Helicobacter pylori and gastroesophageal reflux disease: the bug may not be all bad

Abstract

Peptic ulcer disease and gastric cancer of the antrum and body have been declining in the 20th century. In contrast, a new group of diseases are increasingly rapidly in Western countries: gastroesophageal reflux disease, Barrett's esophagus, and adenocarcinoma of the distal esophagus. Recent studies suggest this phenomenon may be related to the simultaneous fall in the prevalence of Helicobacter pylori (H. pylori) colonization, especially by the virulent cagA + strains. H. pylori infection with the cagA+ strain is potentially protective against the spectrum of gastroesophageal reflux disease because it lowers intragastric acidity as the result of a pangastritis, frequently with multifocal gastric atrophy and possibly increased intragastric ammonia production. Assuming that some types of H. pylori strains are protective, our entire approach to the worldwide elimination of this organism, sometimes indiscriminately, will need critical reevaluation.

Patients with Helicobacter pylori infection have less severe gastroesophageal reflux disease: a study using endoscopy, 24-hour gastric and esophageal pH metry

“…The PG-I/ PG-II ratio did not correlate with gastric acidity; this might be related to the fact that our study population included patients with antral (high acid) and pangastritis (reduced acid) both among H. pylori infected group, thus balancing the effect of each other. Secondly, presence of H. pylori itself increases the gastric pH probably due to inflammation of the stomach and buffering of acid because of ammonia [47,48]. However, among patients without H. pylori infection, higher PG-I/PG-II ratio correlated with gastric acidity.…”

Incidence of Esophageal Carcinoma Among Malays in North-Eastern Peninsular Malaysia: An Area with an Exceptionally Low Prevalence of Helicobacter pylori Infection

“…It has been proposed that gastric atrophy induced by chronic H. pylori infection results in hypoacidity and in turn reduces the tendency for chronic gastresophageal reflux, Barrett's and esophageal carcinoma [4]. Absence of H. pylori would thus enhance the esophageal acid load for those who experienced gastresophageal reflux leading to more severe clinical disease, a higher incidence of Barrett's esophagus, and subsequently adenocarcinoma of the esophagus.…”

“…This rise has been linked to the increasing prevalence of obesity, gastresophageal reflux, and Barrett's esophagus. It has also been suggested that the decline in the prevalence of Helicobacter pylori (H. pylori) and the consequent changes in gastric acid homeostasis resulting in a higher esophageal acid load may be contributory [1][2][3][4]. Indeed an inverse relationship has been suggested between H. pylori infection and the risk of esophageal adenocarcinoma [5][6][7][8].…”

Helicobacter Pylori

“…This has not proven to be the case in the available US studies. At present, the higher dose of clarithromycin is recommended within the United States [4,48].…”

“…The inflammatory and neurohumoral effects induced by H. pylori differ from individual to individual, likely related to host and bacterial strain heterogeneity. This heterogeneity may explain why some individuals develop antral predominant gastritis and duodenal ulcer while others develop body-predominant gastritis, intestinal metaplasia, and gastric malignancy [4]. In fact, recent studies suggest that there may be an inverse relationship between duodenal ulcer and gastric cancer [5].…”