The researchers investigated the prevalence of Helicobacter pylori infection in a population of 150 consecutive outpatients with atrophic body gastritis (ABG). They reported their findings in the September issue of Helicobacter.
All patients had a detailed assessment, including measurement of specific anti-H. pylori antibodies, parietal cell antibodies, and fasting gastrin. In addition, gastroscopy with biopsies from gastric antrum and body were conducted.
The investigators found that 25% of patients were histologically and serologically negative (Group A).
A further 53% of patients had no H. pylori detected on histology. However, in all these subjects, IgG to H. pylori was elevated (Group B).
The final group consisted of 23% of patients, who were found to be positive at histology in the corpus mucosa. All but one of these patients had elevated circulating IgG to H. pylori (Group C).
Mean corporal atrophy score in Group B patients was statistically lower than in Group A patients (2.43 vs. 2.75), but was statistically higher than in Group C patients (1.79). Thus, in corporal mucosa a gradient of atrophy was shown.
A similar gradient was observed for the presence of pernicious anemia. This was lowest in Group C (12%), increasing to 46% in Group B and being highest in Group C (76%).
A statistical correlation was obtained between the histological score of corporal atrophy and the titer of antibodies to parietal cells. An inverse correlation was obtained between the histological score of corporal atrophy and IgG to H. pylori.
|H. pylori may induce gastric atrophic damage and gastric autoimmunity.|
Bruno Annibale, of the University ‘La Sapienza', Rome, said on behalf of his colleagues, "Our study shows that two-thirds of ABG patients have evidence of H. pylori infection.
"This suggests that atrophic gastritis of the corpus is a spectrum of damage, where H. pylori is a key agent able to induce gastric atrophic damage and also gastric autoimmunity," he concluded.