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Chronic gastritis has a high incidence in adults, causing progressive destruction of glandular structures, favoring the development of gastric atrophy. The association of chronic gastritis with intestinal type metaplasia of gastric mucosa has a poor outcome as intestinal metaplasia is regarded as a precancerous lesion. Metaplasia is common in patients with Helicobacter pylori infection and also heavy smokers. The aim of our study was to evaluate the relationship between chronic gastritis and intestinal metaplasia. The study was conducted on a total of 1218 patients, aged between 5 and 90 years, who presented for dyspeptic disorders in the period 2007-2010 and were examined clinically and endoscopically. During the gastroscopic examination, fragments of gastric mucosa were collected for the histopathological study and for highlighting the H. pylori infection. For the histopathological study, the Hematoxylin-Eosin and PAS-Alcian Blue stains were performed, while for the immunohistochemical study the anti-TAG72 and anti-PCNA antibodies were used. A diagnosis of gastritis was established in 615 patients, representing approximately 50.5% of all cases. Most cases with gastritis were found in people of middle age. Gastritis was present in almost all age groups, from teenagers to the elders. Of the 615 cases of gastritis, urease test was positive in 353 patients, representing approximately 57.40% of all patients with gastritis. Histopathological examination identified the presence of intestinal metaplasia in 61.60% of patients with chronic gastritis, mostly complete metaplasia. PCNA immunohistochemistry revealed that cell proliferation processes are intensified in intestinal metaplasia. This study highlights the importance of chronic gastritis, intestinal metaplasia, and H. pylori infection in the etiopathogeny of gastric cancer.

Metaplasia represents the process of transforming a well-differentiated adult tissue into another type of adult tissue. Pancreatic metaplasia of the gastric mucosa represents the process in which the normal mucosa of the stomach is replaced with pancreatic formations, which mimic the structure of pancreatic acini. We describe the case of a male patient aged 39 who was admitted for abdominal pain, vomiting, hematemesis, melena, pale teguments, intense perspiration and nausea. The patient underwent surgery for suturing a perforated duodenal ulcer five years prior to this episode (2002). A gastric ulcer complicated with superior digestive bleeding and a chronic duodenal ulcer complicated with partial stenosis and perivisceritis were found during surgery. Gastric wall fragments were harvested and underwent usual histological techniques and immunohistochemistry. We found an ulceration from the gastric mucosa to the submucosa, covered by fibrino-leukocytic detritus. In the mucosal chorion we found numerous round or oval shaped nested formations which occupied the lower two thirds of the chorion, to the muscularis mucosae. Some metaplasic acini contain cells variable in shape, color and immunophenotype. Surrounding the nested acini we found tubular formations, formed of cubic shaped cells, representing excretory canals which were continued by gastric glands or opened directly in the crypts of the gastric epithelium.