Severe atrophic gastritis with Helicobacter pylori infection and gastric cancer

Abstract

Abstract:Background. We conducted a case-control study to evaluate whether patients with severe gastric atrophy (indicated by serum pepsinogen concentration) have a high risk of gastric cancer. Methods. At the time of diagnosis of gastric cancer, sera from 301 patients (cases) and 602 sex-and age-matched cancer-free individuals (controls) were tested for the presence of antiHelicobacter pylori IgG antibody (HM-CAP enzyme-linked immunoassay [ELISA] kit; Kyowa Medix, Tokyo, Japan) and serum pepsinogen (PG) levels (PG I and II Riabead Kits; Dainabot, Tokyo, Japan). We defined positivity for pepsinogen a pepsinogen I concentration of less than 70 ng/mL and a PG I/II ratio of less than 3.0. We categorized the subjects according to serum pepsinogen levels and anti-Helicobacter pylori IgG antibody, creating four categories. Results. Of the 301 cancer cases, 177 had positive serum pepsinogen levels, and 172 were positive for anti-Helicobacter pylori IgG antibody. The category in which subjects had positive serum pepsinogen levels and were negative for antiHelicobacter pylori IgG antibody had the highest proportion (76.9%) of individuals with gastric cancer and the highest odds ratio (4.20) of the four categories. The odds ratios were 2.55 (95% confidence interval; 1.92-3.88) for positive serum pepsinogen levels and 0.93 (95% confidence interval; 0.63-1.27) for positive anti-Helicobacter pylori IgG antibody. Conclusion. These results suggest that patients with positive serum pepsinogen levels who are negative for IgG antibody to Helicobacter pylori, constitute a high-risk group for gastric cancer. Helicobacter pylori infection is associated with the development of gastric cancer by providing a suitable environment i.e., severe gastric atrophy, for carcinogenesis of the gastric mucosa.

Association of the interleukin-1 * genetic polymorphism and gastric cancer risk in Japanese

“…In patients with extensive mucosal atrophy, the spontaneous disappearance of H. pylori was also observed, indicating that the mucosa of IM or CAG patients without H. pylori infection had undergone precancerous mucosal changes. 10,16 In this study, the frequency of the C allele in the IM or CAG without H. pylori infection group was significantly higher than that in the H. pylori-negative noncancer controls. This result indicated that this Ϫ511 T-to-C base transition may be important for the mucosal atrophy of the stomach.…”

Effect of Helicobacter pylori Infection Combined with CagA and Pepsinogen Status on Gastric Cancer Development among Japanese Men and Women: A Nested Case-Control Study

“…Compared with ''normal'' pepsinogen and negative H. pylori antibody group, the hazard ratios (95% CI) of developing gastric cancer for normal pepsinogen and positive H. pylori antibody group, atrophic pepsinogen and positive H. pylori antibody group, and atrophic pepsinogen and negative H. pylori antibody group were 1.1 (0.4-3.4), 6.0 (2.4-14.5), and 8.2 (3.2-21.5), respectively. In addition, a casecontrol study conducted in Japan showed the largest OR of gastric cancer in the positive pepsinogen and negative H. pylori infection group compared with other combination groups (53). In our study, although a statistically significant, f5-fold risk of developing gastric cancer was observed among those who were H. pylori IgG-seronegative and pepsinogen-positive, the PAF (95% CI) was calculated as only 2.6% (1.0-4.3%).…”

Study of clinicopathological factors associated with the occurrence of synchronous multiple gastric carcinomas

“…The results showed that multiple gastric carcinomas were correlated signifi cantly to the distribution of atrophic mucosa in the stomach and the degree of intestinal metaplasia in the surrounding mucosa, and multivariate analysis confi rmed the latter as a signifi cant independent factor. Recent studies have shown that H. pylori not only causes peptic ulcer and gastritis but also exhibits a strong correlation to gastric carcinomas [27][28][29]. The WHO/International Agency for Research on Cancer (IARC) recognized H. pylori as a defi nite carcinogen in 1994 [30].…”