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.
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.