Does impaired gallbladder function contribute to the development of Barrett's esophagus and esophageal adenocarcinoma?

Abstract

Introduction: Esophageal 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.

Aims: This study aims to compare gallbladder function in patients with Barrett's esophagus, adenocarcinoma, and controls.

Methods: Three 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.

Results: The 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%).

Conclusion: Gallbladder 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.