World J Gastroenterol. 2013 Feb 14;19(6):786-9. doi: 10.3748/wjg.v19.i6.786.
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.
胃食管反流病（GORD）在普通人群中非常普遍。在过去的十年中，已经有人声称幽门螺杆菌（H. pylori）的根除与 GORD 的发生之间存在潜在关系。主要的假设机制是在那些以胃体为主的胃炎患者中，细菌治愈后胃酸分泌过多。我们对该领域中复杂的发病机制和临床数据进行了批判性重新评估。十二指肠溃疡患者在 H. pylori 根除后发生食管炎归因于胃酸分泌过多，这可能在体胃炎愈合后发展。然而，生理病理学和临床研究都证明了这些患者没有胃酸分泌过多的状态。事实上，根除 H. pylori 后，十二指肠溃疡的复发几乎被消除。此外，食管内 pH 记录研究未能证明在细菌根除后酸反流增加。此外，食管测压研究表明，根除 H. pylori 会减少而不是促进胃酸反流到食管。最后，临床研究数据表明，H. pylori 的根除与反流症状或糜烂性食管炎的发生没有显著关联，一些数据还表明，当食管炎已经存在时，根除感染也有优势。因此，“疯狂的酸”的传说——就像所有其他传说一样——仍然是一个迷人但虚构的故事。
