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study (7), we observed the presence of atrophic gastritis in 62% of 24 cagApositive patients, compared with 32% of 34 cagA-negative patients, corresponding with an odds ratio (OR) of 3.48 (95% confidence interval [CI] = 1.0212.2). In a previous, prospective, nested case-control study (2), we observed the development of gastric cancer in 109 subjects who had had a phlebotomy 13 ± 5 years (mean ± standard deviation) earlier. On the basis of serologic testing, 103 (94%) of these subjects had been infected with H. pylori at the time of bleeding. In an extension of this study, it appeared that 90 (87%) of these 103 patients with gastric cancer had been infected with cagA-positive strains (J). This proportion was 78% in 103 matched H. py/on-infected control subjects who did not develop gastric cancer during follow-up, corresponding with an OR of 1.9 (95% CI = 0.9-4.0) (3). The association between infection with a cagA-positive H. pylori strain and gastric cancer was strongest for intestinal-type carcinomas of the distal stomach (OR = 2.3; 95% CI = 1.0-5.2) (J). Ponzetto et al. found cagA antibodies in 96% (95% CI = 87-100) of 51 patients with gastric cancer. This percentage is in agreement with our previous findings, but is remarkably high considering that the specimens were from patients who already were diagnosed as having cancer. During the process of the development of atrophy and cancer, signs of a pre-existing H. pylori infection may disappear (4). The 18% prevalence of cagA antibodies in the control subjects, on the other hand, seems rather low when compared with other studies. It is not clear whether or not all of the 555 consecutive individuals tested were H. pylori positive.

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