The etiology of chronic gastritis has long remained unclear, resulting in the absence of ideal long-term prevention and treatment methods. In 1982, Australian scholar Marshall observed that a bacterium called Helicobacter pylori (abbreviated as HP) in the gastric mucosa was associated with the onset of chronic gastric diseases.
(1) In volunteers with normal gastric mucosa, oral administration of HP suspension can cause gastritis symptoms and pathological changes.
(2) HP detection rates are extremely high in patients with chronic gastritis, while the bacterium cannot be detected in individuals with normal gastric mucosa.
(3) Serum HP antibodies are significantly elevated in chronic gastritis patients, and anti-HP immunoglobulins can be detected in gastric fluid, indicating that HP is a pathogenic antigen (pathogen).
(4) Targeted treatment against HP leads to marked improvement in gastric mucosa of chronic gastritis patients.
(5) HP is detectable in the gastric antrum of 60%-80% of gastric ulcer patients and 70%-100% of duodenal ulcer patients. Serological testing confirms elevated HP antibody titers in their serum.
(6) Refractory ulcers unresponsive to conventional anti-ulcer drugs often heal after switching to anti-HP therapy.
(7) Infection of rhesus monkeys with HP induces chronic gastritis, exhibiting gastric mucosal pathological changes similar to human infection. This successfully established an animal model for HP gastritis. The above evidence conclusively demonstrates the correlation between HP and chronic gastric diseases.
(8) In volunteer trials, Helicobacter pylori infection also causes persistent halitosis and strong breath odor that is difficult to eliminate.
The medical community now holds the following consensus: HP is definitively the causative agent of chronic gastritis and is also closely linked to peptic ulcers and gastric cancer. In other words, HP is the primary culprit and root cause of chronic gastric diseases.