*EMBARGOED All research presented at the ACG Annual Scientific Meeting is strictly embargoed until Monday, October 17, 2016 at 8:00 am EDT.

Dr. Elizabeth T. Jensen
Elizabeth T. Jensen, MPH, PhD

Oral 20 Gene-environment Interaction in Pediatric Eosinophilic Esophagitis

Author Insight from Elizabeth T. Jensen, MPH, PhD, Wake Forest School of Medicine, University of North Carolina at Chapel Hill

What’s new here and important for clinicians?

The rapidly increasing incidence of eosinophilic esophagitis (EoE) suggests that environmental factors contribute to disease development. Candidate and genome-wide association studies have identified genetic variants in association with disease risk, but these variants do not explain the rapid increase in disease incidence. Studies of gene-environment interaction may be used to elucidate novel mechanisms for disease, through identification of novel loci that may only be associated with disease in the setting of certain exposures. Studies of gene-environment interaction may also inform our understanding of possible factors that increase or ameliorate disease risk in people with certain genetic variants. In this study, we observed evidence that breastfeeding, NICU admission, and not having a fury pet in infancy modified the risk of developing EoE in those with certain gene variants that have been associated with the disease. We are planning additional studies to assess replication of these findings.

What do patients need to know?

EoE is becoming much more common. While there are known genetic factors that increase the risk for developing disease, these factors do not explain the increase in disease occurrence. Research is being conducted to help us better understand the potential causes of EoE, including examining possible risk factors in people who may be genetically predisposed for developing disease. Our research found evidence that some early-life factors may increase risk or prevent disease, depending on an individual’s underlying genotype. We are planning additional studies to examine these associations with further detail, in hopes that we will ultimately be able to use this information to evaluate a patient’s risk for disease or, in families where there is a strong family history of disease, to potentially reduce the risk of developing disease.

Read the Abstract

Author Contact

Elizabeth T. Jensen, MPH, PhD, Wake Forest School of Medicine, University of North Carolina at Chapel Hill

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