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Endoscopic surveillance of premalignant gastric lesions
  1. S Sebastian,
  2. J Seery,
  3. C O’Morain,
  4. M Buckley
  1. Department of Gastroenterology, Adelaide and Meath Hospital, Dublin, Ireland.
  1. Correspondence to:
    Dr M Buckley Department of Gastroenterology, Adelaide and Meath Hospital, Tallaght, Dublin 24, Ireland;
    martin.buckley{at}amnch.ie

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We read with interest the study by Whiting and colleagues (Gut 2002:50:37881). The study has further highlighted the importance of early detection of gastric cancer and also given further emphasis on ways to prevent the multistep progression in gastric carcinogenesis. However, we would like to make the following comments.

Firstly, one in five patients in this group had lesions which, according to Whiting et al, should be followed up by yearly endoscopies. Despite the low acceptance rate in screening programmes as noted by the authors, this would create an enormous workload on already over burdene endoscopic units. Clearly, further modes of selection of high risk patients with atrophy and metaplasia is desirable. Mutations in p53, APC, and mismatch repair genes have been reported in intestinal metaplasia. Some of these mutations are associated with an enhanced progression to advanced lesions in the multistep sequence of gastric carcinogenesis.1 High throughput methods for the detection of gene polymorphisms associated with increased cancer risk, such as interleukin 1 polymorphisms, are likely to be available in the near future .2 In addition, alteration in gastric secretion of pepsinogen may be used as an aid in early detection of premalignant lesions.

Secondly, the authors have not provided us with data regarding the Helicobacter pylori status of the patients. Their results may have been different if successful eradication of H pylori was achieved in the follow up group, a situation more relevant to current practice. It is now universally accepted that H pylori infection is the most important factor in gastric carcinogenesis with both host and bacterial virulence factors playing a role.3

The European Helicobacter pylori Study Group strongly recommended H pylori eradication for patients with atrophic gastritis, after gastric cancer resection, and first degree relatives of patients with gastric cancer (presented at the Maastricht 2–2000 conference4). There are emerging data that intestinal metaplasia may be replaced by normal gastric mucosa following H pylori eradication.5

In summary, we feel that less invasive and more cost effective modes for detection and follow up of premalignant gastric lesions are required and hopefully are on the horizon. In the meantime, it appears that a screen and treat strategy for H pylori constitutes one of the most important interventions in the prevention of gastric cancer.

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