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The subtleties of intestinal metaplasia
  1. Institut Curie-Research Division
  2. Paris, France
  1. Dr S Robine, Institut Curie-Research Division, UMR 144 CNRS Laboratory, Morphogenesis et Cellular Signalisation, 26 Rue D'Ulm, Fr-75231, Paris Cedex 05, France.sylvie.robine{at}

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Even if its incidence has decreased due to the influence of environmental and nutritional factors, gastric carcinoma remains a major concern because of its very poor prognosis. Screening for precancerous conditions, including intestinal metaplasia, is one method of improving the prognosis of gastric carcinoma. Nevertheless, the implications for the use of endoscopic surveillance in patients with intestinal metaplasia of the stomach are still unknown.

As suggested by Grötzinger et al in this issue of Gut,1 molecular changes (gain or loss of protein expression) are undoubtedly the first sign of metaplasia; the use of antibodies against specific proteins of the small intestine such as LI-cadherin or villin may help to diagnose metaplasia (see page 73).2 None the less, we cannot substitute the histological definition of intestinal metaplasia with molecular changes or “subtle metaplasia”, as it is called by the authors, until the prognostic value, and particularly the relationship between protein expression and risk of cancer, have been assessed in greater detail.

Intestinal metaplasia of the stomach is characterised by morphological similarity to the enterocytes, Paneth cells, and goblet cells; it shows characteristics of absorbing mucosa, the presence of a striated border, and brush border structures. Histopathological and histochemical studies allow the identification of at least two types of intestinal metaplasia: (1) complete type, also designated type I, which is characterised by the presence of absorptive cells, Paneth cells, and goblet cells secreting sialomucins, and corresponds to the small intestine phenotype; and (2) incomplete type, including types II and III, which is characterised by the presence of columnar and goblets cells secreting sialomucins (type II) and sulphomucins (type III).3 It has been shown that type III intestinal metaplasia is associated with an increased risk of malignant transformation whereas the putative value of types I and II intestinal metaplasia remains controversial.4 Intestinal metaplasia of the stomach is frequent and we should continue to find markers that can distinguish between patients at low and high risk of developing carcinoma. The subcellular distribution of LI-cadherin or semiquantative estimation of immunoreactivity according to the type of metaplasia have to be studied: they may be helpful in discriminating between patients in terms of prognosis.

The currently accepted hypothesis is that gastric carcinogenesis involves a series of histological stages from normal gastric epithelium to intestinal-type gastric carcinoma, constituting sequential steps in the process of human gastric carcinogenesis. However, it is not clear whether intestinal metaplasia constitutes a precancerous lesion in itself or provides a milieu conducive to cancer growth in the surrounding mucosa. Grötzinger et alspeculate on a role for LI-cadherin in the morphogenesis of tumour cells. Early induction of LI-cadherin in metaplasia and late loss of expression in undifferentiated adenocarcinoma may merely reflect differentiation rather than a role for LI-cadherin in the morphogenesis of tumour cells. On the other hand, the different patterns of LI-cadherin localisation in the various types of neoplasia may suggest a role in morphogenesis.

See article on page 73


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