Helicobacter pylori infection and the risks of Barrett's oesophagus: A population‐based case–control study

Abstract

Infection with Helicobacter pylori is associated with significantly reduced risks of oesophageal adenocarcinoma, however few studies have examined the association between H pylori and Barrett's oesophagus (BO), the precursor lesion. We explored the relationship between H pylori infection and BO and sought to identify potential modifiers. We compared the prevalence of positive H pylori serology among 217 adults with simple BO (without dysplasia), 95 with dysplastic BO and 398 population controls sourced from the metropolitan Brisbane area. We determined H pylori serostatus using enzyme-linked immunosorbent assay. To estimate relative risks, we calculated odds ratios (OR) and 95% confidence intervals (CI) using multivariable logistic regression in the entire sample and stratified by factors known to cause BO. The prevalence of H pylori seropositivity was 12%, 3% and 18% respectively, among patients with simple BO, dysplastic BO and population controls. BO patients were significantly less likely to have antibodies for H pylori (Simple BO: OR=0.51, 95% CI: 0.30-0.86; Dysplastic BO: OR=0.10, 95% CI: 0.03-0.33) than population controls. For simple BO, the association was diminished after adjustment for frequency of gastro-oesophageal reflux (GOR) symptoms. Adjustment for frequency of GOR symptoms did not substantially alter the observed effect for dysplastic BO. While there was some variation in the magnitude of risk estimates across strata of age, sex, GOR symptoms, and use of PPIs or H2-receptor antagonists, the differences were uniformly nonsignificant. H pylori infection is inversely associated with BO, and our findings suggest that decreased acid load is not the only mechanism underlying the H pylori protective effect.

Gastric Helicobacter pylori Infection Affects Local and Distant Microbial Populations and Host Responses

“…Despite the significance of H. pylori as a pathogen, concerns have been raised about the consequences of the loss of an organism that has colonized humans for >100,000 years (Moodley et al, 2012). Observations of inverse associations of H. pylori with diseases include early onset-asthma (Arnold et al, 2011a; Chen and Blaser, 2007, 2008), gastrointestinal (Cohen et al, 2012; Higgins et al, 2011; Rothenbacher et al, 2000) and systemic (Perry et al, 2010) infections, and Barrett’s esophagus and its consequences (Corley et al, 2008; Rubenstein et al, 2014; Thrift et al, 2012). In mice, the age at which H. pylori is acquired is critical in influencing outcomes; challenged adult mice developed pre-neoplastic lesions, but neonatal mice were protected against severe pathology by immune tolerance (Arnold et al, 2011b).…”

Risk factors associated with Barrett’s epithelial dysplasia

“…Esophageal adenocarcinoma derived from BE is not common in Japan as compared with western countries, whereas gastric carcinoma is more prevalent in Japan. This inverse relationship may reflect the high prevalence of H. pylori infection in Japan and the low prevalence in western countries [24,39,40] . Another notable epidemiological difference between these regions is the length of BE; that is, SSBE is common in Japan but LSBE is more prevalent in western countries [27,28,30,31] .…”

Carcinogenesis of Barrett’s esophagus: a review of the clinical literature

“…Thrift et al [87] reported a populationbased case-control study which found that H. pylori infection was inversely associated with BE, whereas there was some variation in the magnitude of risk estimates across strata of age, gender, reflux symptoms, and use of proton pump inhibitors (PPIs) or H 2 -receptor antagonists (H 2 RAs Further studies are needed to test this association, and the studies should enroll patients prospectively to ensure standard BE diagnostic methods, H. pylori detection methods, and overall high study quality.…”