Does Impaired Gallbladder Function Contribute to the Development of Barrett’s Esophagus and Esophageal Adenocarcinoma?

Abstract

IntroductionEsophageal adenocarcinoma is aetiologically associated with gastro-esophageal reflux, but the mechanisms responsible for the metaplasia–dysplasia sequence are unknown. Bile components are implicated. Impaired gallbladder function may contribute to duodenogastric reflux (DGR) and harmful GERD. AimsThis study aims to compare gallbladder function in patients with Barrett’s esophagus, adenocarcinoma, and controls. MethodsThree groups of patients, all free of gallstone disease, were studied. Group 1: (n = 15) were normal controls. Group 2: (n = 15) were patients with >3-cm-long segment of Barrett’s esophagus. Group 3: (n = 15) were patients with esophageal adenocarcinoma. Using real-time ultrasonography unit, gallbladder volume was measured in subjects following a 10-h fast. Ejection fraction was calculated before and after standard liquid meal and compared between the groups. ResultsThe mean percentage reduction in gallbladder volume was 50% at 40 min in the adenocarcinoma group compared with 72.4% in the control group (p < 0.001). At 60 min, gallbladder filling had recommenced in the control group to 64.1% of fasting volume while continuing to empty with further reduction to 63% in the Barrett’s group and to 50.6% (p = 0.008) in the adenocarcinoma group. The mean gallbladder ejection fraction decreased progressively from controls to Barrett’s to adenocarcinoma and was significantly lower in Barrett’s group (60.9%; p = 0.019) and adenocarcinoma group (47.9%; p < 0.001) compared with normal controls (70.9%). ConclusionGallbladder function is progressively impaired in Barrett’s esophagus and adenocarcinoma. Gallbladder malfunction increases duodenogastric reflux, exposing the lower esophagus to an altered chemical milieu which, in turn, may have a role in promoting metaplasia–dysplasia–neoplasia sequence in the lower esophageal mucosa.