Incidental Gastric Eosinophils in Patients With Eosinophilic Esophagitis: Do They Matter?
Male
Adolescent
Anti-Inflammatory Agents
Stomach Diseases
Infant
Eosinophilic Esophagitis
3. Good health
Androstadienes
Eosinophils
Leukocyte Count
03 medical and health sciences
0302 clinical medicine
Gastric Mucosa
Child, Preschool
Fluticasone
Humans
Female
Endoscopy, Digestive System
Child
DOI:
10.1097/mpg.0b013e3181d98e6c
Publication Date:
2010-07-01T07:36:11Z
AUTHORS (4)
ABSTRACT
ABSTRACTBackground 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.
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