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      Nodular gastritis in association with gastric cancer development before and after Helicobacter pylori eradication

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          Abstract

          Background and Aim

          Nodular gastritis is caused by Helicobacter pylori infection and is associated with the development of diffuse‐type gastric cancer. This study examined the clinical characteristics of patients with nodular gastritis, including cancer incidence before and after H. pylori eradication.

          Methods

          This was a retrospective study of patients who underwent upper endoscopy and were positive for H. pylori infection. We examined the clinical findings and follow‐up data after H. pylori eradication in patients with and without nodular gastritis.

          Results

          Of the 674 patients with H. pylori infections, nodular gastritis was observed in 114 (17%). It was more prevalent in women (69%) and young adults. Among patients with nodular gastritis, six (5%) had gastric cancer, all of which were of the diffuse type. Among the 19 (4%) patients with gastric cancer and no nodular gastritis, 16 had intestinal‐type cancer. White spot aggregates in the corpus, a specific finding in patients with nodular gastritis, were more frequently observed in patients with gastric cancer than in those without (83% vs 26%, P = 0.0025). Of 82 patients with nodular gastritis who had H. pylori eradicated successfully, none developed gastric cancer over a 3‐year follow‐up period, while 7 (3%) of 220 patients without nodular gastritis developed gastric cancer after H. pylori eradication.

          Conclusions

          In patients with nodular gastritis, white spot aggregates in the corpus may indicate a higher risk of developing diffuse‐type gastric cancer. Nodular gastritis may be an indication for eradication therapy to reduce the risk of cancer development after H. pylori eradication.

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          Most cited references27

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          An Endoscopic Recognition of the Atrophic Border and its Significance in Chronic Gastritis

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            Cancer development based on chronic active gastritis and resulting gastric atrophy as assessed by serum levels of pepsinogen and Helicobacter pylori antibody titer.

            Our study investigated the relationship between gastric cancer development and activity of Helicobacter pylori-associated chronic gastritis or the resulting chronic atrophic gastritis (CAG). A cohort of 4,655 healthy asymptomatic subjects, in whom serum pepsinogen (PG) and H. pylori antibody titer had been measured to assess the activity and stage of H. pylori-associated chronic gastritis, was followed for up to 16 years, and cancer development was investigated. In subjects with a serologically diagnosed healthy stomach (H. pylori-negative/CAG-negative), cancer incidence rate was low, at 16/100,000 person-years. With the establishment of H. pylori infection and progression of chronic gastritis, significant stepwise cancer risk elevations were seen from CAG-free subjects (H. pylori-positive/CAG-negative) [hazard ratio (HR) = 8.9, 95% confidence interval (CI) = 2.7-54.7] to subjects with CAG (H. pylori-positive/CAG-positive) (HR = 17.7, 95% CI = 5.4-108.6) and finally to subjects with metaplastic gastritis (H. pylori-negative/CAG-positive) (HR = 69.7, 95% CI = 13.6-502.9). In H. pylori-infected CAG-free subjects, significantly elevated cancer risk was observed in the subgroup with active inflammation-based high PG II level or potent immune response-based high H. pylori antibody titer; the former was associated with a particularly high risk of diffuse-type cancer, and both subgroups showed high cancer incidence rates of around 250/100,000 person-years, comparable to that in subjects with CAG. No such risk elevation was observed in H. pylori-infected subjects with CAG. These results clearly indicate that gastric cancer develops mainly from the gastritis-atrophy-metaplasia-cancer sequence and partly from active inflammation-based direct carcinogenesis, and that serum levels of PG and H. pylori antibody titer provide indices of cancer development in H. pylori-infected subjects. © 2013 UICC.
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              The effect of eradicating helicobacter pylori on the development of gastric cancer in patients with peptic ulcer disease.

              Infection with Helicobacter pylori is a risk factor for the development of gastric cancer. However, it is not known whether eradication therapy can prevent the development of gastric cancer in persons in whom the cancer is not yet established. In the present study, we investigated whether the eradication of H. pylori in patients with peptic ulcer disease reduces the likelihood of their developing gastric cancer. Prospective posteradication evaluations were conducted in 1,342 consecutive patients (1,191 men and 151 women; mean age: 50 yr) with peptic ulcer diseases who had received H. pylori eradication therapy. After confirmation of eradication, endoscopy and a urea breath test were performed yearly. A total of 1,120 patients completed more than 1-yr follow-up and were followed for up to 8.6 yr (a mean of 3.4 yr). Gastric cancer developed in 8 of 944 patients cured of infection and 4 of 176 who had persistent infection (p= 0.04; log-rank test). All the gastric cancer developed in patients with gastric ulcer, but none in patients with duodenal ulcer (p= 0.005; Fisher's exact test). In patients with gastric ulcer, persistent infection was identified as a significant factor for the risk of developing gastric cancer (hazard ratio: 3.35; 95% confidence interval: 1.00-11.22; p= 0.04; Cox's proportional-hazards model). H. pylori eradication may reduce their risk of developing gastric cancer in patients with gastric ulcer. Large-scale studies in additional populations of this important international public-health issue are warranted.
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                Author and article information

                Contributors
                hidaka-naishikyo@hidakagh.gobo.wakayama.jp
                Journal
                JGH Open
                JGH Open
                10.1002/(ISSN)2397-9070
                JGH3
                JGH Open: An Open Access Journal of Gastroenterology and Hepatology
                Wiley Publishing Asia Pty Ltd (Melbourne )
                2397-9070
                25 March 2018
                June 2018
                : 2
                : 3 ( doiID: 10.1002/jgh3.v2.3 )
                : 80-86
                Affiliations
                [ 1 ] First Department of Internal Medicine Hidaka General Hospital Wakayama Japan
                [ 2 ] Second Department of Internal Medicine Wakayama Medical University Wakayama Japan
                [ 3 ] Nakata Medical Clinic Wakayama Japan
                Author notes
                [*] [* ] Correspondence

                Izumi Nishikawa, First Department of Internal Medicine, Hidaka General Hospital, 116‐2 Sono, Gobo City, Wakayama 644‐0002, Japan.

                Email: hidaka-naishikyo@ 123456hidakagh.gobo.wakayama.jp

                Author information
                http://orcid.org/0000-0001-5799-8930
                Article
                JGH312049
                10.1002/jgh3.12049
                6207053
                30483568
                cfcc8e32-5fc4-42d2-93ae-b73729894f91
                © 2018 The Authors. JGH Open: An open access journal of gastroenterology and hepatology published by Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 28 September 2017
                : 24 January 2018
                : 23 February 2018
                Page count
                Figures: 4, Tables: 3, Pages: 8, Words: 4906
                Categories
                Original Article
                Original Articles
                Custom metadata
                2.0
                jgh312049
                June 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.5.1 mode:remove_FC converted:25.10.2018

                eradication,gastric cancer,gastritis,helicobacter pylori

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