HELICOBACTER PYLORI INFECTION AND ESOPHAGEAL PATHOLOGY
Abstract
Helicobacter pylori (H. pylori) is the most well-known gram-negative spiral-shaped bacterium that infects the mucous membrane of the stomach and duodenum and is an etiological factor in the development of chronic gastritis, duodenitis, gastric ulcer or duodenal ulcer as well as stomach malignancies. According to some studies, the mucous membrane of the esophagus can be an additional reservoir for the infection: the incidence of H. pylori in the lower esophagus ranges from 20 to 70 %. However, the relationship between the persistence of this microorganism and the pathology of the esophagus is a complex issue as well as a subject of discussion due to contradicting results. This review presents an analysis of the literature on possible mechanisms of H. pylori influence on the development of esophageal diseases, such as gastroesophageal reflux disease (GERD), Barrett’s esophagus and esophageal cancer. The review also describes the risks of developing esophageal pathology after H. pylori eradication. It is noteworthy that most authors note a lower incidence of H. pylori in patients with GERD than in the general population. A meta-analysis of 84 717 cases of Barrett’s esophagus has shown that H. pylori reduces the risk of developing Barrett’s esophagus, and a meta-analysis involving 345 886 patients has not revealed a significant difference in the prevalence of H. pylori in patients with esophageal adenocarcinoma and control group patients. It can be assumed that the persistence of infection in different parts of the upper digestive tract triggers different pathogenetic mechanisms; as a result, the presence of a microbe in the stomach becomes a protective factor in the development of esophageal diseases, and H. pylori invasion in the esophagus, on the contrary, potentiates the development of its pathology. On the other hand, an increase in the occurrence and deterioration of the esophageal pathology after successful eradication of the microorganism may be a consequence of translocation of the pathogen into the mucous membrane of the esophagus. In addition, under the conditions of H. pylori persistence, atrophy of the gastric mucosa develops, which can indirectly due to a decrease in acidity reduce the aggressive effect of gastric juice on the esophageal mucosa in patients with GERD. The problem of H. pylori invasion of the esophageal mucosa also requires further study for a more comprehensive understanding of the mechanisms of this pathology.
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