Helicobacter pylori infection and the risk of Barrett's oesophagus: a community-based study

Abstract

Objective-Gastric colonization with the Helicobacter pylori bacterium is a proposed protective factor against oesophageal adenocarcinoma, but its point of action is unknown. We evaluated its associations with Barrett's oesophagus, a metaplastic change that is a probable early event in the carcinogenesis of oesophageal adenocarcinoma. Design-A case-control studySetting-The Kaiser Permanente Northern California population, a large health services delivery organization Patients-Persons with a new Barrett's oesophagus diagnosis (cases) were matched to subjects with gastrooesophageal reflux disease (GORD) without Barrett's oesophagus and to population controls. Main Measures-Subjects completed direct in-person interviews and antibody testing forHelicobacter pylori and its cagA protein.Results-Serologic 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 Helicobacter pylori (odds ratio [OR] = 0.42, 95% confidence interval [CI] 0.26-0.70) than population controls; this inverse association was stronger among those with lower body mass indexes (BMI<25 OR=0.03, 95% CI 0.00 -0.20) and those with cagA+ strains (OR=0.08, 95% CI 0.02-0.35). The associations were diminished after adjustment for GORD symptoms. The H. pylori status was not an independent risk factor for Barrett's oesophagus compared to 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 Helicobacter pylori colonization protects against Barrett's oesophagus and that the association may be at least partially mediated through GORD.

Association between Helicobacter pylori seropositivity anddigestive tract cancers

“…The exact mechanism by which H pylori infection affects the development of EA and esophageal SCC is still puzzling. The strongest risk factor of distal EA is Barrett's esophagus, a condition secondary to long-term gastroesophageal reflux disease, and H pylori colonization may protect against Barrett's esophagus [11,13,26] . Richwww.wjgnet.com Compared to KMUH or NTUH controls: adjusting for age (continuous), gender (female vs male), educational levels (≤ primary school vs > high school; junior and high schools vs > high school), cigarette smoking (yes vs no), alcohol consumption (yes vs no) and betel nut chewing (yes vs no); Compared to community controls: Adjusting for the above factors except for betel nut chewing.…”

“…Recently, cumulative evidence has indicated that H pylori infection plays a protective role in the development of reflux esophagitis [10,11] and esophageal adenocarcinoma (EA) [6,8,12,13] . In contrast, the relationship between H pylori infection and esophageal squamous cell carcinoma (SCC) is still inconclusive [8,[14][15][16][17] .…”

Gastroesophageal reflux disease and the relationship with Helicobacter pylori

“…The relationship between H.pylori and BE development seems somewhat complicated. In the literature, there are studies that reach different results on this issue; in addition to the studies reporting that the presence of H.pylori is a risk factor for BE development, there are studies reporting that it does not influence the development of BE or it prevents BE development (20)(21)(22)(23)(24)(25)(26)(27)(28)(29). In the study by Vaezi et al (29), it was found that being infected with H.pylori had a protective effect for development of BE and its malignant complications.…”

Risk factors associated with Barrett’s epithelial dysplasia

“…Table 5 Relationship between the level of p53 expression and grade of dysplasia weight as risk factors associated with the presence of BE [7][8][9][10][11][12][13][14][15][16] . One of the most notable findings from epidemiological reports has been a strong inverse association between H. pylori infection and dysplasia of Barrett's epithelium [17,18,[21][22][23][24][25][26] . Esophageal adenocarcinoma derived from BE is not common in Japan as compared with western countries, whereas gastric carcinoma is more prevalent in Japan.…”

“…Moreover, Helicobacter pylori (H. pylori) infection may play a key role in suppression of BE. Two main inhibiting roles for development of BE have been postulated in H. pylori infection: H. pylori-induced atrophic gastritis resulting in less gastric acid secretion; and neutralization of the gastric acid by ammonia produced by H. pylori independently of gastric atrophy [17][18][19][20][21][22][23] . Cag-A positive H. pylori infection is strongly associated with a reduced risk of esophageal adenocarcinoma, and the association is independent of gastric atrophy, suggesting the involvement of a mechanism other than reduced acidic gastric reflux [24][25][26] .…”