The protracted inflammation of the gastric mucosa induces profound changes in the microenvironment of the gastric cells. These changes modify the molecular signals that orchestrate morphogenesis and cell differentiation in the stem cells of the crypts. The expression of this adjustment to the new microenvironment is evidenced by the appearance of differentiated metaplastic cells (intestinal, bronchial—ciliated, pancreatic or (pseudo) pyloric, all deriving from the same embryological origin). The inability of stem cells to readapt to the new microenvironment may lead to genomic aberrations such as the retention of cellular products (glassy cells) or to neoplastic transformation. In this report, parameters such as gastric mucosal inflammation, Helicobacter pylori, atrophy, intestinal metaplasia and/or pseudopyloric metaplasia found in gastric biopsy specimens were individually classified according to their extension in sections as grade 1 (focal distribution in sections from individual biopsy specimens) and grade 2 (present in the entire width—distance across—in sections from individual biopsy specimen). The rationale is that a biopsy grade 2 was harvested from a larger mucosal area having that particular change. Each individual parameter gives a score, and the sum of all individual scores gives the total score. The proposed system might allow monitoring the results of treatment in follow-up biopsies. Divergent clinical results in the frequency/incidence of gastritis (including body–autoimmune gastritis), of H pylori strains, of various metaplasias and neoplasias, in disparate geographical regions substantiate the conviction that these parameters are much influenced by the environment. This knowledge is crucial, considering that environmental diseases are theoretically preventable.
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Published Online First 8 September 2006
Competing interests: None declared.
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