Eosinophilic Gastritis in Children

Clinicopathological Correlation, Disease Course, and Response to Therapy

Huaibin M Ko MD; Raffaella A Morotti MD; Oksana Yershov MS; Mirna Chehade MD; MPH


Am J Gastroenterol. 2014;109(8):1277-1285. 

In This Article

Abstract and Introduction


Objectives: Eosinophilic gastritis (EG), defined by histological criteria as marked eosinophilia in the stomach, is rare, and large studies in children are lacking. We sought to describe the clinical, endoscopic, and histopathological features of EG, assess for any concurrent eosinophilia at other sites of the gastrointestinal (GI) tract, and evaluate response to dietary and pharmacological therapies.

Methods: Pathology files at our medical center were searched for histological eosinophilic gastritis (HEG) with ≥70 gastric eosinophils per high-power field in children from 2005 to 2011. Pathology slides were evaluated for concurrent eosinophilia in the esophagus, duodenum, and colon. Medical records were reviewed for demographic characteristics, symptoms, endoscopic findings, comorbidities, and response to therapy.

Results: Thirty children with severe gastric eosinophilia were identified, median age 7.5 years, 14 of whom had both eosinophilia limited to the stomach and clinical symptoms, fulfilling the clinicopathological definition of EG. Symptoms and endoscopic features were highly variable. History of atopy and food allergies was common. A total of 22% had protein-losing enteropathy (PLE). Gastric eosinophilia was limited to the fundus in two patients. Many patients had associated eosinophilic esophagitis (EoE, 43%) and 21% had eosinophilic enteritis. Response to dietary restriction therapy was high (82% clinical response and 78% histological response). Six out of sixteen patients had persistent EoE despite resolution of their gastric eosinophilia; two children with persistent HEG post therapy developed de novo concurrent EoE.

Conclusions: HEG in children can be present in the antrum and/or fundus. Symptoms and endoscopic findings vary, highlighting the importance of biopsies for diagnosis. HEG is associated with PLE, and with eosinophilia elsewhere in the GI tract including the esophagus. The disease is highly responsive to dietary restriction therapies in children, implicating an allergic etiology. Associated EoE is more resistant to therapy.


Eosinophil-associated gastrointestinal (GI) disorders encompass a series of diseases characterized by eosinophilic inflammation in different segments of the GI tract, in the absence of known causes for eosinophilia (e.g., drug reactions, parasitic infestation, inflammatory bowel disease, and malignancy).[1] Eosinophil-associated GI disorders include eosinophilic esophagitis (EoE), eosinophilic gastritis (EG), eosinophilic gastroenteritis (EGE), eosinophilic enteritis, and eosinophilic colitis.[1] In contrast to EoE, the entities EG, enteritis, and gastroenteritis in children are not well characterized. They are considered a heterogeneous group of overlapping disorders, with variation in the degree of disease involvement of the stomach and small intestine, and further heterogeneity in the depth of involvement of the different layers of the GI tract.[1,2]

To date, the largest reported series of EGE in the literature are in adults, and very little information exist on this disease in children[3,4] The entity of EG, defined as a clinicopathological disorder with both histological evidence of gastric eosinophilia limited to the stomach and clinical symptoms, has not been well studied. Our aim was to characterize severe histological eosinophilic gastritis (HEG) in children where no known etiology for the tissue eosinophilia is found. Specifically, we sought to correlate pathological findings in HEG with clinical and endoscopic features, and investigate associations of HEG with eosinophilia in other sites of the GI tract. We also aimed to compare clinical characteristics of those with eosinophilia limited to the stomach (qualifying them as having EG) to those with concurrent eosinophilia at other sites (HEG with esophageal and/or duodenal eosinophilia). Furthermore, we aimed to determine whether HEG in children and EG in particular are triggered by food antigens, by examining the allergic profile of patients with HEG with/without eosinophilia in other organs, as well as their clinical and histological responses to various therapies including dietary restrictions when available.