摘要
Gastroesophageal reflux disease (GORD) is highly prevalent in the general population.In the last decade,a potential relationship between Helicobacter pylori (H.pylori) eradication and GORD onset has been claimed.The main putative mechanism is the gastric acid hypersecretion that develops after bacterial cure in those patients with corpus-predominant gastritis.We performed a critical reappraisal of the intricate pathogenesis and clinical data available in this field.Oesophagitis onset after H.pylori eradication in duodenal ulcer patients has been ascribed to a gastric acid hypersecretion,which could develop following body gastritis healing.However,the absence of an acid hypersecretive status in these patients is documented by both pathophysiology and clinical studies.Indeed,duodenal ulcer recurrence is virtually abolished followingH.pylori eradication.In addition,intra-oesophageal pH recording studies failed to demonstrated increased acid reflux following bacterial eradication.Moreover,oesophageal manometric studies suggest that H.pylori eradication would reduce-rather than favor-acid reflux into the oesophagus.Finally,data of clinical studies would suggest that H.pylori eradication is not significantly associated with eitherreflux symptoms or erosive oesophagitis onset,some data suggesting also an advantage in curing the infection when oesophagitis is already present.Therefore,the legend of "crazy acid" remains-as all the others a fascinating,but imaginary tale.
Gastroesophageal reflux disease (GORD) is highly prevalent in the general population. In the last decade, a potential relationship between Helicobacter pylori (H. pylori) eradication and GORD onset has been claimed. The main putative mechanism is the gastric acid hypersecretion that develops after bacterial cure in those patients with corpus-predominant gastritis. We performed a critical reappraisal of the intricate pathogenesis and clinical data available in this field. Oesophagitis onset after H. pylori eradication in duodenal ulcer patients has been ascribed to a gastric acid hypersecretion, which could develop following body gastritis healing. However, the absence of an acid hypersecretive status in these patients is documented by both pathophysiology and clinical studies. Indeed, duodenal ulcer recurrence is virtually abolished following H. pylori eradication. In addition, intra-oesophageal pH recording studies failed to demonstrated increased acid reflux following bacterial eradication. Moreover, oesophageal manometric studies suggest that H. pylori eradication would reduce - rather than favor - acid reflux into the oesophagus. Finally, data of clinical studies would suggest that H. pylori eradication is not significantly associated with either reflux symptoms or erosive oesophagitis onset, some data suggesting also an advantage in curing the infection when oesophagitis is already present. Therefore, the legend of “crazy acid” remains - as all the others - a fascinating, but imaginary tale.
