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      Risk of gastric cancer in Helicobacter pylori infection in a 15-year follow-up

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          Abstract

          Objective: We investigated the risk of gastric cancer among men with Helicobacter pylori ( H. pylori) infection or atrophic gastritis (AG) in a 15-year follow-up.

          Materials and methods: Study population consists of 12,016 men aged 50–65 years at the beginning of the follow-up in 1994–1996. Serum levels of pepsinogen I (SPGI) and antibodies (IgG) to H. pylori (HpAb) were assayed from serums collected in 1994–1996. Incidence of gastric cancer in the study population was assessed in follow-up from 1994 to 2011 by data from the nationwide cancer registry. Based on SPGI and HpAb values, standardized incidence ratios (SIRs) of gastric cancer were calculated in three subgroups, that is, in those with a healthy stomach, those with H. pylori infection but without AG and those with AG. Risk ratios (RR) of gastric cancer were calculated using SIR of subgroups.

          Results: During 15 years, seven gastric cancers appeared per 79,928 person years among men with healthy stomachs, 50 cancers per 92,533 person years in men with H. pylori infection but without AG, and 8 per 8658 person years in men with AG. Risk ratio (RR) of stomach cancer in men with H. pylori infection was 5.8 (95%CI: 2.7–15.3) compared to men with healthy stomachs, and 9.1 (95%CI: 2.9–30.0) in men with AG. There were no differences in cancer risk between cardia and distal stomach.

          Conclusions: Risk of gastric cancer is low in men with healthy stomachs. It is significantly increased in those with H. pylori infection and more in those with AG.

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          Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration.

          B J Marshall, J R Warren (1984)
          Biopsy specimens were taken from intact areas of antral mucosa in 100 consecutive consenting patients presenting for gastroscopy. Spiral or curved bacilli were demonstrated in specimens from 58 patients. Bacilli cultured from 11 of these biopsies were gram-negative, flagellate, and microaerophilic and appeared to be a new species related to the genus Campylobacter. The bacteria were present in almost all patients with active chronic gastritis, duodenal ulcer, or gastric ulcer and thus may be an important factor in the aetiology of these diseases.
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            Schistosomes, liver flukes and Helicobacter pylori. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Lyon, 7-14 June 1994.

            CD Bucana, Y Kitadai, T Kuwai … (1994)
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              Opposing risks of gastric cardia and noncardia gastric adenocarcinomas associated with Helicobacter pylori seropositivity.

              Jarmo Virtamo, Farin Kamangar, Christian C Abnet … (2006)
              Colonization with Helicobacter pylori is a risk factor for gastric adenocarcinoma, but the magnitude of this association and its relationship to anatomic location of the cancer, duration of follow-up, age at diagnosis, histologic subtype, and H. pylori strain differences are less clear. We conducted a prospective nested case-control study of H. pylori serology to address these questions. Case and control subjects were selected from the 29,133 50- to 69-year-old males recruited into the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. At baseline, detailed demographic data and a serum sample were collected. From 1985 to 1999, 243 incident cases of gastric adenocarcinoma were diagnosed in cohort members. Serum samples from 234 case subjects (173 with noncardia gastric cancers and 61 with gastric cardia cancers) and 234 age-matched control subjects were assayed for antibodies against H. pylori whole-cell and CagA antigens. We fit conditional logistic regression models to estimate the unadjusted and adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for the association of H. pylori seropositivity, defined as seropositivity to either whole-cell or CagA antigens, with noncardia gastric and gastric cardia cancers. All statistical tests were two-sided. H. pylori seropositivity was strongly associated with the risk of noncardia gastric cancer (adjusted OR = 7.9, 95% CI = 3.0 to 20.9) but was inversely associated with the risk of gastric cardia cancer (adjusted OR = 0.31, 95% CI = 0.11 to 0.89). H. pylori seropositivity rates did not vary statistically significantly by length of follow-up, age at diagnosis, or histologic subtype. A calculation of rates showed that the absolute risks of noncardia gastric and cardia gastric adenocarcinomas in the H. pylori-positive participants of this cohort would be 63 and 12 per 100,000 person-years, respectively, whereas corresponding rates in H. pylori-negative participants would be 8 and 37 per 100,000 person-years, respectively. H. pylori is a strong risk factor for noncardia gastric cancer but is inversely associated with the risk of gastric cardia cancer. These findings bolster the hypothesis that decreasing H. pylori prevalence during the past century may have contributed to lower rates of noncardia cancer and higher rates of cardia cancer in Western countries.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Scand J Gastroenterol
                Journal ID (iso-abbrev): Scand. J. Gastroenterol
                Journal ID (archive): IGAS
                Journal ID (publisher-id): igas20
                Title: Scandinavian Journal of Gastroenterology
                Publisher: Taylor & Francis
                ISSN (Print): 0036-5521
                ISSN (Electronic): 1502-7708
                Publication date (Print): 2 October 2016
                Publication date (Electronic): 24 June 2016
                Volume: 51
                Issue: 10
                Pages: 1159-1164
                Affiliations
                [ a ]Department of Public Health, University of Eastern Finland , Kuopio, Finland
                [ b ]Finnish Cancer Registry , Helsinki, Finland
                [ c ]Department of Epidemiology, Finnish Cancer Registry , Helsinki, Finland
                [ d ]Department of Clinical Chemistry, University of Helsinki , Helsinki, Finland
                [ e ]Department of Biostatistics, Finnish Consulting Group , Helsinki, Finland
                [ f ]Department of Pathology, Patolab Oy , Espoo, Finland
                Author notes
                CONTACT Ilkka Vohlonen ilkka.vohlonen@ 123456uef.fi University of Eastern Finland, Public Health , BOX 1627, Kuopio 70100, Finland
                Article
                Publisher ID: 1183225
                DOI: 10.1080/00365521.2016.1183225
                PMC ID: 4960513
                PubMed ID: 27338132
                SO-VID: a82ecd35-95ce-4cc4-98f2-b6e2f5df53b3
                Copyright © © 2016 University of Eastern Finland Published by Informa UK Limited, trading as Taylor & Francis Group
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License ( http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

                History
                Date received : 4 March 2016
                Date revision received : 20 April 2016
                Date accepted : 23 April 2016
                Page count
                Pages: 6, Words: 4973
                Categories
                Subject: Article
                Subject: Original Article

                ScienceOpen disciplines: Gastroenterology & Hepatology
                Keywords: atrophic gastritis,gastric cancer,helicobacter pylori
                Data availability:
                ScienceOpen disciplines: Gastroenterology & Hepatology
                Keywords: atrophic gastritis, gastric cancer, helicobacter pylori

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