OBJECTIVES: Because of the relationship between food and eosinophilic diseases, we hypothesize that patients with eosinophilic esophagitis (EE) may be repeatedly exposed to nonacid ingested foodstuffs compared with patients without EE. Because inflammation is found throughout the esophagus in patients with EE, we further hypothesize that there would be more full-column reflux in EE patients compared with patients with gastroesophageal reflux disease (GERD) and control patients. MATERIALS AND METHODS: We retrospectively reviewed pH-multichannel intraluminal impedance tracings of EE patients who were age-matched with control and GERD patients and compared the reflux profiles among the 3 groups. RESULTS: There were no significant differences between the mean numbers of nonacid reflux events in EE patients (4.7 +/- 3.3) compared with GERD (7.5 +/- 5.3) or control patients (6.8 +/- 4.6) (P = 0.36). There were significantly more acid reflux events in patients with GERD (47.4 +/- 17.1) compared with patients with EE (24.9 +/- 20.0) and control patients (28.4 +/- 16.5) (P = 0.02). Patients with EE did not have a higher percentage of full-column reflux (31.9 +/- 20.9) compared with control patients (24.4 +/- 19.8) or patients with GERD (30.5 +/- 14.9) (P = 0.64). CONCLUSIONS: Neither full-column reflux nor nonacid reflux is a significant contributor to the pathogenesis of EE.
OBJECTIVES: Because of the relationship between food and eosinophilic diseases, we hypothesize that patients with eosinophilic esophagitis (EE) may be repeatedly exposed to nonacid ingested foodstuffs compared with patients without EE. Because inflammation is found throughout the esophagus in patients with EE, we further hypothesize that there would be more full-column reflux in EE patients compared with patients with gastroesophageal reflux disease (GERD) and control patients. MATERIALS AND METHODS: We retrospectively reviewed pH-multichannel intraluminal impedance tracings of EE patients who were age-matched with control and GERDpatients and compared the reflux profiles among the 3 groups. RESULTS: There were no significant differences between the mean numbers of nonacid reflux events in EE patients (4.7 +/- 3.3) compared with GERD (7.5 +/- 5.3) or control patients (6.8 +/- 4.6) (P = 0.36). There were significantly more acid reflux events in patients with GERD (47.4 +/- 17.1) compared with patients with EE (24.9 +/- 20.0) and control patients (28.4 +/- 16.5) (P = 0.02). Patients with EE did not have a higher percentage of full-column reflux (31.9 +/- 20.9) compared with control patients (24.4 +/- 19.8) or patients with GERD (30.5 +/- 14.9) (P = 0.64). CONCLUSIONS: Neither full-column reflux nor nonacid reflux is a significant contributor to the pathogenesis of EE.
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