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Risk of gastric carcinoma in patients with atrophic gastritis and intestinal metaplasia
  1. J Y Kang,
  2. C Finlayson,
  3. J D Maxwell,
  4. P Neild
  1. Departments of Gastroenterology and Histopathology, St George’s Hospital, London, UK.
  1. Correspondence to:
    J Y Kang, Department of Gastroenterology, St George’s Hospital, Blackshaw Road, London SW17 0QT, UK;
    jykang{at}sghms.ac.uk

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We read with interest the study of Whiting et al (

) in which they reported an 11% risk of development of malignancy among patients with atrophic gastritis and intestinal metaplasia over a 10 year period. We agree with their conclusion that their findings should be further evaluated in larger studies, as confirmation of a high risk of malignancy would have important implications for clinical practice. We would however like to raise two issues.

Firstly, in Whiting’s study, biopsies were taken only when there was macroscopic abnormality. These patients may therefore not be representative of the general population of dyspeptic patients with intestinal metaplasia.

We analysed 100 consecutive patients endoscoped for uncomplicated gastro-oesophageal reflux disease or functional dyspepsia for whom two biopsies were taken routinely from the antrum, body, and cardia, irrespective of macroscopic findings. The proportions of our patients with intestinal metaplasia, atrophic gastritis, both, or either were 17%, 27%, 6%, and 38%, respectively. Twenty of 27 patients with atrophy had mild changes: seven had moderate changes and none had severe atrophic gastritis. In four of 17 patients, intestinal metaplasia was widespread: 13 had focal changes. Thirty seven patients had Helicobacter pylori gastritis: 23 of these had concomitant atrophic gastritis and/or intestinal metaplasia. It seems unlikely that 4% (38%×11%) of our patients will develop gastric cancer over the next 10 years.

Our patients with atrophic gastritis and intestinal metaplasia are more representative of the general dyspeptic population and a different group from those studied by Whiting et al. Perhaps the high risk of malignancy they describe is associated with a combination of macroscopic abnormalities, the severity of the changes, the type of intestinal metaplasia, concomitant occurrence of intestinal metaplasia, atrophic gastritis, and H pylori infection rather than the histological findings per se. Long term follow up of a representative population of UK patients with uncomplicated dyspepsia is warranted. Meanwhile, we are concerned that their findings should not be uncritically extrapolated as the basis for surveillance recommendations for patients with uncomplicated dyspepsia and atrophic gastritis and/or intestinal metaplasia.

Secondly, what was the H pylori status of their patients with intestinal metaplasia and atrophic gastritis? In Uemura et al’s follow up study of 1526 Japanese patients over a mean period of 7.8 years,1 gastric cancers developed in 2.9% of patients infected with H pylori but in none of the uninfected patients. Among patients with H pylori infection, those with severe gastric atrophy, intestinal metaplasia, and corpus predominant gastritis were at significantly higher risk. If the patients described by Whiting et al were H pylori positive, antibiotic treatment may be a more cost effective approach compared with endoscopic surveillance.3

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