Alimentary Pharmacology and Therapeutics
Letters to the Editors Letter: incidence rates of Barrett’s oesophagus and oesophageal adenocarcinoma in the UK and the Netherlands C. Matuchansky Lariboisiere St-Louis Faculty of Medicine, Paris Diderot University, Paris, France. E-mail: [email protected] doi:10.1111/apt.12843
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, 5 Second, 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
ACKNOWLEDGEMENT Declaration of personal and funding interests: None. REFERENCES 1. Masclee GM, Coloma PM, Wilde M, Kuipers EJ, Sturkenboom MC. The incidence of Barrett’s oesophagus and oesophageal adenocarcinoma in the United Kingdom and the Netherlands is levelling off. Aliment Pharmacol Ther 2014; 39: 1321–30. 2. Savarino V, Di Mario F, Scarpignato C. Proton pump inhibitors in GORD. An overview of their pharmacology, efficacy and safety. Pharmacol Res 2009; 59: 135–53. 3. Cooper BT, Chapman W, Neumann CS, Gearty JC. Continuous treatment of Barrett’s oesophagus patients with proton pump inhibitors up to 13 years: observations on regression and cancer incidence. Aliment Pharmacol Ther 2006; 23: 727–33. 4. Kastelein F, Spaander MC, Steyerberg EW, et al. Proton pump inhibitors reduce the risk of neoplastic progression in patients with Barrett’s esophagus. Clin Gastroenterol Hepatol 2013; 11: 382–8. 5. Singh S, Garg SK, Singh PP, Iyer PG, El-Serag HB. Acidsuppressive medications and risk of oesophageal adenocarcinoma in patients with Barrett’s oesophagus: a systematic review and meta-analysis. Gut 2013; doi:10.1136/ gutjnl-2013-305997 [Epub ahead of print]. 6. Oberg S, Peters JH, DeMeester TR, et al. Inflammation and specialized intestinal metaplasia of cardiac mucosa is a manifestation of gastroesophageal reflux disease. Ann Surg 1997; 226: 522–32. 7. Bhat SK, McManus DT, Coleman HG, et al. Oesophageal adenocarcinoma and prior diagnosis of Barrett’s oesophagus: a population-based study. Gut 2014; doi: 10.1136/gutjnl-2013305506 [Epub ahead of print]. 8. Sharma P, Weston AP, Morales T, Topalovski M, Mayo MS, Sampliner RE. Relative risk of dysplasia for patients with intestinal metaplasia in the distal oesophagus and in the gastric cardia. Gut 2000; 46: 9–13. 9. Chandrasoma P, Wijetunge S, Demeester SR, Hagen J, Demeester TR. The histologic squamo-oxyntic gap: an accurate and reproducible diagnostic marker of gastroesophageal reflux disease. Am J Surg Pathol 2010; 34: 1574–81.
AP&T invited editoral and correspondence columns are restricted to letters discussing papers that have been published in the journal. A letter must have a maximum of 300 words, may contain one table or figure, and should have no more than 10 references. It should be submitted electronically to the Editors via http://mc.manuscriptcentral.com/apt.
ª 2014 John Wiley & Sons Ltd
403
Letters to the Editors Letter: incidence rates of Barrett’s oesophagus and oesophageal adenocarcinoma in the UK and the Netherlands C. Matuchansky Lariboisiere St-Louis Faculty of Medicine, Paris Diderot University, Paris, France. E-mail: [email protected] doi:10.1111/apt.12843
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, 5 Second, 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
ACKNOWLEDGEMENT Declaration of personal and funding interests: None. REFERENCES 1. Masclee GM, Coloma PM, Wilde M, Kuipers EJ, Sturkenboom MC. The incidence of Barrett’s oesophagus and oesophageal adenocarcinoma in the United Kingdom and the Netherlands is levelling off. Aliment Pharmacol Ther 2014; 39: 1321–30. 2. Savarino V, Di Mario F, Scarpignato C. Proton pump inhibitors in GORD. An overview of their pharmacology, efficacy and safety. Pharmacol Res 2009; 59: 135–53. 3. Cooper BT, Chapman W, Neumann CS, Gearty JC. Continuous treatment of Barrett’s oesophagus patients with proton pump inhibitors up to 13 years: observations on regression and cancer incidence. Aliment Pharmacol Ther 2006; 23: 727–33. 4. Kastelein F, Spaander MC, Steyerberg EW, et al. Proton pump inhibitors reduce the risk of neoplastic progression in patients with Barrett’s esophagus. Clin Gastroenterol Hepatol 2013; 11: 382–8. 5. Singh S, Garg SK, Singh PP, Iyer PG, El-Serag HB. Acidsuppressive medications and risk of oesophageal adenocarcinoma in patients with Barrett’s oesophagus: a systematic review and meta-analysis. Gut 2013; doi:10.1136/ gutjnl-2013-305997 [Epub ahead of print]. 6. Oberg S, Peters JH, DeMeester TR, et al. Inflammation and specialized intestinal metaplasia of cardiac mucosa is a manifestation of gastroesophageal reflux disease. Ann Surg 1997; 226: 522–32. 7. Bhat SK, McManus DT, Coleman HG, et al. Oesophageal adenocarcinoma and prior diagnosis of Barrett’s oesophagus: a population-based study. Gut 2014; doi: 10.1136/gutjnl-2013305506 [Epub ahead of print]. 8. Sharma P, Weston AP, Morales T, Topalovski M, Mayo MS, Sampliner RE. Relative risk of dysplasia for patients with intestinal metaplasia in the distal oesophagus and in the gastric cardia. Gut 2000; 46: 9–13. 9. Chandrasoma P, Wijetunge S, Demeester SR, Hagen J, Demeester TR. The histologic squamo-oxyntic gap: an accurate and reproducible diagnostic marker of gastroesophageal reflux disease. Am J Surg Pathol 2010; 34: 1574–81.
AP&T invited editoral and correspondence columns are restricted to letters discussing papers that have been published in the journal. A letter must have a maximum of 300 words, may contain one table or figure, and should have no more than 10 references. It should be submitted electronically to the Editors via http://mc.manuscriptcentral.com/apt.
ª 2014 John Wiley & Sons Ltd
403
