Personal view: to treat or not to treat? Helicobacter pylori and gastro‐oesophageal reflux disease — an alternative hypothesis

Abstract

Summary Helicobacter pylori causes acute on chronic gastritis and is responsible for most peptic ulcers and gastric cancer. However, recent papers have suggested that it may protect against gastro‐oesophageal reflux, Barrett's oesophagus and oesophageal cancer. Furthermore, the rapid increase in gastro‐oesophageal reflux disease, Barrett's oesophagus and adenocarcinoma of the oesophagus in the developed world has been attributed by some to the falling prevalence of H. pylori. These considerations have led to the suggestion that H. pylori infection should not necessarily be treated, especially in patients with gastro‐oesophageal reflux disease. Conversely, data from prospective randomized studies have shown that H. pylori eradication does not cause gastro‐oesophageal reflux disease in patients with duodenal ulcer or in the normal population, nor does it worsen the outcome of pre‐existing gastro‐oesophageal reflux disease. Therefore, although H. pylori is negatively associated with gastro‐oesophageal reflux disease, its eradication does not induce the disease. A hypothesis is presented suggesting that the increased prevalence of gastro‐oesophageal reflux disease is a result of rising acid secretion in the general population, which, in turn, is a consequence of the increased linear height (a predictor of acid secretion). The greater acid secretion could also explain the decline in the prevalence of H. pylori and perhaps account for the inverse relationship between H. pylori and gastro‐oesophageal reflux disease. These considerations are explored in discussing whether H. pylori infection should be treated in infected patients presenting with gastro‐oesophageal reflux disease.

Increasing incidence of Barrett's oesophagus in the general population

“…23 It has been suggested that the incidence of gastro-oesophageal reflux disease is linked with an increasing average body weight, 24 and with an increasing average body height in association with a decreasing prevalence of Helicobacter pylori infection in the population. 25 The rise in incidence of BO that we observed was most pronounced in men less than 60 years of age (fig 3). A possible explanation could be that men are now exposed to risk factors for BO at a younger age than they were in the past.…”

Update on therapeutic options for Helicobacter pylori-related diseases

“…It now clearly appears that the association between high proportion of GERD and low prevalence of H. pylori infection observed in some studies is not causal. It has even been proposed that it could be just the opposite, ie, that increasing acid secretion in the general population, which is considered to be a consequence of increased height, may not only result in GERD but also in a decrease in the prevalence of H. pylori, because the bacterium is less likely to colonize the stomach [49].…”

Helicobacter pylori infection and gastric cancer

“…26 There is accumulating evidence that acid secretory capacity is crucial in determining the distribution and natural history of H. pylori infection. 27,28 In hosts with low secretory capacity (genetically determined or secondary to pharmacologic inhibition) the organism is capable of colonising a wider niche than would be possible in the presence of high volumes of acid. Colonisation of a wider niche including the corpus mucosa, leads to corpus gastritis with resultant functional inhibition of acid secretion.…”