Helicobacter Pylori Infection and Serum Pepsinogen 1 Concentration in Peptic Ulcer Patients: Effect of Bacterial Eradication

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Abstract
In order to test the hypothesis that H. pylori infections in the gastric antrum increase pepsinogen I release, fasting serum pepsinogen I concentrations were compared in peptic ulcer patients with and without H. pylori infection. A randomized prospective study was performed to determine whether the increased serum pepsinogen I concentrations associated with H. pylori infection respond to treatment that eradicates H. pylori. Fasting serum pepsinogen I concentrations were measured by RIA in 736 patients with endoscopically and histologically confirmed benign peptic ulcer with and without H. pylori infection. Out of 511 patients with H. pylori infection, 110 patients (group 1) were randomly selected and were treated with metronidazole and tripotassium dicitrato bismuthate combined with ranitidine and antacid, and 97 patients (group 2) were treated only with ranitidine and antacid. The third group, 54 patients free of H. pylori infection, was designed to evaluate the influence of H2-receptor antagonist and antacid on the change of pepsinogen I. Fasting pepsinogen I concentration and H. pylori status were compared before and after the treatment. Patients infected by H. pylori (gastric ulcer 208, duodenal ulcer 303; total 511) had significantly higher fasting serum pepsinogen I concentrations than H. pylori negative patients (gastric ulcer 110, duodenal ulcer 115: total 225). Mean pepsinogen I level of the former was 124.3±46.9 and that of the latter was 77.9±25.8 ng/ml. (p0.57) None of the patients who were initially H. pylori-negative has been reinfected during the period of the study and their serum pepsinogen I concentrations were not changed. (pre-treatment value 75.1±8.0 ; post-treatment value 77.3±24.5 mg/ml)(p<0.75) Four-to six-week therapy of H2-receptor antagonist and antacid did not exert any influence on serum pepsinogen I concentrations. On the basis of our results, we have confirmed that the chronic infection of H. pylori of gastric antrum in peptic ulcer patients causes increased pepsinogen I release into the circulation, and eradication of the organism results in significant fall in serum pepsinogen I concentrations.