Gastric biopsies with prominent eosinophils: Clinicopathologic features and response to therapy

The use of the term 'histologic eosinophilic gastritis' (EoG) has been proposed for cases with ≥30 eosinophils/high power field (HPF) in five separate HPF and with no known associated causes of eosinophilia. This study evaluates the clinical presentation, pathologic characteristics of 'histologic eosinophilic gastritis'.

Gastric biopsies with prominent mucosal eosinophils over 23 years were retrieved yielding 87 qualifying cases. Clinical information and follow-up data were retrieved from medical records. Of the 72 cases with no discernible aetiology, 56 satisfied the criteria for 'histologic eosinophilic gastritis' (Group 1), while 16 had prominent eosinophils without satisfying these criteria (Group 2). There were no differences in clinical presentation, endoscopic findings, morphologic features or treatment response between these groups. The cases with a secondary aetiology (Group 3), included Crohn disease (n = 5), concurrent or prior history of Helicobacter pylori gastritis (n = 5), strongyloidiasis (n = 1), collagenous gastritis (n = 1), hyper-eosinophilic syndrome (n = 1), autoimmune atrophic gastritis (n = 1) and systemic mastocytosis (n = 1). Of the 10 patients with histologic eosinophilic gastritis who were treated with steroids (with or without a combination of other therapies), seven (70%) had documented response to steroid-based therapy, with three (30%) patients who were symptomatically steroid non-responsive. No histologic differences were identified in patients with steroid-responsive disease. Two patients developed relapsing disease characterized by severe abdominal pain dependent on steroid therapy.

The criteria for 'histologic eosinophilic gastritis' can miss cases with clinically significant eosinophilia and our study results argue against using this term for pathology diagnosis. The majority of patients with increased gastric mucosal eosinophils present with non-specific GI symptoms and endoscopic findings. While a significant proportion of patients improve symptomatically without treatment or with anti-acid therapy, a small proportion of patients develop steroid-dependent, relapsing idiopathic disease that warrants additional clinical follow-up.