Review of research area Intestinal metaplasia of the stomach (IM) is generally considered a precancerous lesion and is associated with a small increase in the risk of developing gastric cancer (GC). Endoscopic monitoring has been proposed to control the risk of endangered populations. However, due to the lower incidence of GC in the United States and other Western countries, there is no specific monitoring protocol. In general, there are no widely accepted guidelines for IM management. Recently, the European Endoscopic Society as well as other European academic companies have developed documented guidelines for the management of patients with IM.~These guidelines emphasize the increased risk of cancer in patients with gastric atrophy and IM and the need for staging in cases of high-grade dysplasia. Risk factors for IM include Helicobacter pylori infection, high NaCl intake, smoking, alcohol consumption and chronic biliary reflux.~The development of intestinal-type gastric carcinoma occurs in four stages: non-atrophic gastritis, multifocal atrophic gastritis, IM, and dysplasia. The IM of the gastric cardia and the Barrett's esophagus differ in the risk of malignancy. Elevated serum pepsinogen levels have been suggested as an indicator of extensive gastric atrophy. Currently, there are no reliable markers of gastric dysplasia or gastric cancer.~Based on the available data, it appears that the IM of the gastric cardia is a possible precursor to the development of intestinal-type carcinoma of the stomach. It has been found that 45% of patients with gastric carcinoma had residual IM, supporting the idea that IM is a particularly important precursor to its development. Histologically, the IM may be complete or incomplete. Complete (type I) intestinal metaplasia is defined by the mucosa of the small intestinal type with mature absorbent cells, cell cups, and a brush-like outline. Incomplete intestinal metaplasia (type II) secretes cialomycin and is similar to colonic epithelium with columns of intermediate cells at various stages of differentiation, irregular mucosal droplets and the absence of a brush limit. The highest risk of gastric cancer is associated with incomplete and / or extensive IM.~Recent studies show that microbial changes are related to the histological stages of gastric oncogenesis. Chronic H. pylori infection can cause inflammation of the mucosa and cause histological changes. It is also recognized as an important risk factor for GC. However, only 3% of patients infected with H. pylori develop GC. In addition, H. pylori has been found to be usually undetectable in GC samples. These studies suggest that H. pylori infection may only be an early event for the gastric mucosa, which will undergo further oncogenic changes and indicate the possible role of mucosal microbes, with the exception of H. pylori in the gastric carcinoma.~The dominant germ type in the gastric mucosa was found to be protein-secreted bacteria, in both H. pylori negative and positive for H. pylori samples. Two previous studies have shown that the microbial count in IM patients was found to be partially overlapped with the group of gastritis and cancer among patients with H. pylori infection. Li et al (2017) found that the microbial amount in gastritis samples overlapped mostly with that of IM samples. In contrast, the microflora of patients with IM and GC had significantly lower microbial richness, while the biodiversity of the microbiology of patients with overt gastritis (EG), chronic gastritis (CG) and IM was similar in total, with the exception of those with GC. These conflicting results suggest that IM may be the key point in microbial change and that there may be other qualitative factors involved in gastric oncogenesis, especially in patients with IM.~Research subject and objectives The study will be performed on patients undergoing gastroscopy who have IM and / or GC findings. In patients with IM, the microbiome will be analyzed and correlated with the type of IM (complete-incomplete). The same will be done for patients with GC (intestinal-type cancer).~Thematic area The aim of the study will be to analyze the microbiome in the blood and stomach in patients with intestinal metaplasia (IM) and / or gastric cancer (GC). As far as IM is concerned, it has been found that the incomplete type is related to GC mainly intestinal-type. Studies show differences in the microbiome in patients with IM and in patients with GC, but do not specify whether these differences are related to histological types.~Our intention is to further analyze the microbiome based on histological types. Most studies on stomach cancer have focused on the microbiota of gastric microbiota. Recent data have shown that the microbiome of the small intestine, especially the mucosa, can play a key role in the condition of the gastrointestinal tract. Disturbance of the microbiome of the small intestine has been found in celiac disease, chronic liver disease, diabetes and irritable bowel syndrome. However, information on the role of the microbiome in IM remains limited.~Keywords Gastric intestinal metaplasia, Complete Type, Incomplete Type, Gastric Cancer, Microbiome
The aim of the study will be to analyze the microbiome in the blood and stomach in patients with intestinal metaplasia (IM) and / or gastric cancer (GC). As far as IM is concerned, it has been found that the incomplete type is related to GC mainly intestinal-type. Studies show differences in the microbiome in patients with IM and in patients with GC, but do not specify whether these differences are related to histological types.~Our intention is to further analyze the microbiome based on histological types. Most studies on stomach cancer have focused on the microbiota of gastric microbiota. Recent data have shown that the microbiome of the small intestine, especially the mucosa, can play a key role in the condition of the gastrointestinal tract. Disturbance of the microbiome of the small intestine has been found in celiac disease, chronic liver disease, diabetes and irritable bowel syndrome. However, information on the role of the microbiome in IM remains limited.