RESUMO
BACKGROUND/AIMS: Mucosal atrophy is defined as the loss of appropriate glands in the gastric mucosa; such a finding suggests that this malady is associated with an excessive ratio of apoptotic cells to proliferating epithelial cells. However, exactly why the genesis and progression of the atrophic changes takes place in the gastric mucosa of some, but not all of the subjects infected with H. pylori, is seldom described. TGF-beta1 (transforming growth factor-beta1) is a potent growth inhibitor in epithelial tissues, and it also induces apoptosis of epithelial cells. We evaluated its role in the pathogenesis of atrophic gastritis by analyzing the expression of TGF-beta1. METHODS: The subjects were 14 patients with chronic atrophic gastritis and 43 patients with chronic gastritis. The exclusion criteria were as follows; those patients who had a previous history of gastrectomy, PPI, H. pylori eradication, NSAIDs, stomach cancer and/or a severe bleeding tendency. Biopsy specimens were obtained from the antrum, angle and body of the stomach, respectively and we performed RT-PCR for determining the expression of TGF-beta1 mRNA with using an additional angle specimen. RESULTS: The clinical parameters were similar in both groups. The rate of H. pylori infection was also similar in both groups. The TGF-beta1 levels were significantly higher for the chronic atrophic gastritis group than for the chronic gastritis group. CONCLUSIONS: The results that the TGF-beta1 levels are significantly higher in the chronic atrophic gastritis group suggest that TGF-beta1 is associated with the development of atrophic gastritis. The apoptotic process induced by TGF-beta1 may be linked to the development of atrophic gastritis.