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Helicobacter pylori infection and gastroesophageal reflux in a population-based study (The HUNT Study).
Helicobacter 2007; 12(1):16-22H

Abstract

BACKGROUND AND AIM

It has been suggested that Helicobacter pylori infection may prevent gastroesophageal reflux, possibly through gastric atrophy. Since, however, previous results are contradictory and no population-based studies are available, the relationship between H. pylori and reflux remains uncertain. The aim of this study was to investigate this relationship in a population-based, nested, case-control study.

METHODS

From a cohort of 65,363 individuals, representing 71.2% of the adult population in the Norwegian county of Nord-Trondelag, we randomly selected 472 persons with recurrent reflux symptoms (cases) and 472 without such symptoms (controls). Occurrence of H. pylori and its virulence factor cagA was determined serologically, using an immunoblot assay. Gastric atrophy was assessed through serum levels of pepsinogen I. Odds ratios (OR) with 95% confidence intervals (CI), adjusted for potential confounding factors, represented relative risks.

RESULTS

H. pylori infection was not associated with a decreased risk of reflux symptoms (OR 1.1, 95% CI 0.8-1.6), irrespective of positive cagA status (OR 1.1, 95% CI 0.8-1.5). Gastric atrophy reduced the risk of reflux symptoms (OR 0.2, 95% CI 0.0-0.6). Infection with H. pylori entailed a ninefold increase in the risk of gastric atrophy compared to non-infection (OR 8.9, 95% CI 2.0-39.9).

CONCLUSIONS

H. pylori infection, irrespective of cagA status, did not affect the occurrence of reflux symptoms in this population-based setting. Infected individuals are at increased risk of gastric atrophy, which in turn reduces reflux symptoms, but due to the low frequency of gastric atrophy among infected individuals overall, there was no association with reflux symptoms on a population level.

Authors+Show Affiliations

Unit of Esophageal and Gastric Research, Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden. helena.nordenstedt@ki.seNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17241296

Citation

Nordenstedt, Helena, et al. "Helicobacter Pylori Infection and Gastroesophageal Reflux in a Population-based Study (The HUNT Study)." Helicobacter, vol. 12, no. 1, 2007, pp. 16-22.
Nordenstedt H, Nilsson M, Johnsen R, et al. Helicobacter pylori infection and gastroesophageal reflux in a population-based study (The HUNT Study). Helicobacter. 2007;12(1):16-22.
Nordenstedt, H., Nilsson, M., Johnsen, R., Lagergren, J., & Hveem, K. (2007). Helicobacter pylori infection and gastroesophageal reflux in a population-based study (The HUNT Study). Helicobacter, 12(1), pp. 16-22.
Nordenstedt H, et al. Helicobacter Pylori Infection and Gastroesophageal Reflux in a Population-based Study (The HUNT Study). Helicobacter. 2007;12(1):16-22. PubMed PMID: 17241296.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Helicobacter pylori infection and gastroesophageal reflux in a population-based study (The HUNT Study). AU - Nordenstedt,Helena, AU - Nilsson,Magnus, AU - Johnsen,Roar, AU - Lagergren,Jesper, AU - Hveem,Kristian, PY - 2007/1/24/pubmed PY - 2007/3/16/medline PY - 2007/1/24/entrez SP - 16 EP - 22 JF - Helicobacter JO - Helicobacter VL - 12 IS - 1 N2 - BACKGROUND AND AIM: It has been suggested that Helicobacter pylori infection may prevent gastroesophageal reflux, possibly through gastric atrophy. Since, however, previous results are contradictory and no population-based studies are available, the relationship between H. pylori and reflux remains uncertain. The aim of this study was to investigate this relationship in a population-based, nested, case-control study. METHODS: From a cohort of 65,363 individuals, representing 71.2% of the adult population in the Norwegian county of Nord-Trondelag, we randomly selected 472 persons with recurrent reflux symptoms (cases) and 472 without such symptoms (controls). Occurrence of H. pylori and its virulence factor cagA was determined serologically, using an immunoblot assay. Gastric atrophy was assessed through serum levels of pepsinogen I. Odds ratios (OR) with 95% confidence intervals (CI), adjusted for potential confounding factors, represented relative risks. RESULTS: H. pylori infection was not associated with a decreased risk of reflux symptoms (OR 1.1, 95% CI 0.8-1.6), irrespective of positive cagA status (OR 1.1, 95% CI 0.8-1.5). Gastric atrophy reduced the risk of reflux symptoms (OR 0.2, 95% CI 0.0-0.6). Infection with H. pylori entailed a ninefold increase in the risk of gastric atrophy compared to non-infection (OR 8.9, 95% CI 2.0-39.9). CONCLUSIONS: H. pylori infection, irrespective of cagA status, did not affect the occurrence of reflux symptoms in this population-based setting. Infected individuals are at increased risk of gastric atrophy, which in turn reduces reflux symptoms, but due to the low frequency of gastric atrophy among infected individuals overall, there was no association with reflux symptoms on a population level. SN - 1083-4389 UR - https://www.unboundmedicine.com/medline/citation/17241296/Helicobacter_pylori_infection_and_gastroesophageal_reflux_in_a_population_based_study__The_HUNT_Study__ L2 - https://doi.org/10.1111/j.1523-5378.2007.00466.x DB - PRIME DP - Unbound Medicine ER -