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        위 십이지장 질환들의 위액내 Bile Acid 와 Lysolecithin 농도에 관한 관찰

        정정명(Jung Myung Chung),정봉균(Bong Kun Jeon),김수찬(Soo Chan Kim),주영돈(Young Don Joo),설상영(Sang Young Soel),최하진(Ha Jin Choi) 대한내과학회 1989 대한내과학회지 Vol.37 No.3

        N/A A peptic ulcer is a benign ulcerative lesion in the alimentary tract developed by corrosive and digestive action of acid and pepsin in gastric juice and its cause is thought to be due to the imbalance of aggressive factors and defense mechanisms in gastric juice. But there are many controversies about the etiologic factors of peptic ulcer and further studies are needed for understanding of the pathophysiologic mechanisms. Recently it has been reported that bile and pancreatic juice could be refluxed into the upper duodenum or stomach under certain conditions, so gastric and duodenal ulcers could be induced by those digestive actions. This reflux phenomenon is supposed to be an important etiologic factor of gastric ulcer. More specifically, bile acid and lysolecithin of the refluxed duodenal contents increase back diffusion of hydrogen ions in the stomach and this back diffusion of hydrogen ions could induce acute or chronic gastritis and gastric ulcer. Moreover, it is carefully presumed that this reflux-induced acute and chronic gastritis acts as a factor of non-ulcer dyspepsia, and chronic stimulation of refluxed bile acid and lysolecithin seems likely to be an etiological factor for the development of stump cancer in gastrectomized patients. In this study, we have investigated the levels of bile acid and lysolecithin concentration in gastric juice for the evaluation of some influences of gastroduodena1 reflux on several gastroduodenal diseases. The results were as follows: 1) Bile acid concentration of gastric juice was 46.5±31.0 μmol/l in 13 normal controls, 202.2±109,2 μmol/l in 20 cases of duodenal ulcer, 329.1±101.5 μmol/1 in 28 cases of gastric ulcer 241.8±147.7 μmon/1 in 14 cases of stomach cancer and 352.1±88.7 μmol/1 in 18 cases of non-ulcer dyspepsia. 2) Lysolecithin concentration in gastric juice was 81.0±22.9 μmol/1 in 10 normal controls, 114.3±40.1 μmol/ l in 12 cases of duodenal ulcer, 170.4±43.9 μmol/1 in 10 cases of gastric ulcer, 230.3±172.0 μmol/1 in 6 cases of stomach cancer and 238.9±187.6 μmol/l in 7 cases of non-ulcer dyspepsia. 3) Average bile acid concentration in gastric juice showed a significant increase in each disease group and it was more prominent in gastric diseases including non-ulcer dyspepsia and gastric ulcer than in other groups. 4) Lysolecithin concentration in gastric juice also showed a significant increase in each disease group and it was more prominent in gastric ulcer than in duodenal ulcer. Lysolecithin concentration in the non-ulcer dyspepsia and stomach cancer groups showed a more prominent increase than the control group and duodenal ulcer group but we could not apprehend the clinical significance because the number of cases was negligible. 5) There was no specific correlation between bile acid and lysolecithin concentration of gastric juice in 20 cases of gastric and duodenal ulcers, From our findings, the constant increase of bile acid or lysolecithin concentration in gastric juice might be one of the etiologic factors in development of gastroduodenal diseases, particularly in gastric diseases. However, further study about this problem is thought to be needed.

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