That gastroesophageal reflux and eosinophilic esophagitis (EoE) may both lead to esophageal eosinophilia is well known. What is not known is how, if at all, these entities interact to contribute to this pathologic entity in specific patients and how often they occur in patients as synergistic contributors to the disease as opposed to distinct processes. There are several hypotheses by which gastroesophageal reflux disease (GERD) and EoE might interact to cause esophageal eosinophilia. These include (1) reflux of food from the stomach with increased antigenic exposure to esophageal epithelium; (2) reflux-induced dilation of intercellular spaces in the epithelium facilitating dendritic cell and antigen movement through the mucosa, and (3) a common inflammatory pathway activated by both GERD and EoE. Although these hypotheses appear plausible, supporting clinical data is not readily available. For example, it is unclear if the beneficial effect of proton pump inhibitors on esophageal eosinophilia is mediated through control of acid exposure to esophageal mucosa or independent anti-inflammatory effects. There is also a lack of definitive evidence to support an increased incidence of GERD in the pediatric population in the absence of evident risk factors such as obesity. One would think if GERD were an important cofactor in this disease, the incidence of GERD would rise similarly to EoE. It is speculated that GERD and EoE coexist and in some patients interact to facilitate esophageal eosinophilia and its sequelae. However, the presence and degree of this interaction likely varies remarkably. Their presence could be influenced by other factors such as age of the patient and genetic predisposition to EoE.
- Dilated intercellular spaces
- Eosinophilic esophagitis
- Gastroesophageal reflux disease
ASJC Scopus subject areas