Is non-atrophic gastritis serious?

Non-atrophic gastritis refers to a lesion that is not accompanied by gastric mucosal atrophy. At this time, the gastric mucosa is often infiltrated with a chronic inflammatory cell infiltration dominated by lymphocytes and plasma cells. It is generally divided into body gastritis, antral gastritis, pangastritis, etc. This is also a relatively serious gastrointestinal disease. Sometimes patients will show discomfort in the upper abdomen, which often leads to upper abdominal distension, sometimes belching symptoms, nausea and other symptoms, and often cause indigestion in patients.

Is non-atrophic gastritis serious?

Most patients with chronic non-atrophic gastritis may not have any symptoms. Those with symptoms mainly present with non-specific indigestion symptoms such as upper abdominal pain or discomfort, upper abdominal distension, early satiety, belching and nausea. Patients with functional dyspepsia may or may not have chronic gastritis. After eradication of Helicobacter pylori, the histology of chronic gastritis can be significantly improved, but it cannot alleviate the dyspepsia symptoms of most patients with histological improvement, indicating that chronic gastritis is not closely related to dyspepsia symptoms.

Cause 1. Helicobacter pylori infection Helicobacter pylori infection is the main cause of chronic non-atrophic gastritis. The relationship between the two meets the four basic requirements proposed by Koch for determining the pathogen as the cause of infectious diseases, namely, the pathogen exists in patients with the disease, the distribution of the pathogen is consistent with the distribution of lesions in the body, the disease can improve after the pathogen is eliminated, and in animal models, the pathogen can induce diseases similar to those in humans. There are two prominent types of Helicobacter pylori-associated chronic non-atrophic gastritis: antral predominant pangastritis and corpus predominant pangastritis. The former can increase gastric acid secretion, thereby increasing the risk of duodenal ulcer; the latter reduces gastric acid secretion, increasing the risk of gastric ulcer and gastric cancer.