Thomas W G
Lancet. 1980 Nov 29;2(8205):1166-8. doi: 10.1016/s0140-6736(80)92598-2.
The increased duodeno-gastric reflux often associated with gastric or duodenal ulcer disease causes hypersecretion of acid in response to pentagastrin and hypergastrinaemia in response to meal. It is proposed that these functional changes are mediated by an alteration in somatostatin activity that is produced by the alkaline nature or pancreatic component of the reflux. When duodenal reflux is confined to the antrum, an increased acid output from normal secretory mucosa is delivered to the duodenum where ulceration may occur. When alkaline reflux affects the body of the stomach, gastritis is produced, with local fundic hypersecretion, which may lead to ulceration of the damaged gastric mucosa. Duodenal reflux may therefore be a common factor in the pathogenesis of gastric and duodenal ulcer, and it probably acts by producing a hormonal defect.
十二指肠-胃反流增加常与胃溃疡或十二指肠溃疡病相关，可导致对五肽胃泌素的胃酸分泌过多以及进食后高胃泌素血症。有人提出，这些功能变化是由反流的碱性性质或胰腺成分所产生的生长抑素活性改变介导的。当十二指肠反流局限于胃窦时，正常分泌黏膜增加的酸分泌会进入十二指肠，可能导致溃疡形成。当碱性反流影响胃体时，会产生胃炎，伴有局部胃底分泌过多，这可能导致受损胃黏膜溃疡。因此，十二指肠反流可能是胃溃疡和十二指肠溃疡发病机制中的一个共同因素，它可能通过产生激素缺陷而起作用。
