British Society of Gastroenterology guidelines for the diagnosis of Barrett's oesophagus: are we casting the net too wide?

We read with interest the British Society of Gastroenterology guidelines for the diagnosis and management of Barrett's columnar‐lined oesophagus¹ and the related commentary by Professor Playford (Gut 2006;55:442–3). One of the new recommendations in these guidelines relates to the diagnosis of Barrett's oesophagus. The guidelines state that “the presence of areas of intestinal metaplasia, although often present, is not a requirement for diagnosis”. This is out of step with guidelines from the US, where intestinal metaplasia is required to establish a diagnosis of Barrett's oesophagus.² The rationale for the British guidelines is that sampling errors at initial endoscopy may miss areas affected with intestinal metaplasia. The evidence used to support this is an article from a Continuing Professional Development bulletin.³ The authors in this bulletin conclude that “if a sufficient number of biopsies are taken over an adequate period of time, IM can usually be demonstrated (in the majority of these patients)”. Although this may at first seem logical, the results of a study from Northern Ireland do not support this logic.

We carried out a population‐based study of Barrett's oesophagus and examined pathology reports relating to all sets of oesophageal biopsies carried out in Northern Ireland (population 1.7 million) between January 1993 and December 1999.⁴ Biopsy specimens of Barrett's oesophagus were subdivided into those in which intestinal metaplasia was present and those in which it was absent. Patients in the cohort were followed up until death or development of oesophageal malignancy. A total of 4955 sets of biopsy specimens from 2969 patients met the criteria for Barrett's oesophagus. After a mean follow‐up of 3.7 (range 1–8) years, 29 oesophageal malignancies were found to have developed in the cohort. The incidence of oesophageal malignancy overall (per 100 person years of follow‐up) was 0.26; for patients with intestinal metaplasia the risk was 0.40 (95% confidence interval (CI) 0.26 to 0.59) and for those without intestinal metaplasia the risk was 0.06 (95% CI 0 to 0.32). In other words, if intestinal metaplasia was absent in biopsy specimens, the risk of oesophageal malignancy was not significantly higher than that in the normal population. Further, we found 93% concordance among the 2969 patients between intestinal metaplasia status on the first biopsy and that on any subsequent biopsy (unpublished data). Intestinal metaplasia seems to be either there from the start or absent. Given that these data are derived from “real world practice”, where probably few biopsy specimens per patient were taken and hence sampling error might have occurred, it is reassuring to find that the risk of malignancy in patients in whom intestinal metaplasia was not shown was low. These patients may have a “patchy” distribution of intestinal metaplasia in the segment of columnar mucosa that is biologically distinct from those where the distribution of intestinal metaplasia is uniform, but this is purely speculative.

Patients with Barrett's oesophagus are at low risk of oesophageal adenocarcinoma; refinement of surveillance programmes is needed to focus resources on those most likely to benefit from surveillance—perhaps concentrating on those patients in whom intestinal metaplasia is evident at initial endoscopy is one way to do this?