THE EFFECT OF TREATMENT OF HELICOBACTER-PYLORI INFECTION 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), sh ow a similar tendency as the previously found alterations in gastric c arcinomas. These observations provided additional support for the poss ible involvement of H. pylori associated gastritis in the pathogenesis of gastric carcinoma. The present study was performed to determine wh ether these altered t-PA and u-PA levels and activities in H. pylori a ssociated gastritis are reversed to normal when successful treatment o f the infection is achieved. Subjects, Materials and Methods: In 64 pa tients 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 wer e determined by sandwich ELISAs in homogenates of biopsy specimens obt ained before and eight weeks after successful treatment for H, pylori infection. Plasminogen activator activities were determined spectropho tometrically in ten patients of both groups before and after successfu l treatment. Results: After therapy t-PA antigen levels were significa ntly higher than before treatment in antral (p=0.003 in both groups) a nd corpus (OME/AB p=0.02, RAN/AB p=0.005) mucosa. In contrast, u-PA an tigen levels after treatment were significantly lower than before trea tment in antral (p<0.001) as well as corpus (p less than or equal to 0 .001) mucosa in both treatment groups. t-PA activity was also signific antly 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 foun d after treatment. Conclusion: The alterations in t-PA and u-PA levels and activity found in H. pylori associated gastritis are reversed whe n successful treatment of the infection is achieved.