Ethnic and gender variation in distal esophageal acid exposure

A79

Introduction: It is well recognized that African Americans (AA) develop Barrett’s esophagus and esophageal adenocarcinoma at a lower rate than non-Hispanic whites (nHw). Gastroesophageal reflux disease (GERD) is commonly accepted as one of the major contributors in the development of both Barrett’s esophagus and esophageal adenocarcinoma. This suggests that there may be less distal esophageal acid exposure in AA than nHw. Very little is known about distal esophageal acid exposure in AA in comparison to nHw. The aim of the present investigation was assess distal esophageal acid exposure in healthy adult AA volunteers and compare it to the exposure observed in healthy nHw volunteers to determine if ethnic variation exists in this physiologic parameter.
 Methods: Healthy AA and nHw volunteers were recruited from the Jacksonville metropolitan area. Ethnicity was self-reported. Exclusion criteria were symptoms suggestive of esophageal disease, medication use or concurrent illness that could affect distal esophageal acid exposure. 24 hour pH testing was performed in all volunteers with the distal sensor 5 cm above the manometrically determined lower esophageal sphincter. Number of total number of distal esophageal acid reflux episodes, longest episode and total time below pH 4 were measured. Mean and standard deviation were compared using t-test.
 Results: 80 volunteers had distal esophageal acid exposure measured for a 24 hour period. 41 were AA (20 M/21 F) and 39 were nHw (18 M/21 F). Distal esophageal acid exposure was significantly different between AA females (mean + SD, 20.8 + 21.4 min) and nHw males (38.4 + 32.2 min, p < 0.05). No difference was observed between ethnicities and/or gender with regard to total number of distal esophageal reflux episodes or longest distal reflux episode.
 Conclusions: AA females had significantly less acid exposure than nHw males. Other distal esophageal acid exposure measures were equivalent between groups. Further study is needed to determine the etiology of the variation in distal esophageal acid exposure observed and its impact in the development of Barrett’s esophagus and esophageal adenocarcinoma.