Microbiome Analysis in Patients With Gastric Intestinal Metaplasia and in Patients With Gastric Cancer and Correlation With the Subtypes of the Lesions

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.