risk children, without peanut allergy at study entry, had a higher proportion of peanut allergy development and lower proportion of peanut allergy outgrowing than typically reported. The model requires further validation in high-risk infants and may not be generalizable to low-risk infants. Infants referred at a younger age, lacking breastfeeding, and with higher levels of sensitization to peanut were identified by the model as having the highest likelihood of peanut allergy development and may benefit from even closer monitoring than typical for this high-risk group. However, strategies for prevention of peanut allergy, such as early dietary peanut introduction, should be applied to all high-risk infants.