Baron J H
Scand J Gastroenterol Suppl. 1982;80:1-10.
In duodenal ulcer disease, peptic digestion and ulceration of the duodenal mucosa can be related to increased duodenal acidity, which in about half the patients is due to inherited gastric hypersecretion, with too many parietal and chief cells. The others, normosecretors, may have parietal and chief cells excessively stimulated by, and/or specially sensitive to, gastrins and the vagus, together with inadequate suppression of the release of antral gastrin and the secretion of gastric acid. The abnormality is gastric hypersecretion with inappropriate hypergastrinaemia. The reserve capacities of the duodenal defence mechanisms are probably normal, but there seems to be a functional impairment with inadequate defence by decreased bicarbonate secretion into the duodenum, but as yet no clear impairment of the release of mucosal hormones. There are marked hereditary factors in gastric ulcer too. Some ulcers are related to gastric irritants (salicylates, tobacco). Oi's anatomical dual-control mechanism explains why gastric ulcers are usually solitary and at one site. Gastritis and duodenal reflux are probably the most important factors in type 1, body ulcers. Gastric stasis may be a factor in type 2, combined ulcers. Type 3 prepyloric ulcers resemble duodenal ulcers, both in blood group and hypersecretion.
在十二指肠溃疡病中，十二指肠黏膜的消化性溃疡可能与十二指肠酸度增加有关，约半数患者的十二指肠酸度增加是由于遗传性胃酸分泌过多，壁细胞和主细胞过多。其他胃酸分泌正常者，壁细胞和主细胞可能受到胃泌素和迷走神经的过度刺激和/或对其特别敏感，同时胃窦胃泌素释放和胃酸分泌的抑制不足。异常表现为胃酸分泌过多伴不适当的高胃泌素血症。十二指肠防御机制或许储备能力正常，但似乎存在功能损害，即十二指肠内碳酸氢盐分泌减少导致防御不足，不过目前黏膜激素释放尚无明显损害。胃溃疡也有显著的遗传因素。一些溃疡与胃刺激物（水杨酸盐、烟草）有关。Oi的解剖学双重控制机制解释了为何胃溃疡通常是单发且位于同一部位。胃炎和十二指肠反流可能是1型胃体部溃疡最重要的因素。胃潴留可能是2型复合性溃疡的一个因素。3型幽门管溃疡在血型和胃酸分泌过多方面与十二指肠溃疡相似。
