Over 60% of chronic gastritis patients harbor HP infection. The progression pathway—HP infection → chronic superficial gastritis → atrophic gastritis → intestinal metaplasia or dysplasia → gastric cancer—has been clinically validated. HP primarily spreads through person-to-person transmission via oral-oral or fecal-oral routes. HP infection invariably causes gastric mucosal inflammation, and the body typically struggles to clear it, leading to chronic infection.
Etiology
(1) Helicobacter pylori Infection
Helicobacter pylori is the primary cause of chronic gastritis. It damages cells through ammonia production and secretion of substances like vacuolating toxin A (VacA). Its cytotoxin-associated gene (cagA) protein induces intense inflammatory responses, while its bacterial cell wall serves as an antigen triggering immune reactions.The prolonged presence of these factors leads to chronic inflammation of the gastric mucosa.
Spontaneous clearance of H. pylori infection is rare, resulting in the persistent existence of chronic gastritis. A minority of chronic non-atrophic gastritis cases may progress to chronic multifocal atrophic gastritis. In extremely rare instances, chronic multifocal atrophic gastritis may evolve into gastric cancer after prolonged progression.Epidemiological studies indicate that patients with chronic multifocal atrophic gastritis have a significantly higher risk of gastric cancer than the general population. Approximately 15%–20% of gastritis cases caused by Helicobacter pylori infection develop into peptic ulcers. Chronic gastritis induced by Helicobacter pylori infection is also occasionally associated with the occurrence of gastric mucosa-associated lymphoid tissue (MALT) lymphoma.The varying consequences of Helicobacter pylori infection among individuals in different populations across regions are considered the result of interactions among bacterial, host, and environmental factors. (2) Dietary and Environmental Factors Global comparative studies reveal that regional differences in the incidence of atrophy and intestinal metaplasia largely parallel regional variations in gastric cancer incidence.This suggests that factors beyond Helicobacter pylori infection contribute to the development and progression of chronic atrophic gastritis. Epidemiological studies indicate that diets high in salt and low in fresh fruits and vegetables are closely associated with gastric mucosal atrophy, intestinal metaplasia, and gastric cancer development.
(III) Autoimmunity
Autoimmune gastritis primarily involves atrophy of the parietal cell-rich corpus mucosa;Patients exhibit autoantibodies such as parietal cell antibodies (PCA) in their blood. Those with pernicious anemia may also test positive for intrinsic factor antibodies (IFA). This condition may coexist with other autoimmune diseases like Hashimoto's thyroiditis or vitiligo. These manifestations suggest the disease belongs to the autoimmune category.Autoantibodies attack parietal cells, reducing their total number and leading to decreased or absent gastric acid secretion. Intrinsic factor antibodies bind to intrinsic factor, impairing vitamin B12 absorption and causing pernicious anemia.
(IV) Other Factors
When the pyloric sphincter is dysfunctional, duodenal fluid containing bile and pancreatic juice refluxes into the stomach, weakening the gastric mucosal barrier function.Other external factors, such as alcohol abuse, use of NSAIDs (e.g., aspirin, cold and flu capsules), and certain irritating foods, can repeatedly damage the gastric mucosa.
Disease Prevention
Preventing chronic gastritis is more important than treating it. The following principles should be followed:
1. Maintain a positive mental state.Depression, excessive stress, or fatigue can disrupt pyloric sphincter function, leading to bile reflux and chronic gastritis.
2. Quit smoking and avoid alcohol. Harmful components in tobacco increase gastric acid secretion, irritating the gastric mucosa. Excessive smoking can cause bile reflux.Excessive or prolonged consumption of strong alcoholic beverages can cause gastric mucosal congestion, edema, or even erosion, significantly increasing the incidence of chronic gastritis.
3. Exercise caution or avoid medications harmful to the gastric mucosa. Long-term misuse of such drugs damages the gastric lining, leading to chronic gastritis and ulcers.
4. Avoid highly acidic, spicy, or other irritating foods, as well as raw, cold, or indigestible items. Chew food thoroughly and slowly to ensure adequate mixing with saliva, which aids digestion and reduces gastric irritation. Maintain regular, measured meals rich in nutrients, particularly vitamins A, B, and C. Refrain from consuming stimulating beverages like strong tea or coffee.