消化管ホルモンからみた胃潰瘍の病態生理・十二指腸潰瘍の病態生理

Pathogenesis of Peptic Ulcer from the Viewpoint of Gut Hormones

　消化性潰瘍の成因に，胃液分泌を介して消化管ホルモンが重要な役割を演ずることは，古くより指摘され，多くの研究がなされてきた．そして，既に10種を越える消化管ホルモンが発見され，その多くが生理的胃液分泌調節に何らかの関与をしていることも知られているが，消化性潰瘍の病態生理に及ぼす役割については，ガストリン，セクレチンを除いてはほとんど知られていないのが現状である．

　一方，消化性潰瘍という名称の中に総合される胃潰瘍および十二指腸潰瘍は，それぞれ胃液分泌動態をめぐって著明な相違が認められることは周知の事実である^1)～4)．本稿では，胃液分泌，ガストリン分泌を中心としたわれわれの形態学的研究を紹介することにより，胃潰瘍と十二指腸潰瘍の病態の相違を述べることより始めて，消化性潰瘍の病態生理に及ぼす消化管ホルモンの意義について話を展開していきたい．

　We investigated how gut hormones (mainly gastrin and secretin) were related to a pathogenesis of peptic ulcer. Our morphological study of the resected specimen showed that duodenal ulcer had more increased number of total G-cell as well as IGR than gastric ulcer-suggesting a relationship of cause and effect between the hyperacidity and the duodenal ulcer. However, considering the IGR in healthy controlled group, it is clear that the total number of the G-cell and IGR are strongly influenced by a degree of mucosal atrophy or intestinal metaplasia of the antrum.

　Therefore, it is necessarv to make a more close comparative study to define the relationship between the peptic ulcer and gastrin by considering length of ulcer history and its locational classification.

　On the other hand, there were many reports stating that the pathogenesis of duodenal ulcer was due to deranged secretin secretion or enhanced its inactivation, and the pathogenesis of the peptic ulcer has still not well defined. Perhaps, it is quite difficult to define the pathogenesis of the peptic ulcer as long as a single gut hormone is discussed as a causative factor, and we should study neuro-humoral interaction including automatic nerves together with mucosal defense mechanism including vascular system to cralify its pathogenesis. Zollinger-Ellison syndrome has been well known to have hyperacidity due to tumor-secreting gastrin and clinical feature of persistent peptic ulcer, demonstrating clear-cut relationship of cause and effect between the gut hormone and peptic ulcer. We reported our case of Zollinger-Ellison syndrome and discussed its pathogenesis, diagnosis and therapy.