Eosinophilic Gastrointestinal Disorders Affect More Than Just the Esophagus.

I n 1937, Dr R. Kaisjer provided the first description of eosinophilic gastroenteritis after reviewing surgical resections taken from various parts of the gastrointestinal (GI) tract (1). During the next few decades, other descriptions, again derived from whole tissue surgical specimens, followed. With the advent of flexible endoscopy in the 1960s, physicians were provided the necessary tools to procure mucosal biopsy samples from patients, escorting in a new era of defining the resident and pathological inflammatory cells of the intestinal mucosae. In the early 1980s, 2 publications identified eosinophils as markers of gastroesophageal reflux disease (2,3). The association of esophageal eosinophilia with gastroesophageal reflux disease held firm until the early 1990s when 3 publications provided the first descriptions of eosinophilic esophagitis (EoE) as a distinct disease entity (4,5,5a). Since then, 3 consensus recommendations and a European guideline have been published identifying and refining the diagnostic criteria for EoE (6–9). The emergence of EoE as an increasingly recognized distinct clinicopathological entity rekindled interest and raised questions about the role of the eosinophil in GI health and disease; for example, do eosinophils play a role in innate host defense and increase as a compensatory mechanism or is their increased presence a manifestation of a pathological inflammatory or allergic condition? (10,11). The latter explanation has certainly garnered more attention, and when tissue eosinophilia is seen in the context of organ-specific symptoms, with peripheral eosinophilia, without evidence of infection, and with resolution after steroid treatment, the diagnosis of an eosinophilic GI disease (EGIDs) is strongly considered.