胃液Prostaglandin Eの研究 第2編 消化性潰瘍および急性ビラン性胃炎における検討

Prostaglandin E (PGE) in the gastric juice of patients with peptic ulcer and acute erosive gastritis was determined by a radioimmunoassay. In gastric and duodenal ulcer patients, the concentration and output of PGE in the gastric juice were not significantly different from those of normal subjects both basally and after pentagastrin stimulation, but in acute erosive gastritis patients they showed significantly lower levels. The concentration of PGE in the gastric juice was lower in all cases after pentagastrin stimulation compared to the basal level because of dilution due to an increased gastric juice volume. After pentagastrin stimulation, PGE output tended to increase in all groups, but this increase was not statistically significant and probably was caused by an increased gastric juice volume. No correlation could be found among acid output, pepsin output and gastric PGE output. These results do not support the concept that endogenous PGE deficiency may be an etiological factor in peptic ulcer disease, and seem to argue against a possible inhibitory role of PGE in gastric acid secretion by a negative feedback mechanism in man. However, a low level of endogenous PGE may be intimately related to the pathogenesis of acute erosive gastritis.