Difference in Expression of Helicobacter Gastritis in Antrum and Body pylori

Seven hundred seventy biopsy specimens obtained from 10 different sites in stomachs of 77 patients were examined for the presence of active chronic gastritis (ACG) and Helicobacfer pylori to investigate the characteristics of gastritis in the antrum and body. Forty-eight patients with ACG at one or more sites were all H. pylori positive. H. pylori was not found in 20 patients who had chronic gastritis with no activity or in 9 patients who had histologically normal mucosa. In patients with ACG in at least one biopsy site, a strong positive topographic association between H. pyZori colonization and ACG was seen in the Warthin-Starry stain. The frequency of H. pylori colonization was similar in the antrum and body. However, the incidence of ACG declined significantly proximal to the borderline between, the antrum and body (P < 0.001). The average grade of gastritis at the individual biopsy sites was distributed evenly throughout the antrum but decreased markedly in the body (P < 0.0001). In the same manner, the average grade of H. pylori colonization decreased in the body (P < 0.0027). The grade of H. pylori colonization in the individual biopsy specimens was closely related to the grade of gastritis (r = 0.51); also, the grade of neutrophil infiltration was related to the grade of gastritis (r = 0.79). A good correlation existed between the grade of H. pylori colonization and the grade of neutrophi1 infiltration (r = 0.70). The results of this study show a different expression of H. pylori gastritis in the antrum and body, which is the main subtype of chronic type B gastritis. The close topographic and graded association between the presence of H. pyZori and the activity and grade of gastritis lend further support to the major pathogenic role of H. pyZori in active chronic gastritis. The different expression of gastritis in antrum and body is suggested to be increased reactivity of the antral mucosa to the infection, possibly on the basis of an enhanced immunologic response to H. pylori in this region. T he clinical significance of chronic gastritis (CG) has changed dramatically since the detection of Helicobacter pylori (formerly Campylobacter pylori). Today, it is accepted as the main precursor condition for duodenal and gastric ulceration’~2 in a large proportion of ulcer patients. Further, it is under discussion as a clinical entity of its own in some patients with abdominal complaints.‘~’ Our increased knowledge of the pathogenesis of gastritis has led to the first attempts at a pathogenetic classification of gastritis3s4 In 1973, Strickland and Mackay published a classification of gastritis based on their findings in gastric tube suction biopsy specimens.5 They classify patients as having type A gastritis if they show inflammatory and atrophic changes in the body, in conjunction with the detection of serum antibodies against parietal cells and intrinsic factor. However, most forms of gastritis @go%) are referred to as type B gastritis, which probably originates in the antrum and spreads continuously towards the cardia.