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We read with interest the paper by Whiting et al (Gut 2002;50:378–81) regarding the surveillance of premalignant gastric lesions. The authors reported that over 10 years, 12 cancers (11.5%) were diagnosed in 104 patients with intestinal metaplasia and/or atrophic gastritis. Therefore, they suggest that these patients have an increased risk of developing gastric cancer, and benefit from annual endoscopic follow up.
Although we agree with the major conclusions of the study, our experience is somehow different. In fact, we have recently investigated the timing of first endoscopic-histological follow up of patients with body predominant atrophic gastritis and demonstrated that four years seems a satisfactory interval for the first follow up of these patients.1 The timing of surveillance should be safe enough not to miss malignancies at early stages but very close follow up may affect compliance. In fact, Whiting et al underlined how the proposed annual surveillance protocol was accepted by less than 50% of their patients. Thus it may be speculated that a number of cancers equal to those diagnosed may have been missed. In our population compliance was similar among patients who had follow up proposed at two or four years (73% v 64.5%), and we found no malignancies at the two year follow up, with only one carcinoid tumour at four years, despite a detailed histological sampling, including an accurate evaluation of ECL cell patterns.1 In fact, we have demonstrated that this approach can address further evaluations for patients at high risk of developing carcinoid tumours.2 Unfortunately, in Whiting’s paper the time interval from the diagnosis of atrophy and/or metaplasia to that of cancer is not clearly reported, making comparisons difficult, given also the lower number of our patients and the different ethnicities.
Furthermore, while we evaluated only patients with atrophy and metaplasia of the gastric body, in Whiting’s paper histological details are not given. It is well known that the diagnosis of atrophic gastritis is difficult, with poor agreement even among expert pathologists and it has been recommended to diagnose “atrophy” only when appropriate gastric glands are replaced by intestinal epithelium or by fibrosis.3 Therefore, as the authors state that patients were included in the group at higher risk when more than one risk factor was present, we assume that all intestinal metaplasia patients had atrophy also. The number and site of biopsies needed to define the topography of atrophy and metaplasia in the antral or corporal mucosa are also important. In fact, it has been demonstrated that corpus predominant gastritis related hypoachlorhydria is a key factor in the multistep carcinogenesis cascade.4
Moreover, in Whiting’s study, Helicobacter pylori infection was not mentioned, even in patients enrolled between 1984 and 1988 and followed annually for 10 years, a period in which it has become widely accepted that patients with H pylori infection and premalignant changes deserve antimicrobial therapy,5 even if the possible effect of H pylori cure in premalignant conditions is still a matter of discussion.6
It would therefore have been interesting to know whether in Whiting’s study malignancies at follow up occurred more frequently in patients with atrophic changes and metaplasia in the gastric body or in those who were H pylori positive, but these data were not provided.
In conclusion, while we agree that surveillance of patients with atrophic gastritis is an important goal that deserves attention, we believe that other large prospective studies are needed to establish the best timing of follow up and histological protocols to optimise resources and join compliance and early diagnosis of gastric malignancies.
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