Segment Of Columnar-lined Esophagus Research Articles

Radiofrequency Ablation and Dilated Columnar-Lined Esophagus

To the Editor: It is with interest that we read the article by Pouw et al. (1) entitled Properties of the neosquamous epithelium after ablation of Barrett's esophagus containing neoplasia, which has been published in a recent issue of The American Journal of Gastroenterology. The fascinating finding of the study was that 2 years after radiofrequency ablation (RFA) for Barrett's esophagus containing dysplasia and early cancer, the esophagus was covered by a normal squamous epithelium. In addition to the normalization of histology (i.e., the absence of columnar-lined esophagus), genetic abnormalities had also been reversed (replacement with a normal stem cell pool). These outstanding data indicate that RFA is a promising tool for the effective endoscopic treatment of Barrett's esophagus and for the elimination of cancer risk. RFA eradicates columnar lining within the tubular esophagus. However, in patients with gastroesophageal reflux disease, the anatomical esophagogastric junction does not coincide with the level of the rise of endoscopically visible gastric-type folds (2). A segment of columnar-lined esophagus is interposed between the tubular esophagus and the proximal stomach (2). Because of the reflux-induced loss of the function of the lower esophageal sphincter and columnar lining, this part of the esophagus is dilated, resulting in a gastric-type appearance during endoscopy (i.e., columnar lining with gastric-type folds), which has therefore been named dilated end-stage esophagus (2). Recent studies indicated a similar oncological potential for columnar-lined esophagus with (Barrett's esophagus) and without intestinal metaplasia (i.e., cardiac and oxyntocardiac mucosa, respectively) (3). In addition, after RFA, patients are put on high-dose proton pump inhibitor therapy, which seems to favor the development of squamous epithelium within the ablated segments of the tubular esophagus (1,4). Due to its proximity to the stomach, the dilated end-stage esophagus is exposed to the highest concentrations of the oncogen (i.e., reflux) (2). Preexisting dysplasia and early cancer in the study by Pouw et al. (1) indicate that the esophageal mucosa (including the epithelium of the untreated dilated end-stage esophagus) was at an increased cancer risk. Supporting this notion, recent studies found that dysplasia was a significant risk factor for the development of esophageal adenocarcinoma (5,6). Because of saccular morphology, the dilated end-stage esophagus is not suitable for balloon catheter ablation (1,2). Therefore, an effective laparoscopic fundoplication around the dilated end-stage esophagus for the elimination of reflux should be considered after successful RFA. Otherwise, the development of adenocarcinomas within the untreated dilated columnar-lined esophagus may be observed. The authors are kindly asked to address the above considerations.

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

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. 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. 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. 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. 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.

Determinants of intestinal metaplasia within the columnar-lined esophagus.

The clinical and physiological features of patients with short segments of columnar-lined esophagus (CLE) with and without intestinal metaplasia (IM) are distinct. Retrospective case series. University tertiary referral center. Sixty-five consecutive patients with a 2-cm or shorter length of endoscopically visible CLE. The type of CLE and the presence of Helicobacter pylori were determined by histopathologic examination of esophageal and gastric antrum biopsy specimens. All patients underwent esophageal manometry and simultaneous 24-hour pH and bilirubin monitoring. Clinical and physiological data were compared in patients with and without IM. Thirty-six patients had IM and 29 had cardiac-type mucosa without IM in biopsy specimens from the CLE. There was no significant difference in age or sex distribution, but the duration of symptoms was significantly longer in patients with IM (10 vs 5 years; P = .03). Abnormal esophageal acid exposure was found in 30 (83%) of 36 patients with IM and 23 (79%) of 29 patients without IM. The prevalence of abnormal bilirubin exposure was significantly higher in patients with IM (75% [27/36]) than in those without IM (41% [12/29]; P = .01). There was no significant difference in the prevalence of H pylori infection between the 2 groups (8% vs 10%; P >.99). Patients with short segments of CLE and IM have similar esophageal acid exposure but significantly higher frequency of abnormal bilirubin exposure and longer median duration of reflux symptoms than patients without IM. Therefore, CLE, regardless of histological type, is a manifestation of gastroesophageal reflux disease. The presence of duodenoesophageal reflux and the duration of reflux seem to be important in the pathogenesis of IM.