Summary of the first international gastrointestinal eosinophil research symposium

The recent explosion of literature and increasing clinical experiences have established EE as a chronic disease. Few patients, if any, outgrow their illness. As such, a number of clinical management issues and basic research questions have emerged. Although the First International Gastrointestinal Eosinophil Researcher Symposium provided much in the way of clinical advice and new knowledge, it also raised important questions that will take time to answer: Etiology and pathogenesis Maintenance treatment strategies Endpoints for treatment Natural history and complications Optimalmethod to identify food antigens/aeroallergens Methods to differentiate eosinophilia associated with GERD and EE Noninvasive technologies to assess disease activity Evaluation and management of asymptomatic patient with esophageal eosinophilia The most pressing clinical issues focus on the natural history of the disease and the necessity and determination of appropriate maintenance treatments. These areas are undeniably linked; if patients are free from long-term morbidity, then the importance of chronic treatments is diminished. This scenario does not appear to be the case for most patients who experience a waxing and waning course that can affect daily life in an untoward manner. As more physicians recognize the chronicity of the disease, a larger body of experience dictates that complications and long-term problems may arise. Although strictures and narrow-caliber esophagus are the bestknown sequelae in adults, EE is certainly associated with a less well-defined but clinically important impact on a child's eating behavior. Along these same lines, the best treatment endpoint has yet to be determined. To date, research protocols have focused primarily on tissue eosinophilia as an endpoint because many clinicians are somewhat reluctant to leave the esophagus with any degree of inflammation. Using clinical phenotypes (allergic vs nonallergic) along with noninvasive or mucosal biomarker profiles (ie, eotaxin-3, IL-5) may hold promise for future identification of patients who will benefit, or not, from more targeted therapeutic intervention and monitoring. For example, the suggestion that there may be allergic and nonallergic phenotypes may guide future treatment into different approaches (nutritional vs medical). Each of these areas demands careful documentation and basic studies to know the mechanisms by which eosinophils affect the esophageal mucosa. Eight years ago, Dr David Landon made the following observation: "My suspicion is that some EEs evolve into the fibrotic variety. Only one of these has reversed on fluticasone. The problem would seem to be that once fibrosis becomes truly established, the disease seems irreversible. Whether other therapy, or a more basic attack, would change this outcome, I don't know." As collaborative basic and clinical research projects continue to address these unresolved problems, we will gain increasing clarity as to the best manner in which to provide immediate and long-term care for our patients.