OBJECTIVE
To perform a comprehensive assessment of the gastric mucosa in neuroendocrine neoplasm (NET) in patients of the North-Western regiom of Russia to identify the most significant risk factors for this type of malignant tumors.
MATERIAL AND METHODS
The study involved 6007 patients (4066 of them were women and 1941 men) who underwent video esophagogastroduodenoscopy with a test for H. pylori and OLGA biopsy and immunohistochemical typing, according to indications. Stomach malignancies of various types were detected in 126 patients (63 women and 63 men).
RESULTS
The group with NETs consisted of 23 patients, including 19 women and 4 men. During endoscopic examination, signs of atrophy were noted in most cases, only in 6 cases intestinal metaplasia was visually determined, and in 10 cases NET was suspected. Histological examination of biopsies was carried out in 20 out of 23 cases. No background chronic disease was detected in one patient, and chronic autoimmune atrophic gastritis was detected in the remaining 19 cases. The severity of OLGA atrophy was stage II or III. In all cases of fundal gastritis, pseudopyloric and intestinal metaplasia of the epithelium is noted. Neuroendocrine cell hyperplasia was detected in 3 studies, pancreatic metaplasia in 2. In one case, H. pylori infection was detected with contamination in all parts of the stomach. In the remaining patients, there was no inflammatory process in the antrum and no infection was detected.
CONCLUSION
The study brought us closer to understanding the background conditions in the gastric mucosa accompanying the formation of NETs. Analysis of changes in the gastric mucosa in our case showed that, in at least 19 cases out of 23, we were dealing with type I NETs (82.6%). The severity of atrophic changes does not always directly affect this process, and the presence of such additional findings as neuroendocrine cell hyperplasia and pancreatic metaplasia may be additional risk factors, and H. pylori infection, on the contrary, can be considered as a potential protective factor of this disease.
