중증간경변증 환자에서 위산분비 및 혈청 Gastrin치의 동정
- 박재호; 강영우; 박승국
- Alternative Author(s)
- Park, Jae Ho; Kang, Young Woo; Park, Soong Kook
- Publication Year
- Gastric acid output; Gastrin; Liver cirrhosis
- Increased incidences(5-40%) of peptic ulceration in the patients with liver cirrhosis have been observed but the pathogenesis has nit been clarified. Furthermore, elevated levels of gut hormones have been pointed out in cirrhotic patients, and an impairment of the inaction process at the liver was suggested as a mechanism of the elevation of some of gut hormones. And there was a tendency to correlate a pathogenesis of peptic ulcer with changes of acid output. This study was conducted to investigate the pathogenesis of peptic ulcer in liver cirrhosis, and the changes of acid output and serum gastin concentrations to the pentagasrin in patients with advanced liver cirrhosis and normal control subjects were checked. Fifteen patients with advanced liver cirrhosis and 10 normal control subjects were randomly selected for this study, and the basal acid output(BAO) and maximal acid output(MAO) after pentagastrin injection were measured. At the same time serum gastrin concentrations of each subject were measured before and 15, 45, 90, 120 minutes after pentagastrin injection(6ug/kg). The response of acid output to the pentagastrin was adequate in the patients with advanced liver cirrhosis as well as in the normal control group. There was no significant difference in amount and pattern of acid output between two groups. After injection of pentagastrin, the serum gastrin concentration increased significantly at 15 minutes in both groups, and it may be partially due to cross reaction of pentagastrin and serum gastrin. There was no significant difference in serum gastrin concentration between two groups. These results suggested the concentration of serum gastrin and gastric acid output did not seem to de direct relationship with pathogenesis of peptic ulcer in the patients with liver cirrhosis. Because the role of defense mechanisms in peptic ulceration was overlooked, further comprehensive study to evaluate their role is needed to make clear the payhogensis of peptic ulcer formation in liver cirrhosis.
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