The effect of treatment of Helicobacter pylori infection on gastric mucosal plasminogen activators

Background and objective: Long-term H. pylori associated gastritis is recognized as a pathogenic factor in gastric carcinogenesis. Recently, we demonstrated that the alterations in the plasminogen activator (PA) profile found in H. pylori associated gastritis, i.e., a decrease in tissue-type PA (t-PA) and an increase in urokinase-type PA (u-PA), show a similar tendency as the previously found alterations in gastric carcinomas. These observations provided additional support for the possible involvement of H. pylori associated gastritis in the pathogenesis of gastric carcinoma. The present study was performed to determine whether these altered t-PA and u-PA levels and activities in H. pylori associated gastritis are reversed to normal when successful treatment of the infection is achieved. Subjects, materials and methods: In 64 patients of two different treatment groups [omeprazole, clarithromycin, and metronidazole (OME/AB, n = 34), and ranitidine, clarithromycin, and metronidazole (RAN/AB, n = 30)] t-PA and u-PA antigen concentrations were determined by sandwich ELISAs in homogenates of biopsy specimens obtained before and eight weeks after successful treatment for H. pylori infection. Plasminogen activator activities were determined spectrophotometrically in ten patients of both groups before and after successful treatment. Results: After therapy t-PA antigen levels were significantly higher than before treatment in antral (p = 0.003 in both groups) and corpus (OME/AB p = 0.02, RAN/AB p = 0.005) mucosa. In contrast, u-PA antigen levels after treatment were significantly lower than before treatment in antral (p <0.001) as well as corpus (p ≤ 0.001) mucosa in both treatment groups. t-PA activity was also significantly higher after treatment in antral (OME/AB p = 0.02, RAN/AB p = 0.002), but not in corpus mucosa. u-PA activity was not affected by therapy. In four patients in whom H. pylori infection persisted no significant changes in the altered t-PA and u-PA antigen concentrations were found after treatment. Conclusion: The alterations in t-PA and u-PA levels and activity found in H. pylori associated gastritis are reversed when successful treatment of the infection is achieved.