SIRS, I read with great interest the article by Masclee et al.1 who showed, in a dynamic population-based retrospective cohort study in the UK and the Netherlands that the incidence rates of Barrett's oesophagus (BO) increased from 2000 to 2003, but levelled off thereafter. I have two main concerns regarding their article. First, the relevant medical information, in the population-based registries which served as data sources, included drug prescriptions and/or use. It would have been worth knowing the yearly incidence rates, throughout the study period, of prescriptions [particularly of proton pump inhibitors (PPIs)], as compared with BO and oesophageal adenocarcinoma (OAC) incidence rates. Indeed, despite the strong rationale for the use of PPIs in BO, many clinical trials using PPIs did not show relevant BO regression.2, 3 Yet, once BO is installed, PPIs have been associated with a significant decrease in highgrade dysplasia and OAC arising from BO.
4, 5Second, Masclee et al. outline that, in contrast to BO, the OAC incidence rate continued to increase until now, which may reflect the long lag time between BO and high-grade dysplasia and OAC. Another hypothesis may be raised: as no evidence of BO is found in most cases of incident diagnoses of OAC,6,7 at least part of these might arise from high-grade dysplasia developed in specific intestinal metaplasia in the gastric cardia, at the anatomical gastro-oesophageal junction (GOJ) and without evidence of classical or short-segment BO.Intestinal metaplasia in the GOJ region may comprise two distinct entities: short-segment BO (specific intestinal metaplasia in the distal oesophagus), and metaplastic gastric carditis. 8 The possible pre-malignant role of the latter has been minimised, 8 but prospective studies separating these two entities are lacking. Carditis and intestinal metaplasia of the GOJ have indeed been considered as early histological indicators of gastro-oesophageal reflux disease.6, 9