BACKGROUND AND AIM: Some patients with eosinophilic esophagitis (EE) (>15 eosinophils/high-power field on esophageal mucosal biopsies and lack of response to acid suppression and/or normal pH probe study) demonstrate incidental eosinophilic inflammation of the gastric mucosa. It is unclear whether patients with EE and normal gastric biopsies (EE-N) are phenotypically different from patients with EE and gastric mucosal abnormalities (EE-A) (ie, >10 eos/hpf on gastric biopsies). The aim of the study was to compare the clinical features and response to therapy among patients with EE-N and EE-A. PATIENTS AND METHODS: Medical records of all of the EE-A and a random group of patients with EE-N diagnosed during an 8-year period were reviewed. A subgroup analysis of patients treated with swallowed fluticasone with a repeat esophagogastroduodenoscopy within 6 months of starting therapy was also performed. RESULTS: During the study period, 41 patients had EE-A. When compared to 50 random patients with EE-N, no clinical differences were noted, including sex, age, presenting symptoms, esophageal histology, and atopy history. Eleven (27%) of the 41 EE-A and 14 (28%) of the 50 EE-N patients were treated with swallowed fluticasone, and the response was similar among the groups. The mean esophageal eosinophils/high-power field among the EE-A group dropped from 47 to 8 compared with a 46 to 7 drop among the EE-N group treated with fluticasone therapy (P = 0.91). In 9 (82%) of the 11 patients with EE-A treated with fluticasone, there was resolution (7 of 9) or significant improvement (2 of 9) of gastric eosinophilia. CONCLUSIONS: Patients with EE-A and EE-N have similar clinical presentations. Incidental gastric inflammation does not predict a worse response of esophageal inflammation to fluticasone and should not exclude its use in patients with EE-A. In fact, gastric inflammation responded to swallowed fluticasone in the majority of patients with EE-A. This observation should foster further investigation into pathogenesis of EE and presumed esophagogastric inflammatory axis.
BACKGROUND AND AIM: Some patients with eosinophilic esophagitis (EE) (>15 eosinophils/high-power field on esophageal mucosal biopsies and lack of response to acid suppression and/or normal pH probe study) demonstrate incidental eosinophilic inflammation of the gastric mucosa. It is unclear whether patients with EE and normal gastric biopsies (EE-N) are phenotypically different from patients with EE and gastric mucosal abnormalities (EE-A) (ie, >10 eos/hpf on gastric biopsies). The aim of the study was to compare the clinical features and response to therapy among patients with EE-N and EE-A. PATIENTS AND METHODS: Medical records of all of the EE-A and a random group of patients with EE-N diagnosed during an 8-year period were reviewed. A subgroup analysis of patients treated with swallowed fluticasone with a repeat esophagogastroduodenoscopy within 6 months of starting therapy was also performed. RESULTS: During the study period, 41 patients had EE-A. When compared to 50 random patients with EE-N, no clinical differences were noted, including sex, age, presenting symptoms, esophageal histology, and atopy history. Eleven (27%) of the 41 EE-A and 14 (28%) of the 50 EE-Npatients were treated with swallowed fluticasone, and the response was similar among the groups. The mean esophageal eosinophils/high-power field among the EE-A group dropped from 47 to 8 compared with a 46 to 7 drop among the EE-N group treated with fluticasone therapy (P = 0.91). In 9 (82%) of the 11 patients with EE-A treated with fluticasone, there was resolution (7 of 9) or significant improvement (2 of 9) of gastric eosinophilia. CONCLUSIONS:Patients with EE-A and EE-N have similar clinical presentations. Incidental gastric inflammation does not predict a worse response of esophageal inflammation to fluticasone and should not exclude its use in patients with EE-A. In fact, gastric inflammation responded to swallowed fluticasone in the majority of patients with EE-A. This observation should foster further investigation into pathogenesis of EE and presumed esophagogastric inflammatory axis.