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EDITORIALS: Thomas J McGarrity Barrett's oesophagus: the continuing conundrum BMJ 2000; 321: 1238-1239 [Full text]

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Barrett’s oesophagus: the conundrum changes!

J A Eksteen   (20 November 2000)

Barrett's screening is a fad

John R Bennett   (22 November 2000)

Selecting patient's for follow-up in Barrett's oesophagus.

Richard A Carr   (1 December 2000)

Barrett's oesophagus: the continuing conundrum

K Ragunath   (16 January 2001)

Barrett’s oesophagus: the conundrum changes! 20 November 2000
J A Eksteen, Lecturer Gastroenterology University of Birmingham, Queen Elizabeth Hospital Send response to journal: Re: Barrett’s oesophagus: the conundrum changes!	We read with much interest the paper by Macdonald et al. (1), and the accompanying editorial by McGarrity (2) regarding the value of endoscopic surveillance of Barrett’s oesophagus. Both articles highlighted the major problems with detection of oesophageal adenocarcinoma in an unselected group of individuals with Barrett’s oesophagus. Recently much attention has been devoted to risk stratification of individuals who are at high risk of malignant change in Barrett’s oesophagus. In particular we understand that males over 45 years, those with at least 3cm of Barrett’s metaplasia, those with severe and frequent reflux symptoms (> 3 times week), those with chronic heartburn for 10 years or more, the obese, those taking medication which relaxes the lower oesophageal sphincter (such as nitrates) and perhaps those with eradicated helicobacter pylori organisms are most at risk from Barrett’s associated adenocarcinoma (3). Pathology has also made a major contribution to understanding the pathogenesis since we realise that intestinal-type metaplasia gives rise to dysplastic clones from which the adenocarcinoma arises (3). Molecular genetics has been rigorously applied to samples along the Barrett’s metaplasia-dysplasia- adenocarcinoma sequence and has yielded important information about key genetic alterations (4). Furthermore information of those with a family history of gastro-oesophageal cancer has also yielded rare but none the less important genetic defects, which can and should be considered for application to familial clusters of disease including germ line mutations of the cell-cell adhesion molecule E-cadherin (5). In conclusion we believe, therefore that even in those individuals with Barrett’s oesophagus fit for surgery further selection for repeated endoscopic surveillance should occur. In particular a combination of clinical criteria, and perhaps in the near future genetics, can be used to stratify those of high risk for Barrett’s adenocarcinoma for surveillance. 1. MacDonald CE, Wicks AC, Playford RJ. Final results from 10-year cohort of patients undergoing surveillance for Barrett’s oesophagus: observational study. Brit Med J 2000;321:1252-54 2. McGarrity TJ. Barrett’s oesophagus: the continuing conundrum. Brit Med J 2000;321:1238-39 3. Jankowski J, Wright NA, Meltzer S, Triadafilopoulos G, Geboes K, Casson A, Kerr D, Young LS. Molecular evolution of the metaplasia dysplasia adenocarcinoma sequence in the esophagus (MCS). Am J Pathol 1999;154:965-974. 4. Jankowski J, Harrison RF, Perry I, Balkwill F, Tselepis C. Propagation of Barrett’s metaplasia: the simmering cauldron. Lancet (in press) 5. Jankowski J, Perry I, Harrison RF. Gastro-oesophageal cancer: death at the junction. Understanding changes at the molecular level could lead to screening opportunities. Brit Med J 2000;321:463-4. J A Eksteen MB ChB MRCP Lecturer in Gastroenterology University of Birmingham, Queen Elizabeth Hospital, Edgebaston, Birmingham, B15 2TH B.Eksteen@bham.ac.uk Janusz A Jankowski MD, PhD, FRCP (Edinburgh and London) Reader in Medicine University of Birmingham, Queen Elizabeth Hospital, Edgebaston, Birmingham, B15 2TH
Barrett's screening is a fad 22 November 2000
John R Bennett, Retired gastro-enterologist Send response to journal: Re: Barrett's screening is a fad	On the page before the excellent study by Macdonald et al. showing the ineffectiveness of endoscopic screening of patients with Barrett's you printed an "Endpiece"quoting Pliny the Elder "One is instantly reminded of the malign influence of fashion on medicine, more that any other science. Even nowadays it is subject to fads, although no science is actually more profitable."
Selecting patient's for follow-up in Barrett's oesophagus. 1 December 2000
Richard A Carr, Consultant Histopathologist South Warwickshire General Hospitals NHS Trust Send response to journal: Re: Selecting patient's for follow-up in Barrett's oesophagus.	I read with interest the paper of Madonald et al which presented the results of a 10 year cohort of patient's diagnosed with Barrett's oesophagus. The majority of deaths (n=134, table 2 in their paper)were not related to the stomach or oesophagus, however in total 7 deaths were stated to be due to carcinomas of the oesophagus and stomach i.e. 5.2% in a follow-up period of approximately 10 years. Only 5 patients had mild dysplasia in the study (which includes 409 patients). They concluded that in their cohort the surveilance was not of direct benefit to an individual patient. In my opinion the results of this study cannot be extrapolated to the wider community of patients with Barrett's oesophagus. The risk of death from oesophageal or stomach carcinoma in patients with Barrett's oesophagus in their study of the order of 5.2% in only 10 years of follow- up seems fairly high. Surely if Barrett's oesophagus is only a pre- disposing condition to the development of malignancy and little is known of natural history of the condition it is impossible to state which individual patient's would benefit from regular surveilance. There may be a long time lag e.g. 20 to 40 years between the development of dysplasia and malignancy. Barrett's oesophagus may be only be a risk for developing dysplasia which itself may be present for many years before carcinoma develops. While I wholeheartedly support their comment that "centres that have recruited large numbers of patients into surveillance programmes should formally audit the value of their own programmes and publish the results so that metanalayses can be performed." I would guess that it would require a hugh number of death's and sub-groups analyses e.g. young patients with Barrett's oesophagus and those with dysplasia before results could be used to advise individual patiens of the benefit of surveillance. I worry about extrapolating the results of any study of this nature to individual patients. I think that although there are many consistent variables in the pathways to developing malignancy there are many individual factors both genetic and enviromental that probably suggest that follow-up in any individual patient should be tailored to their individual circumstances. If I was an average 34 year old and had Barrett's oesophagus would I want regular surveillance? Proabably not based on current evidence but if I had some adverse genetic/enviromental/pathological features I might feel very differently. I might also be grateful to know in order to modify risk factors and present earlier if I became symptomatic. The cost/benefit for routine surveillance of uncomplicated (by dysplasia) Barrett's oesophagus in medically fit, asymptomatic, patients does not seem good for the cash/personell strapped NHS where a second class service prevails. In a first class service with unlimited resources however the conclusion might be entirely different particularly for selected patients.
Barrett's oesophagus: the continuing conundrum 16 January 2001
K Ragunath Send response to journal: Re: Barrett's oesophagus: the continuing conundrum	Editor - The editorial by McGarrity1 discuses the current management dilemmas in Barrett's oesophagus. Barrett's oesophagus is premalignant, and acid reflux predisposes to this condition. Inspite of potent acid suppressants the incidence of adenoarcinoma of the oesophagus continues to rise. The study by Lagergen et al2 raises interesting questions and we cannot ignore reflux symptoms lightly. Perhaps more attention should be paid on the management of these symptoms rather than identify a long-term consequence of their presence. McGarrity states that only surgically fit patients with Barrett's oesophagus should be surveyed. He also states that patients with high- grade dysplasia (HGD) should be seriously considered for surgery and a selected group may be subjected to vigorous biopsy protocol or considered for ablative treatment. Oesophagectomy does offer complete cure, but only a minority of patients will fall into this category. However, the mortality and morbidity is significant even in specialist centres. With the emergence of alternative non-surgical (endoscopic) treatment including photodynamic therapy3, argon plasma coagulation4 and endoscopic mucosal resection5, patients who are otherwise surgically unfit or unwilling for surgery should be given the option of surveillance. These endoscopic therapeutic procedures are undergoing assessment but may well become standard treatment in the future. Ablation therapy combined with control of acid reflux is showing great promise as a minimally invasive approach to Barrett's oesophagus with dysplasia. However, the benefits of the treatment remain as yet unproven and the results of controlled trials are awaited. We are learning more about the molecular biology of Barrett's oesophagus, which may help in patient selection. If we selectively survey only surgically fit patients we are not doing justice to the surgically unfit patients or the patients not willing for surgery who may benefit from endoscopic treatment. Considerable attention is being paid by the gastrointestinal community to the identification and management of Barrett's oesophagus, whether by pharmacotherapeutics or anti-reflux surgery. Perhaps a greater emphasis should be placed on the prevention of development of columnar lined oesophagus by the appropriate treatment of reflux symptoms. Competing interest: None declared Dr K Ragunath Research Registrar Professor N Krasner Consultant Gastroenterologist Gastrointestinal Unit, University Hospital Aintree, Liverpool L9 7AL 1. McGarrity TJ. Barrett's oesophagus: the continuing conundrum.BMJ 2000;321:1238-9. 2. Lagergren J, Bergström R, Lindgren A, Nyrén O. Symptomatic gastroesophageal reflux as risk factor for oesophageal adenocarcinoma. N Engl J Med 1999;340:825-31. 3. Overholt BF, Panjehpour M, Haydeck JM. Photodynamic therapy for Barrett's oesophagus: follow-up in 100 patients. Gastrointest Endo 1999;49:1-7. 4. Schulz H, Miehlke S, Antos D, Schentke KU, Veith M et al. Ablation of Barrett's epithelium by endoscopic argon plasma coagulation in combination with high-dose omeprazole. Gastrointest Endo 2000;51:659-63. 5. Ell C, May A, Gossner L, Pech O, Günter E et al. Endoscopic mucosal resection of early cancer and high-grade dysplasia in Barrett's oesophagus. Gastroenterology 2000;118;670-677.