The American journal of gastroenterology · 1994
Effect of eradication of Helicobacter pylori on serum pepsinogen I, gastrin, and insulin in duodenal ulcer patients: a 12-month follow-up study.
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Chen T S, Tsay S H, Chang F Y, Lee S D
Аннотация
OBJECTIVES: To understand the short-term and long-term effects of the eradication of Helicobacter pylori on serum pepsinogen I, gastrin, and insulin concentration, we studied 53 patients with endoscopically proven duodenal ulceration and H. pylori infection.
METHODS: All patients received a 2-wk course of colloidal bismuth subcitrate, amoxycillin, and metronidazole, and endoscopy was performed at 1.5, 3, 6, and 12 months after entry. H. pylori status was assessed by a urease test and histology.
RESULTS: Among 43 patients in whom H. pylori was eradicated throughout the follow-up year, the mean basal pepsinogen I was 108 ng/ml at pretreatment, decreasing significantly to 85, 77, 80, and 75 ng/ml at 1.5, 3, 6, and 12 months, respectively, at posttreatment. The basal gastrin was 100 pg/ml at pretreatment and fell significantly to 72, 64, 65, and 59 pg/ml, respectively, posttreatment. Of the four patients in whom the H. pylori was not eradicated, there was no significant change in the median basal pepsinogen I and gastrin concentration. Among the six patients in whom the H. pylori was again detectable within the follow-up year, the fallen serum concentration of pepsinogen I and gastrin returned to the pretreatment level. There was no significant change of basal insulin concentration after triple therapy in either the successfully eradicated or failed group.
CONCLUSION: We conclude that H. pylori is the leading and direct cause of higher serum concentration of pepsinogen I and gastrin in duodenal ulcer patients.
METHODS: All patients received a 2-wk course of colloidal bismuth subcitrate, amoxycillin, and metronidazole, and endoscopy was performed at 1.5, 3, 6, and 12 months after entry. H. pylori status was assessed by a urease test and histology.
RESULTS: Among 43 patients in whom H. pylori was eradicated throughout the follow-up year, the mean basal pepsinogen I was 108 ng/ml at pretreatment, decreasing significantly to 85, 77, 80, and 75 ng/ml at 1.5, 3, 6, and 12 months, respectively, at posttreatment. The basal gastrin was 100 pg/ml at pretreatment and fell significantly to 72, 64, 65, and 59 pg/ml, respectively, posttreatment. Of the four patients in whom the H. pylori was not eradicated, there was no significant change in the median basal pepsinogen I and gastrin concentration. Among the six patients in whom the H. pylori was again detectable within the follow-up year, the fallen serum concentration of pepsinogen I and gastrin returned to the pretreatment level. There was no significant change of basal insulin concentration after triple therapy in either the successfully eradicated or failed group.
CONCLUSION: We conclude that H. pylori is the leading and direct cause of higher serum concentration of pepsinogen I and gastrin in duodenal ulcer patients.