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Helicobacter pylori infection does not influence the progression from gastroesophageal reflux disease to Barrett's esophagus to esophageal adenocarcinoma.
Edhi, Ahmed; Gangwani, Manesh K; Aziz, Muhammad; Jaber, Fouad; Khan, Zubair; Inamdar, Sumant; Thrift, Aaron P; Desai, Tusar K.
Affiliation
  • Edhi A; Oakland University School of Medicine, William Beaumont Hospital, Royal Oak, MI, USA.
  • Gangwani MK; Department of Medicine, University of Toledo Medical Center, Toledo, OH, USA - gangwani.manesh@gmail.com.
  • Aziz M; Department of Medicine, University of Missouri, Kansas City, MO, USA.
  • Jaber F; Department of Gastroenterology and Hepatology, Mercy Health, Toledo, OH, USA.
  • Khan Z; Department of Gastroenterology and Hepatology, Mercy Health, Saint Louis, MO, USA.
  • Inamdar S; Department of Gastroenterology and Hepatology, University of Arkansas Medical Sciences, Little Rock, AR, USA.
  • Thrift AP; Section of Epidemiology and Population Sciences, Department of Medicine, Baylor College of Medicine, Houston, TX, USA.
  • Desai TK; Oakland University School of Medicine, William Beaumont Hospital, Royal Oak, MI, USA.
Article in En | MEDLINE | ID: mdl-38727697
ABSTRACT

INTRODUCTION:

We conducted a meta-analysis evaluating the overall risk of esophageal adenocarcinoma (EAC) in individuals with Helicobacter pylori infection, and a network meta-analysis to assess the role of H. pylori infection in the progression from Barrett's esophagus (BE) to EAC. EVIDENCE ACQUISITION The MEDLINE, EMBASE and Cochrane databases were searched between 1988 and June 2023 for observational studies of H. pylori infection and the risk of EAC. Summary odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using the DerSimonian-Laird method. I2 statistics were calculated to examine heterogeneity. EVIDENCE

SYNTHESIS:

Thirteen studies were included in the meta-analysis and 3 additional studies were included in the network meta-analysis. For comparisons with controls, individuals with H. pylori infection were 46% less likely to develop EAC than individuals without H. pylori infection (OR, 0.54; 95% CI 0.46, 0.64), with low heterogeneity between studies (I2=4.4%). The magnitude of the inverse association was stronger in the two large cohort studies (OR=0.31) than in the 11 case-control studies (OR=0.55). When comparing to controls, the network meta-analysis of 6 studies showed that H. pylori infection was associated with a lower risk of GERD (OR=0.68) or BE (OR=0.59) or EAC (OR=0.54); however, H. pylori infection was not associated with risk of EAC in patients with BE (OR=0.91; 95% CI 0.68, 1.21).

CONCLUSIONS:

This meta-analysis provides the strongest evidence yet that H. pylori infection is inversely associated with EAC. H. pylori does not appear to be associated with BE progression to EAC.

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Minerva Gastroenterol (Torino) Year: 2024 Document type: Article Affiliation country:

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Minerva Gastroenterol (Torino) Year: 2024 Document type: Article Affiliation country: