<i>Helicobacter pylori</i> Infection: Protection against Barrett’s Mucosa and Neoplasia?

Abstract

Background: Since Helicobacter pylori (Hp) infection provokes intestinal and gastric metaplasia, the question arises whether the specialized metaplasia (Barrett’s mucosa (BM)) and dysplasia or carcinoma in Barrett’s epithelium seen in gastro-oesophageal reflux disease (GORD) might not also be correlated with Hp infection, or whether the latter offers protection against Barrett’s oesophagus and Barrett’s adenocarcinoma. Patients: Gastric and oesophageal biopsies obtained from a total of 2,201 patients were analysed retrospectively. 297 of these patients had GORD (age 53.5 ± 13.4 years; m:f ratio 2.1:1), 1,192 patients had BM (age 62.8 ± 14.6 years; m:f 2.3:1) with or without neoplasia. 1,054 of these patients were diagnosed as having BM alone, 138 patients having BM neoplasia (high-grade dysplasia or adenocarcinoma). Patients with BM and low-grade dysplasia were excluded from this study because of the uncertainty in differentiating low-grade dysplasia from regenerative epithelium. A total of 712 patients with non-ulcer dyspepsia (NUD; average age 40.0 ± 16.1 years; m:f 0.3:1) served as a control group. Results: The percentage of Hp infection did not differ between patients with GORD with (53.3%)/without BM (51.4%) and neoplasia (47.8%), but is statistically significantly lower than in patients with NUD (65.7%). Conclusion: Our analysis shows that patients with GORD and Hp infection have no increased risk for the development of BM or neoplasia in BM. Since Hp infection is significantly less frequent in GORD than in NUD patients, a protective effect of the Hp infection is a possibility worth discussing.

Helicobacter pylori Infection in a Pig Model Is Dominated by Th1 and Cytotoxic CD8+T Cell Responses

“…H. pylori colonization usually does not cause illness, since 85% of infected people remain asymptomatic throughout life, but infection with strains bearing the cag (cytotoxin-associated gene) pathogenicity island can result in peptic ulcer disease, gastric lymphoma, and gastric adenocarcinoma, the second leading cause of cancer-related deaths, in 15% of infected individuals (2,3). Conversely, there also is increasing evidence of H. pylori providing protection against esophageal and cardial pathologies (4)(5)(6)(7), childhood asthma (8)(9)(10), childhood allergies (9,11), and diabetes and obesity (12). This Gram-negative microaerophilic bacterium of the Epsilonproteobacteria has coevolved with humans for at least 50,000 years, indicating high adaptation capacity to the environmental niche of the human gastric mucosa and suggesting the ability to evade the immune system (13) through mechanisms that are incompletely understood.…”

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.…”

Gastritis aus histologischer Sicht

“…Im deutschen Routineuntersuchungsgut liegt der Anteil der CGastritis mittlerweile bei bis zu 30. Auffällig ist eine Häufung bei Patienten mit gastroösophagealer Refluxkrankheit [2]. Relativ selten ist die Autoimmungastritis, die auf die Magenkorpusschleimhaut beschränkt ist (ca.…”