There is an increasing body of evidence that the combination of cutaneous sensitization via a disrupted skin barrier (ie children with eczema or with filaggrin mutations) and environmental peanut exposure influences the development of peanut allergy.
Among children with FLG mutations, for each ln unit increase in the house dust peanut protein level, there was a more than 6-fold increased odds of peanut SPT sensitization, CRD sensitization, or both in children at ages 8 years, 11 years, or both and a greater than 3-fold increased odds of peanut allergy compared with odds seen in children with wild-type FLG.
Subsequent investigations of the role of FLG-null mutations have identified a series of significant associations with atopic disease phenotypes, including atopic asthma, allergic rhinitis, and peanut allergy.