Non-erosive gastritis

Non-erosive gastritis refers to a group of different histological changes that occur mainly as a result of Helicobacter pylori infection. In most patients, the disease is asymptomatic. Changes are detected by endoscopy. Treatment of non-erosive gastritis is aimed at destroying H. Pylori and sometimes suppressing acidity.

Read also:

• Gastritis
• Chronic gastritis caused by Helicobacter pylori
• Erosive gastritis

[1], [2], [3], [4]

Pathomorphology of non-erosive gastritis

Superficial gastritis

Lymphocytes, plasma cells together with neutrophils predominate in the zone of infiltration inflammation. Inflammation, as a rule, is superficial and can seize the antrum, the body of the stomach or both. This process is usually not accompanied by atrophy or metaplasia of the mucosa. The prevalence of the disease increases with age.

Deep gastritis

Deep gastritis, most likely, has a number of clinical manifestations (symptoms) (eg, indeterminate dyspepsia). Mononuclear cells and neutrophils infiltrate the entire mucosa to the muscular layer, but phlegmon or crypt abscesses rarely develop, despite such infiltration. The spread of the process may be heterogeneous. There may be surface gastritis, as well as partial atrophy of glands and metaplasia.

[5], [6]

Gastric atrophy

Atrophy of the gastric glands can be observed with gastritis, most often a prolonged antrum-gastritis (in the presence of Hp-infection is called type B). Some patients with atrophic gastritis detect autoantibodies to parietal cells, usually in association with gastric gastritis (type A) and pernicious anemia.

Atrophy can occur without certain symptoms. Until atrophy progresses, the endoscopically mucous membrane may look normal if vascularization is traced in the submucosal layer. Since atrophy captures all the mucous membrane, acid and pepsin secretion decreases and the development of the internal factor can be completely disrupted, which leads to malabsorption of vitamin B ₁₂.

Metaplasia

There are two types of metaplasia in chronic non-erosive gastritis: metaplasia of mucosal glands and intestinal metaplasia.

Metazplasia of the glands of the mucous (pseudopiloric metaplasia) occurs with the development of pronounced atrophy of the glands of the stomach, which are progressively replaced by mucus-forming cells (antrum mucosa), especially with a small curvature. There may be gastric ulcers (usually in the area of the mucosal transition of the antrum to the body of the stomach), but whether they are the cause or consequence of these metaplastic changes is unclear.

Intestinal metaplasia usually begins in the antrum, in response to chronic damage to the mucous membrane and can migrate to the body. Cells of the gastric mucosa change and resemble the intestinal mucosa with goblet cells, endocrine (enterochromaffine or enterochromaffin-like) cells and rudimentary villi and may even acquire functional (absorption) characteristics. It is histologically classified as complete (most frequent) or incomplete metaplasia. With complete metaplasia, the mucous membrane of the stomach is completely transformed into the mucosa of the small intestine and histologically, and functionally with the ability to absorb nutrients and secrete peptides. With incomplete metaplasia, the epithelium takes a histological structure close to the large intestine, and often demonstrates dysplasia. Intestinal metaplasia can lead to stomach cancer.

Symptoms of non-erosive gastritis

In most patients, the gastritis associated with Helicobacter pylori is asymptomatic, although some patients experience mild dyspepsia or other vague signs.

Diagnosis of non-erosive gastritis

Often, changes are detected with endoscopy performed for a different purpose. The study is not indicated for asymptomatic flow. In the initial detection of gastritis, testing for Helicobacter pylori is indicated.

[7], [8], [9]

Treatment of non-erosive gastritis

Treatment of non-erosive gastritis involves the destruction of Helicobacter pylori. Treatment of patients without symptomatic symptoms is somewhat controversial due to the high prevalence of superficial gastritis associated with Helicobacter pylori and the relatively low percentage of clinical complications (ie, peptic ulcer disease). However, Helicobacter pylori belongs to the 1 st class of carcinogens; The destruction of the microorganism eliminates the risk of developing cancer. In patients with the absence of Helicobacter pylori, treatment is symptomatic and is aimed at drug-induced suppression of acidity (eg, H ₂ -blockers, proton pump inhibitors) and the use of antacids.