Impact of Helicobacter pylori status on GERD, Barrett’s esophagus and esophageal cancer

Helicobacter pylori (H. pylori) is a ubiquitous human pathogen that infects up to 50% of the world's population. Its involvement in the etiology of various gastrointestinal disorders, including gastritis, peptic ulcer disease, and gastric cancer, is well established. In recent years, the relationship between H. pylori infection and gastroesophageal reflux disease (GERD) has garnered significant attention. This review article aims to summarize the current understanding of the impact of H. pylori infection and its eradication on GERD and its related complications, including Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC).

Gastric Acid Secretion and H. pylori Infection

Gastric acid secretion plays a crucial role in acid reflux disease, which can be modulated by H. pylori infection. Studies have shown that H. pylori infection can increase or decrease gastric acid secretion depending on its distribution within the stomach. For instance, antrum-predominant infection has been shown to augment acid secretion by stimulating parietal cells and gastrin induction, ultimately contributing to GERD development. Conversely, corpus-predominant infection can decrease acid secretion, potentially offering protection against GERD.

H. pylori and GERD

While the direct causal link between H. pylori infection and GERD remains controversial, several studies have reported an association between the two conditions. The presence of H. pylori may influence GERD symptoms by altering the composition of the upper gastrointestinal microbiota, modulating gastric acid secretion, and influencing esophageal motility.

Several meta-analyses have evaluated the effect of H. pylori eradication on GERD symptoms. While some studies have reported an increase in GERD symptoms after eradication, others have shown no significant change or even improvement. These inconsistent results highlight the need for further research to clarify the exact role of H. pylori in GERD pathogenesis.

H. pylori and Barrett's Esophagus (BE)

Barrett's esophagus is a premalignant condition that can progress to esophageal adenocarcinoma. Early studies investigating the relationship between H. pylori infection and BE yielded inconclusive results. However, recent meta-analyses have consistently reported a protective effect of H. pylori against BE development. This protective effect is likely mediated through several mechanisms, including downregulation of tumor-promoting inflammatory responses and maintenance of oral microbiota balance.

H. pylori and Esophageal Adenocarcinoma (EAC)

The link between H. pylori infection and esophageal adenocarcinoma is complex. While H. pylori infection appears to confer protection against EAC, the mechanisms underlying this phenomenon are not fully understood. It has been suggested that CagA-positive H. pylori strains may play a role in preventing EAC by downregulating inflammatory responses and maintaining oral microbiota balance. Additionally, H. pylori-induced apoptosis of Barrett's-derived EAC cells has been reported, further supporting its potential protective role.

Clinical Implications and Future Directions

Understanding the relationship between H. pylori infection and GERD-related complications has important clinical implications. The protective effect of H. pylori against BE and EAC highlights the need for caution when considering eradication therapy in patients with these conditions. Further research is needed to elucidate the underlying mechanisms of H. pylori's protective effects and to identify biomarkers that can guide personalized treatment strategies.

Conclusions

In summary, the relationship between H. pylori infection and GERD-related complications is complex and multifaceted. While H. pylori infection appears to offer protection against BE and EAC, its role in GERD symptomology remains uncertain. Further research is necessary to better understand the pathogenesis of these conditions and to develop effective prevention and treatment strategies.

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https://www.xiahepublishing.com/2994-8754/JTG-2023-00020

The study was recently published in the Journal of Translational Gastroenterology.

Journal of Translational Gastroenterology (JTG) dedicates to improving clinical diagnosis and treatment, advancing understanding of the molecular mechanisms, and promoting translation from bench to bedside of gastrointestinal, hepatobiliary, and pancreatic diseases. The aim of JTG is to provide a forum for the exchange of ideas and concepts on basic, translational, and clinical aspects of gastroenterology, and promote cross-disciplinary research and collaboration.

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