胃酸分泌能と胃排出能からみた胃・十二指腸潰瘍の病態生理

The Pathophysiology of Gastric and Duodenal Ulcer from the Viewpoint of Gastric Acid Secretion and Gastric Emptying

　消化性潰瘍の成因を論ずる場合，no acid no ulcerで語られるごとく，胃酸分泌を無視できないことは言うまでもない．しかし胃液酸度のみに原因を負わせることは不可能である．

　胃および十二指腸潰瘍の2つの潰瘍は全く異なった病態であることは，現在では常識的である．日本人と欧米人の消化性潰瘍を疫学的にみると，食生活や社会的環境などが欧米化したことにより胃潰瘍と十二指腸潰瘍の占める割合が逆転し，十二指腸潰瘍の比率が増加していることなどから考えて，攻撃因子としての胃酸分泌能の意義は重要である．

　In previous reports, it has been thought that there were certain differences between gastric ulcer and duodenal ulcer in the etiology and the pathophysiology of ulcer.

　Therefore, in this article, we investigated the pathophysiology of ulcer from the standpoint of gastric acid secretion and gastric emptying using the acetaminophen method.

　The gastric acid secretion in gastric ulcer patients varied from normosecretion to hyposecretion on BAO and MAO stimulated by tetragastrin. According to aging, the progressive atrophic change of the gastric mucosa was seen as to reduce the gastric acid secretion. The gastric emptying in gastric ulcer was delayed more than normal controls and duodenal ulcers, unrelated with the difference in the gastric acid secretion. But especially, the ulcer which is located on the “M” portion including the angle had much more delayed gastric emptying than the other location.

　In duodenal ulcer patients, having the gastric hypersecretion (BAO and MAO), according to atrophic of the gastric mucosa and reduction of the gastric acid secretion were noted and found compared to gastric ulcer. The gastric emptying was more rapid than normal controls and gastric ulcers. And also, the gastric emptying in duodenal ulcer with acid hypersecretion (MAO＞20 mEq/h) was much more rapid than normosecretory patients (MAO＜20).

　Patients with recurrent gastric ulcer had more delayed gastric ulcer, and in those with recurrent duodenal ulcer, more rapid gastric emptying than those without proven recurrence was seen.

　From the viewpoints of the results obtained: 1) The pathophysiology of gastric ulcer may be considered important damage of the mucosal resistance which followed various gastritis and gastric atrophy due to delayed gastric emptying, in spite of the hyposecretion of the gastric secretion.

　2) On the other hand, the pathophysiology of duodenal ulcer may be considered to be both the hypersecretion of the gastric acid output and the rapid gastric emptying, namely, in addition to increasing vagal stimulation, disturbance of negative feed back (duodenal brake) was one of the important factors.