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Helicobacter pylori infection and the risk of Barrett's oesophagus: a community-based study.
Gut. 2008 Jun; 57(6):727-33.Gut

Abstract

OBJECTIVE

Gastric colonisation with the Helicobacter pylori bacterium is a proposed protective factor against oesophageal adenocarcinoma, but its point of action is unknown. Its associations with Barrett's oesophagus, a metaplastic change that is a probable early event in the carcinogenesis of oesophageal adenocarcinoma, were evaluated

METHODS

A case-control study was carried out in the Kaiser Permanente Northern California population, a large health services delivery organisation. Persons with a new Barrett's oesophagus diagnosis (cases) were matched to subjects with gastro-oesophageal reflux disease (GORD) without Barrett's oesophagus and to population controls. Subjects completed direct in-person interviews and antibody testing for H pylori and its CagA (cytotoxin-associated gene product A) protein.

RESULTS

Serological data were available on 318 Barrett's oesophagus cases, 312 GORD patients and 299 population controls. Patients with Barrett's oesophagus were substantially less likely to have antibodies for H pylori (OR = 0.42, 95% CI 0.26 to 0.70) than population controls; this inverse association was stronger among those with lower body mass indexes (BMIs < 25, OR = 0.03, 95% CI 0.00 to 0.20) and those with CagA+ strains (OR = 0.08, 95% CI 0.02 to 0.35). The associations were diminished after adjustment for GORD symptoms. The H pylori status was not an independent risk factor for Barrett's oesophagus compared with the GORD controls.

CONCLUSIONS

Helicobacter pylori infection and CagA+ status were inversely associated with a new diagnosis of Barrett's oesophagus. The findings are consistent with the hypothesis that H pylori colonisation protects against Barrett's oesophagus and that the association may be at least partially mediated through GORD.

Authors+Show Affiliations

Division of Research, Kaiser Permanente, 2000 Broadway, Oakland, CA 94612, USA. Douglas.Corley@kp.orgNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

17895354

Citation

Corley, D A., et al. "Helicobacter Pylori Infection and the Risk of Barrett's Oesophagus: a Community-based Study." Gut, vol. 57, no. 6, 2008, pp. 727-33.
Corley DA, Kubo A, Levin TR, et al. Helicobacter pylori infection and the risk of Barrett's oesophagus: a community-based study. Gut. 2008;57(6):727-33.
Corley, D. A., Kubo, A., Levin, T. R., Block, G., Habel, L., Zhao, W., Leighton, P., Rumore, G., Quesenberry, C., Buffler, P., & Parsonnet, J. (2008). Helicobacter pylori infection and the risk of Barrett's oesophagus: a community-based study. Gut, 57(6), 727-33.
Corley DA, et al. Helicobacter Pylori Infection and the Risk of Barrett's Oesophagus: a Community-based Study. Gut. 2008;57(6):727-33. PubMed PMID: 17895354.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Helicobacter pylori infection and the risk of Barrett's oesophagus: a community-based study. AU - Corley,D A, AU - Kubo,A, AU - Levin,T R, AU - Block,G, AU - Habel,L, AU - Zhao,W, AU - Leighton,P, AU - Rumore,G, AU - Quesenberry,C, AU - Buffler,P, AU - Parsonnet,J, Y1 - 2007/09/25/ PY - 2007/9/27/pubmed PY - 2008/6/19/medline PY - 2007/9/27/entrez SP - 727 EP - 33 JF - Gut JO - Gut VL - 57 IS - 6 N2 - OBJECTIVE: Gastric colonisation with the Helicobacter pylori bacterium is a proposed protective factor against oesophageal adenocarcinoma, but its point of action is unknown. Its associations with Barrett's oesophagus, a metaplastic change that is a probable early event in the carcinogenesis of oesophageal adenocarcinoma, were evaluated METHODS: A case-control study was carried out in the Kaiser Permanente Northern California population, a large health services delivery organisation. Persons with a new Barrett's oesophagus diagnosis (cases) were matched to subjects with gastro-oesophageal reflux disease (GORD) without Barrett's oesophagus and to population controls. Subjects completed direct in-person interviews and antibody testing for H pylori and its CagA (cytotoxin-associated gene product A) protein. RESULTS: Serological data were available on 318 Barrett's oesophagus cases, 312 GORD patients and 299 population controls. Patients with Barrett's oesophagus were substantially less likely to have antibodies for H pylori (OR = 0.42, 95% CI 0.26 to 0.70) than population controls; this inverse association was stronger among those with lower body mass indexes (BMIs < 25, OR = 0.03, 95% CI 0.00 to 0.20) and those with CagA+ strains (OR = 0.08, 95% CI 0.02 to 0.35). The associations were diminished after adjustment for GORD symptoms. The H pylori status was not an independent risk factor for Barrett's oesophagus compared with the GORD controls. CONCLUSIONS: Helicobacter pylori infection and CagA+ status were inversely associated with a new diagnosis of Barrett's oesophagus. The findings are consistent with the hypothesis that H pylori colonisation protects against Barrett's oesophagus and that the association may be at least partially mediated through GORD. SN - 1468-3288 UR - https://www.unboundmedicine.com/medline/citation/17895354/Helicobacter_pylori_infection_and_the_risk_of_Barrett's_oesophagus:_a_community_based_study_ L2 - https://gut.bmj.com/lookup/pmidlookup?view=long&amp;pmid=17895354 DB - PRIME DP - Unbound Medicine ER -