Dysplasia and adenocarcinoma after classic antireflux surgery in patients with Barrett's esophagus -: The need for long-term subjective and objective follow-up

Objective To assess the clinical, endoscopic, and functional results in a group of patients with Barrett's esophagus undergoing classic antireflux surgery in whom dysplasia and adenocarcinoma were found at a late objective follow-up. Summary Background Data There have been isolated reports of patients with Barrett's esophagus undergoing antireflux surgery who show dysplasia or even adenocarcinoma on follow-up. Methods Of 161 patients undergoing surgery, dysplasia developed in 17 (10.5%) at late follow-up and adenocarcinoma developed in 4 (2.5%). These 21 patients represent the group assessed and were compared with 126 surgical patients with long-segment Barrett's in whom dysplasia did not develop. They were evaluated by clinical questionnaire, multiple endoscopic procedures and biopsy specimens, 24-hour pH studies, and 24-hour bilirubin monitoring. Results Of the 17 patients with dysplasia, 3 were asymptomatic at the time that dysplastic changes appeared; all patients with adenocarcinoma had symptoms. Two patients (12%) in the dysplasia group had short-segment Barrett's; all patients with adenocarcinoma had long-segment Barrett's. Manometric studies revealed an incompetent lower esophageal sphincter in 70% of the dysplasia group, similar to nondysplasia patients with recurrence, and in 100% of the adenocarcinoma group. The 24-hour pH study showed pathologic acid reflux in 94% of the patients with dysplasia, similar to patients with recurrence without dysplasia, whereas bilirubin monitoring showed duodenal abnormal reflux in 86% of the patients. Among patients with dysplasia, three different histologic patterns were identified. All patients with adenocarcinoma had initially intestinal metaplasia, with appearance of this tumor 6 to 8 years after surgery. Conclusions Patients with Barrett's esophagus who undergo antireflux surgery need close and long-term endoscopic and histologic surveillance because dysplasia or even adenocarcinoma can appear at late follow-up. Metaplastic changes from fundic to cardiac mucosa and then to intestinal metaplasia and later to dysplasia or adenocarcinoma can clearly be documented. There were no significant differences in terms of clinical, endoscopic, manometric, 24-hour pH, and bilirubin monitoring studies between patients with recurrence of symptoms without dysplastic changes, and patients with dysplasia. Therefore, the high-risk group for the development of dysplasia is mainly the group with failed antireflux surgery.