ATROPHIC GASTRITIS AND INTESTINAL METAPLASIA IN HELICOBACTER-PYLORI INFECTION - THE ROLE OF CAGA STATUS

Objective: Helicobacter pylori (H. pylori) is a major factor in determ ining the risk for development of gastric adenocarcinoma through the i ntermediate steps of atrophic gastritis and intestinal metaplasia. Bec ause H. pylori infection is highly prevalent in asymptomatic populatio ns and only a few people develop cancer, additional factors may influe nce the risk for development of cancer, once infection is established. Some factors may pertain to differences among bacterial strains. Beca use infection by H. pylori strains possessing cagA (cytotoxin-associat ed gene A), a gene encoding a high-molecular-weight immunodominant ant igen (CagA), is associated with enhanced induction of gastritis, the a im of our study was to evaluate potential differences in the prevalenc e and intensity of atrophy and intestinal metaplasia between CagA-posi tive and CagA-negative H. pylori-infected patients. Methods: Eighty H. pylori-infected patients among 120 consecutive dyspeptic patients ref erred for upper gastrointestinal endoscopy were studied. Six bioptic s pecimens were taken from the gastric antrum: five for histological exa mination, and one for urease test. The H. pylori status was determined by histology, CLO test, and serology tin a standardized ELISA) for se rum IgG and IgA directed to H. pylori. The CagA status was determined by Western blotting to detect serum IgG antibodies to CagA. Gastritis was classified according to the Sydney System. A score from 0 to 3 was assigned to each of the following morphological variables: atrophy, i ntestinal metaplasia, and mononuclear and neutrophilic cell infiltrati on. The association between CagA status and histological features was assessed by means of the chi(2) test for trend. Results: Among the 80 H. pylori-infected patients 53 (66%) were CagA seropositive and 27 (34 %) were CagA seronegative. The mean age of the two groups was similar. CagA-positive patients had significantly higher scores for atrophy (p = 0.006), intestinal metaplasia (p = 0.01), and mononuclear (p < 0.00 1) and polymorphonuclear (p = 0.002) cell infiltration than did CagA-n egative patients. No differences in contrast, were found for H. pylori density. Conclusion: Infection with CagA-positive H. pylori strains i s associated with an increased prevalence and intensity of antral atro phy and intestinal metaplasia, in addition to higher degrees of gastri tis. Our results seem to suggest that the CagA status could be a helpf ul parameter to define a subgroup of H. pylori-infected patients at in creased risk of developing gastric adenocarcinoma. (C) 1998 by Am. Col l. of Gastroenterology.