Endoscopic surveillance of columnar-lined esophagus: frequency of intestinal metaplasia detection and impact of antireflux surgery

Abstract

Objective: To quantify the occurrence of intestinal metaplasia in columnar-lined esophagus (CLE) during endoscopic surveillance and to evaluate the impact of antireflux surgery on the development of intestinal metaplasia.

Summary background data: The malignant potential in segments of CLE is mainly restricted to those containing intestinal metaplasia. Patients with segments of CLE in which no intestinal metaplasia can be detected are rarely enrolled in a surveillance program but may still be at increased risk of developing esophageal adenocarcinoma because intestinal metaplasia may be missed or may develop with time.

Methods: The occurrence of intestinal metaplasia on biopsy samples was determined on repeated endoscopies in 177 patients enrolled in a surveillance program for CLE. The incidence of intestinal metaplasia in patients with no evidence of intestinal metaplasia on the two first endoscopies was evaluated on the subsequent endoscopies and compared in patients with medically and surgically treated gastroesophageal reflux disease.

Results: Intestinal metaplasia was found in 53% of the patients (94/177) on their first surveillance endoscopy and was more prevalent in long segments of CLE. The prevalence of intestinal metaplasia increased markedly with increasing number of surveillance endoscopies. Intestinal metaplasia tended to be detected early in patients with long segments of CLE; in patients with shorter segments, intestinal metaplasia was also detected late in the course of endoscopic surveillance. Patients with surgically treated reflux disease were 10.3 times less likely to develop intestinal metaplasia compared with a group receiving standard medical therapy.

Conclusion: Biopsy samples from a single endoscopy, despite an adequate biopsy protocol, are insufficient to rule out the presence of intestinal metaplasia. Patients in whom biopsy specimens from a segment of CLE show no intestinal metaplasia have a significant risk of having undetected intestinal metaplasia or of developing intestinal metaplasia with time. Sampling error is probably the reason for the absence of intestinal metaplasia in segments of CLE longer than 4 cm, whereas development of intestinal metaplasia is common in patients with shorter segments of CLE. Antireflux surgery protects against the development of intestinal metaplasia, possibly by better control of reflux of gastric contents.

Figure 1. Cumulative prevalence of intestinal metaplasia during endoscopic surveillance (endoscopies one through six) in patients with varying lengths of esophageal columnar lining. The lengths of columnar lining were 1 to 2 cm (A), 3 to 4 cm (B), 5 to 6 cm (C), and longer than 6 cm (D). The number of patients at each endoscopy is denoted within the bars.

Figure 2. The relationship between the length of esophageal columnar lining and the time to detect intestinal metaplasia in patients with no intestinal metaplasia on the first endoscopy.

Figure 3. Kaplan-Meier curve for the intestinal metaplasia-free survival during endoscopic surveillance of patients with no evidence of intestinal metaplasia on the first two endoscopies (n = 79).

Figure 4. Kaplan-Meier curve comparing the intestinal metaplasia-free survival during endoscopic surveillance of patients with medically and surgically treated reflux disease. The patients had no evidence of intestinal metaplasia on the first two endoscopies.