Abstract
The aim of the study was to ascertain the existence of intestinal metaplasia in gastric mucosa of patients with gastric carcinoma coupled with H. pylori positive chronic atrophic gastritis and possible connection of IM with the development of gastric carcinoma. The paper presents prospective study that included 50 patients with gastric carcinoma and 50 patients with chronic atrophic H. pylori positive gastritis. All the patients were subjected to gastroscopy as well as biopsy targeted at antrum, lesser curvature and corpus and at the area 1-2 cm removed from tumor lesion. Biopsy samples were sliced by microtome and stained. We analyzed presence, frequency and severity of inflammatory-regenerative, metaplastic and dysplastic changes in the mucosa and evaluated their prognostic value. We typed IM immunohistochemically. This study confirmed responsibility of H. pylori for inflammatory events in gastric mucosa in patients with gastric carcinoma. According to our findings incomplete IM of types IIa and IIb as precancerous lesion is responsible for the development of gastric carcinoma and is associated with chronic atrophic gastritis grade I and II (92% of subjects, p=0.0097, h=1, p=0.01). Thus, the finding of incomplete intestinal metaplasia may be used as an indicator for early gastric carcinoma detection. Patients with patho-histologically verified incomplete intestinal metaplasia associated with active chronic atrophic gastritis of levels I and II represent risk group for the development of gastric carcinoma of intestinal type.
Highlights
H. pylori induced chronic atrophic gastritis (CAG) is a precancerous condition accompanied by gradual loss in epithelia differentiation that eventually leads towards carcinoma
In our research we found incomplete Intestinal metaplasia (IM) type IIb in only ( ) patients with gastric carcinoma
Based on the results of our research we may conclude that IM as precancerous lesion is responsible for the development of gastric carcinoma
Summary
H. pylori induced chronic atrophic gastritis (CAG) is a precancerous condition accompanied by gradual loss in epithelia differentiation that eventually leads towards carcinoma. Intestinal metaplasia (IM) as precancerous lesion is either partial or complete transformation of gastric glands epithelial cells into the intestinal type. It may appear either in antrum or pylorus mucosa or diffusely. Complete type of mature IM is characterized by histology, mucine histochemistry, enzymes and endocrine cells identical to those found in small intestine. Pathohistological features of this type are columnar absorptive cells, multiplied goblet cells that contain predominantly acid mucines, Paneth’s non-differentiated cells and Moendocrine cells. Hyperplastic glands laid with juvenile non-differentiated cells with hyper-chromic nuclei and increased mitotic index develop in the process. Positive correlation between H. pylori infection and IM type II is noted in patients with gastric carcinoma
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