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Gastric pathology associated with Helicobacter pylori.

A bacterium is associated with a specific gastritis. Neutrophils infiltrate the necks of the glands, just deep to the infected foveolae. This infiltration rarely, if ever, occurs without H. pylori infection. Foveolar epithelial damage is common, with loss of cell structure. Electron microscopy suggests that the bacteria cause this damage as they attach to the superficial cell membrane. These features, defined by Whitehead et al as active changes, appear specific for H. pylori infection. The neutrophils and specific epithelial changes disappear within days of starting treatment for Helicobacter. They rapidly recur if the treatment is unsuccessful. Without treatment, the changes remain for decades and are severe in 10% to 20% of cases. Other changes occur in the mucosa. Reduced mucus secretion occurs in damaged or proliferating epithelium. This reduced secretion occurs near healing ulcers or with other types of inflammation but is often severe when Helicobacter is present. It returns to normal within weeks of treating the infection. The bacteria adhering to the cell membrane may cause this change directly. Lymphoid infiltration occurs with any type of chronic inflammation or immune reaction. The infiltration is not specific for Helicobacter, and it reduces slowly in months or years after eradication of H. pylori. Peptic ulceration, particularly duodenal ulceration, although not specific, is particularly common with H. pylori infection. The long-term inflammation probably causes other gastric pathology. Atrophy is common. Epithelial metaplasia occurs in about 20% of patients, usually mild. Other features, such as scarring, epithelial dysplasia, and in situ malignant change, are less common. They show little improvement after eradicating H. pylori. The part played by the bacteria in their cause remains uncertain. Pathologists see a long-standing chronic gastritis clearly related to a bacterium. The inflammation often is severe and commonly damages the mucosa, with ulceration, atrophy, metaplasia, and occasional premalignant changes. Physicians would treat inflammation of this degree in most other parts of the body. This disease is usually symptomless. There is some controversy, but eradicating Helicobacter often fails to improve nonulcer dyspepsia. This failure results in a continuing argument over whether or not to treat the infection. Meanwhile the pathology continues. A temporary solution to the problem is suggested: Patients infected with Helicobacter can give informed consent. Patients can be told about the infection, the pathology, the poor relationship to symptoms, and side effects of therapy, and they can decide.

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