Interactions between Helicobacter pylori and gastroesophageal reflux disease

Abstract

Interactions between Helicobacter Pylori (HP) and gastroesophageal reflux disease (GERD) are a complex issue. Several pathophysiological factors influence the development and the course of GERD, HP infection might be only one of these. Many studies emphasize the co-existence of these diseases. HP infection could contribute to GERD through both a protective and an aggressive role. Gastric acid secretion is a key factor in the pathophysiology of reflux esophagitis. Depending on the type of gastritis related to HP, acid secretion may either increase or decrease. Gastritis in corpus leads to hypoacidity, while antrum gastritis leads to hyperacidity. In cases of antral gastritis and duodenal ulcers which have hyperacidity, the expectation is an improvement in pre-existing reflux esophagitis after eradication of HP. In adults, HP infection is often associated with atrophic gastritis in the corpus. Atrophic gastritis may protect against GERD. Pangastritis which leads to gastric atrophy is commonly associated with CagA strains of HP and it causes more severe gastric inflammation. In case of HP-positive corpus gastritis in the stomach, pangastritis, and atrophic gastritis, reflux esophagitis occurs frequently after eradication of HP. Nonetheless, as a predisposing disease of gastric cancer, HP should be treated. In conclusion, as the determinative factors affecting GERD involving in HP, detailed data on the location of gastric inflammation and CagA positivity should be obtained by the studies at future.

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