Letters

Surveillance for Barrett's oesophagus

BMJ 2001; 322 doi: https://doi.org/10.1136/bmj.322.7294.1124 (Published 05 May 2001) Cite this as: BMJ 2001;322:1124

The conundrum of Barrett's oesophagus is changing

  1. J A Eksteen (B.Eksteen@bham.ac.uk), lecturer in gastroenterology,
  2. Janusz A Jankowski, reader in medicine
  1. University of Birmingham, Queen Elizabeth Hospital, Birmingham B15 2TH
  2. Academic Unit of Epidemiology and Health Services Research, School of Medicine, University of Leeds, Leeds LS2 9JT
  3. Pathology Laboratory, South Warwickshire NHS Trust, Warwick CV34 5BJ
  4. James Paget Hospital, Great Yarmouth NR31 6LA
  5. Imperial College School of Medicine, Hammersmith Hospital, London W12 0NN
  6. Leicester General Hospital, Leicester LE5 4PW

    EDITOR—Macdonald et al in their paper and McGarrity in his accompanying editorial reviewed the value of endoscopic surveillance of Barrett's oesophagus. 1 2 Both articles highlighted the major problems with detection of oesophageal adenocarcinoma in an unselected group of individuals with Barrett's oesophagus.

    Much attention has been devoted to risk stratification of individuals who are at high risk of malignant change in Barrett's oesophagus. Men over 45 years, those with at least 3 cm of Barrett's metaplasia, those with severe and frequent reflux symptoms (>3 times week), those with chronic heartburn for 10 years or more, obese patients, those taking drugs which relax the lower oesophageal sphincter (such as nitrates), and perhaps those with eradicated Helicobacter pylori infection are most at risk of Barrett's associated adenocarcinoma.3

    Pathology has also made a major contribution to understanding the pathogenesis as intestinal type metaplasia gives rise to dysplastic clones from which the adenocarcinoma arises.3 Molecular genetics has been rigorously applied to samples along the sequence encompassing Barrett's metaplasia, dysplasia, and adenocarcinoma, and it 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

    We believe therefore that even in those patients with Barrett's oesophagus who are fit for surgery further selection for repeated endoscopic surveillance should be undertaken. In particular, a combination of clinical criteria, and, perhaps in the near future, genetics, can be used to stratify for surveillance those at high risk of Barrett's adenocarcinoma.

    References

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    It is too early to dismiss surveillance programmes

    1. Christopher Paul Wild (c.p.wild@leeds.ac.uk), professor of molecular epidemiology,
    2. David Forman, professor of cancer epidemiology
    1. University of Birmingham, Queen Elizabeth Hospital, Birmingham B15 2TH
    2. Academic Unit of Epidemiology and Health Services Research, School of Medicine, University of Leeds, Leeds LS2 9JT
    3. Pathology Laboratory, South Warwickshire NHS Trust, Warwick CV34 5BJ
    4. James Paget Hospital, Great Yarmouth NR31 6LA
    5. Imperial College School of Medicine, Hammersmith Hospital, London W12 0NN
    6. Leicester General Hospital, Leicester LE5 4PW

      EDITOR—Macdonald et al conclude that current surveillance strategies for patients with Barrett's oesophagus provide no benefit in terms of reduced …

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