BACKGROUND/AIMS: Previous publications in the literature have reported an association between incidence of Helicobacter pylori (HP) infection and gastric cancer. The role of HP in precancerous gastric lesions or in their evolution towards neoplastic disease is not so clear. MATERIALS AND METHODS: We studied 174 patients with atrophic gastritis. RESULTS: Intestinal metaplasia (IM) was detected in 165 subjects of the patients and different grades of dysplasia were observed in 32 subjects. HP was found in 75 (52.8%) of 165 subjects with IM, in 7 (34.7%) with both IM and dysplasia and in 3 with dysplasia alone. There was no significant difference in the prevalence of HP infection in the three IM types, type I (47.7%), type II (54.7%) and type III (48.4%) (p = n.s.). In contrast, the prevalence of HP positive patients was significantly lower in dysplasia (10/32 vs 22/32; p < 0.005). At the same time, the frequency of HP was significantly lower for subjects with IM and dysplasia than for those with type I IM (41/83 vs 7/32; p = 0.01). CONCLUSIONS: At present, in our experience, HP infection is rather infrequent in type III IM and it is found less often in cases of dysplasia. We have taken these results to suggest that the modified gastric mucosa becomes inhospitable for HP and, consequently, that other factor are probably responsible for promoting gastric carcinogenesis.
BACKGROUND/AIMS: Previous publications in the literature have reported an association between incidence of Helicobacter pylori (HP) infection and gastric cancer. The role of HP in precancerous gastric lesions or in their evolution towards neoplastic disease is not so clear. MATERIALS AND METHODS: We studied 174 patients with atrophic gastritis. RESULTS:Intestinal metaplasia (IM) was detected in 165 subjects of the patients and different grades of dysplasia were observed in 32 subjects. HP was found in 75 (52.8%) of 165 subjects with IM, in 7 (34.7%) with both IM and dysplasia and in 3 with dysplasia alone. There was no significant difference in the prevalence of HP infection in the three IM types, type I (47.7%), type II (54.7%) and type III (48.4%) (p = n.s.). In contrast, the prevalence of HP positive patients was significantly lower in dysplasia (10/32 vs 22/32; p < 0.005). At the same time, the frequency of HP was significantly lower for subjects with IM and dysplasia than for those with type I IM (41/83 vs 7/32; p = 0.01). CONCLUSIONS: At present, in our experience, HP infection is rather infrequent in type III IM and it is found less often in cases of dysplasia. We have taken these results to suggest that the modified gastric mucosa becomes inhospitable for HP and, consequently, that other factor are probably responsible for promoting gastric carcinogenesis.
Authors: S Kikuchi; T Nakajima; O Kobayashi; T Yamazaki; M Kikuichi; K Mori; S Oura; H Watanabe; H Nagawa; R Otani; N Okamoto; M Kurosawa; H Anzai; T Kubo; T Konishi; S Futagawa; N Mizobuchi; O Kobori; R Kaise; T Sato; Y Inaba; O Wada Journal: Jpn J Cancer Res Date: 2000-08