By Andy Skean
The incidence of eosinophilic esophagitis has increased significantly over the past 2 decades and is a leading cause of upper gastrointestinal morbidity. Symptom severity among children varies, but for many, the condition is associated with significant disease burden. The etiologic factors contributing to development are poorly understood, but given the increase in incidence, environmental factors are likely important. Growing evidence supports the hypothesis that early life factors can lead to dysbiosis in the colonization of the gut microbiome. This dysbiosis may lead to downstream immune dysregulation.
With this in mind, my colleagues and I conducted a case-control study—published in The Journal of Allergy and Clinical Immunology—examining the association between early-life factors that have been previously demonstrated to alter microbial colonization in early life in relation to development of eosinophilic esophagitis. Patients were recruited from Cincinnati Children’s and population-based controls were selected from the Greater Cincinnati area.
We identified several factors—including antibiotic use in infancy, admission to the neonatal intensive care unit (NICU), and use of an acid suppressant in infancy—that were associated with eosinophilic esophagitis development. Building on this work, we also recently published a study suggesting that risk of the condition, as it relates to underlying genetic susceptibility, may be modified by early life exposures. Our study identified that breastfeeding modified the association between a calpain 14 susceptibility single-nucleotide polymorphism and eosinophilic esophagitis. The findings from these studies underscore the potential to identify modifiable factors that may ultimately reduce risk for eosinophilic esophagitis, particularly in those who are genetically susceptible.
Jensen E, Kuhl J, Martin L, et al. Early-life environmental exposures interact with genetic susceptibility variants in pediatric patients with eosinophilic esophagitis. J Allergy Clin Immunol. 2018:141(2);632-637. Available at: https://doi.org/10.1016/j.jaci.2017.07.010.