Background: The high frequency of gastroesophageal reflux symptoms reported in patients with eosinophilic esophagitis has suggested that the two disorders may be associated; however, few studies have systematically addressed this issue.
Goals: To determine the frequency of the simultaneous occurrence of esophageal eosinophilia and Barrett esophagus and define the clinical characteristics of patients with both conditions.
Study: From a national pathology database of patients who had esophagogastroduodenoscopy with mucosal biopsies we extracted patients with a diagnosis of Barrett mucosa, eosinophilic esophagitis pattern of injury [(≥15 eosinophils/high-power field (HPF)], or both. We then evaluated their respective clinicopathologic associations.
Results: Among 233,662 unique patients evaluated during the study period, Barrett mucosa without increased eosinophils was diagnosed in 29,733 patients (12.7%; median age 63 y; 67.6% male); eosinophil counts of ≥15/HPF were recorded in 9509 patients without Barrett mucosa (4.1%; median age 44 y; 63.9% male). A simultaneous diagnosis of Barrett mucosa and ≥15 eosinophils/HPF in the squamous epithelium and was made in 404 unique patients (0.17%; median age 56 y; 79.5% male). The observed prevalence of the simultaneous occurrence of the two conditions was one third of that expected if they occurred independently (odds ratio 0.29; 95% confidence interval, 0.27-0.33; P<0.0001).
Conclusions: These data suggest a strong inverse relationship between Barrett metaplasia and eosinophilic infiltrates in the esophageal mucosa. Although the influence of diagnostic bias cannot be excluded, the possibility that eosinophilic infiltrates in the esophageal mucosa prevent subsequent metaplastic changes may deserve to be explored.
*Miraca Research Institute, Miraca Life Sciences, Irving
†Department of Pathology, Dallas VAMC
‡Department of Pathology, University of Texas Medical Center at Dallas, Dallas, TX
M.H.S., R.M.G., P.B.M., and G.M.L. are employees of Miraca Life Sciences; W.L.N. is a gastrointestinal pathology fellow supported by the University of Texas and by Miraca Life Sciences.
The authors declare that they have nothing to disclose.
Reprints: Robert M. Genta, MD, Miraca Life Sciences, 6655 North MacArthur Blvd., Irving, TX 75039 (e-mail: robert.genta@UTSouthwestern.edu).
Received February 1, 2012
Accepted March 20, 2012