Two-thirds of atrophic body gastritis patients have evidence of Helicobacter pylori infection.

Abstract

Helicobacter pylori is involved in the induction of atrophic body gastritis (ABG). During the progression of atrophic gastritis the disappearance of H. pylori has been documented and in time serology is the only sign that indicates a previous infection. It has been shown that a positive serology, in ABG patients without histological evidence of infection, indicates an active H. pylori infection. To investigate in a population of patients with ABG the prevalence of H. pylori infection on the basis of histology and serology. A total of 150 consecutive outpatients with atrophic body gastritis were diagnosed on the basis of a screening system. All patients had a detailed assessment including measurement of specific anti-H. pylori antibodies, parietal cell antibodies, and fasting gastrin, gastroscopy with biopsies from gastric antrum and body. 24.6% of patients were histologically and serologically negative (Group A). 52.7% H. pylori was not detected on histology but IgG to H. pylori were in all these patients elevated (Group B). 22.6% of patients 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 +/- 0.08 vs. 2.75 +/- 0.09; p <.05), but was statistically higher than in Group C patients (1.79 +/- 0.11; p <.001). Thus, in corporal mucosa a gradient of atrophy was shown: Group C < Group B < Group A. A similar gradient was observed for the presence of pernicious anemia being lowest in Group C 11.8% increasing to 45.6% in Group B and being highest in Group C 75.6%. A statistical correlation was obtained (r =.04791, p <.05) between the histological score of corporal atrophy and the titer of antibodies to parietal cells and an inverse correlation was obtained (r = -.2322, p <.0001) between the histological score of corporal atrophy and IgG to H. pylori. This 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.