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Non-erosive gastritis
Last reviewed: 07.07.2025
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Nonerosive gastritis refers to a group of various histological changes that occur primarily as a result of Helicobacter pylori infection. Most patients are asymptomatic. Changes are detected by endoscopy. Treatment of nonerosive gastritis is aimed at eradicating H. pylori and sometimes suppressing acidity.
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[ Pathomorphology of non-erosive gastritis
Superficial gastritis
Lymphocytes, plasma cells, and neutrophils predominate in the area of infiltrative inflammation. The inflammation is usually superficial and may involve the antrum, body, 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 is likely to have a number of clinical manifestations (symptoms) (eg, vague dyspepsia). Mononuclear cells and neutrophils infiltrate the entire mucosa to the muscular layer, but phlegmon or crypt abscesses rarely develop despite such infiltration. The distribution of the process may be heterogeneous. Superficial gastritis may be present, as well as partial atrophy of the glands and metaplasia.
Gastric atrophy
Atrophy of the gastric glands may be observed in gastritis, most often long-term antrum gastritis (called type B in the presence of Hp infection). Some patients with atrophic gastritis have autoantibodies to parietal cells, usually in association with gastritis of the body of the stomach (type A) and pernicious anemia.
Atrophy may occur without specific symptoms. As long as atrophy does not progress, the mucosa may appear normal endoscopically if vascularization is observed in the submucosa. Since atrophy affects the entire mucosa, acid and pepsin secretion are reduced and the production of intrinsic factor may be completely impaired, leading to malabsorption of vitamin B 12.
Metaplasia
There are two types of metaplasia in chronic non-erosive gastritis: metaplasia of the glands of the mucous membrane and intestinal metaplasia.
Metaplasia of the mucosal glands (pseudopyloric metaplasia) occurs with the development of severe atrophy of the gastric glands, which are progressively replaced by mucus-forming cells (antral mucosa), especially along the lesser curvature. Gastric ulcers may be present (usually at the junction of the antral mucosa with the body of the stomach), but whether they are the cause or the consequence of these metaplastic changes is unclear.
Intestinal metaplasia usually begins in the antrum in response to chronic mucosal injury and may extend to the body. The cells of the gastric mucosa change to resemble the intestinal mucosa with goblet cells, endocrine (enterochromaffin or enterochromaffin-like) cells, and rudimentary villi, and may even acquire functional (absorptive) characteristics. It is classified histologically as complete (the most common) or incomplete metaplasia. In complete metaplasia, the gastric mucosa is completely transformed into small intestinal mucosa both histologically and functionally with the ability to absorb nutrients and secrete peptides. In incomplete metaplasia, the epithelium adopts a histological appearance similar to the colon and often exhibits dysplasia. Intestinal metaplasia can lead to gastric cancer.
Symptoms of non-erosive gastritis
Most patients with Helicobacter pylori-associated gastritis are asymptomatic, although some patients experience mild dyspepsia or other vague symptoms.
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Treatment of non-erosive gastritis
Treatment of nonerosive gastritis involves eradication of Helicobacter pylori. Treatment of asymptomatic patients is somewhat controversial because of the high prevalence of superficial gastritis associated with Helicobacter pylori and the relatively low rate of clinical complications (i.e., peptic ulcer disease). However, Helicobacter pylori is a class 1 carcinogen; eradication of the organism eliminates the risk of cancer. In patients without Helicobacter pylori, treatment is symptomatic and involves drug-induced acid suppression (e.g., H2 blockers, proton pump inhibitors) and antacids.
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