Eosinophilic Gastroenteritis

An Update

Alfredo J Lucendo; Angel Arias


Expert Rev Gastroenterol Hepatol. 2012;6(5):591-601. 

In This Article

Abstract and Introduction


Eosinophilic gastroenteritis (EGE) is characterized by dense eosinophilic inflammation of one or several digestive tract sections. The symptoms include abdominal pain, weight loss, vomiting and diarrhea. Biopsy samples taken during endoscopic examination allows the diagnosis of the disease. An infiltration of >30 eosinophils per high-power field in at least five high-power fields, exhibiting signs of eosinophilic degranulation and extending to the muscularis mucosa or submucosa are all histological indications of EGE. EGE is traditionally classified into three forms depending on the depth of inflammation in the wall (mucosal, muscular or serosal). This, together with the digestive tract segments involved, determines the clinical presentation. The natural history of EGE includes three different evolutionary patterns, since patients may suffer a single outbreak, a recurrent course or even chronic disease. Corticosteroids are the most frequently used therapy for EGE; dietary treatments should be also considered. Surgery has been limited to solving obstruction and small bowel perforation.


Eosinophilic gastrointestinal disorders (EGID) constitute a pathology characterized by eosinophilic infiltration of the GI tract, the symptoms of which vary depending on the affected digestive segments and the involvement of the different layers of the digestive wall.

In the case of eosinophilic gastroenteritis (EGE), the typically affected sites are the stomach and small bowel, although any area of the GI tract from the esophagus to the rectum can be also involved. First described in 1937 by Kaijser, interest in EGE has grown in recent years in parallel with an increasing number of case reports and case series from different continents.[1]

The currently accepted diagnostic criteria for EGE were proposed by Klein et al. in 1970[2] and updated by Talley et al in 1990[3] and includes the presence of generally recurrent gastrointestinal symptoms, demonstration of a dense eosinophilic infiltrate in biopsies taken from the GI tract or high eosinophil content in peritoneal fluid and the absence of parasitic or extraintestinal diseases that could cause eosinophilia[4,5] such as vasculitis, drug reactions or neoplasms. Peripheral eosinophilia is currently not required for a positive diagnosis since it is not a universal finding.

Despite being still recognized as a rare disorder, nearly a fourth of all historical descriptions of EGE in the literature come from the last 5 years. However, many aspects of the disease remain unknown. Thus, no definitive epidemiological features have been established, physiopathological data are extremely limited and an established natural history for EGE is lacking and therapeutic options are mostly based on empirical experience. There is a complete lack of controlled and randomized studies that clearly establish definitive information regarding EGE. However, information provided by case reports over a wide range of years and geographical origins allow us to assume some common observations as characteristics for the disease. This article aims to comprehensively review the latest, most relevant published information regarding EGE to provide a guide for understanding this increasingly recognize disorder.