Intestinal
metaplasia is defined as the appearance of intestinal epithelium in the stomach. Intestinal
metaplasia is frequently found in populations with a high incidence of
gastric cancer. Macroscopic demonstration of
sucrase and
trehalase with
Tes-tape in many resected stomachs yielded new information for understanding the nature of intestinal
metaplasia. Intestinal
metaplasia can be classified into two types, complete and incomplete. The former is associated with the presence of
sucrase,
trehalase,
leucine aminopeptidase,
alkaline phosphatase, goblet cells and Paneth cells, and the latter with that of
sucrase,
leucine aminopeptidase and goblet cells, but not
trehalase or Paneth cells. Goblet cells in the complete type of intestinal
metaplasia contain
sialomucin, as does the small intestine, while those in the incomplete type contain
sulphomucin and
sialomucin, as does the large intestine. Well-differentiated
adenocarcinoma is closely related to intestinal
metaplasia, especially the incomplete type. Atypical epithelium of intestinal
metaplasia has been proposed as a more proximate stage of
gastric cancer. Intestinal
metaplasia can be diagnosed by staining with
dye under endoscopic observation. A reduced level of
pepsinogen I in the blood reflects the presence of severe intestinal
metaplasia, which is understood to be a sign of high risk of
gastric cancer. Intestinal
metaplasia is supposed to be produced by components of food.
Mutagens/
carcinogens such as N-methyl-N'-nitro-soguanidine and N-
propyl-N'-nitro-N-nitrosoguanidine can produce intestinal
metaplasia in the glandular stomach of rats and
gastric cancers. The formation of intestinal
metaplasia precedes the appearance of
adenocarcinoma in the glandular stomach. Intestinal
metaplasia, which is a kind of host reaction to environmental agents, may result either from genetic change - change in
DNA structure - or from epigenetic change - change in the differentiation mechanism. Preventive measures could be developed to suppress the development of intestinal
metaplasia and to suppress the process of conversion of metaplastic cells to
cancer cells.