GASTRIC-MUCOSAL PLASMINOGEN ACTIVATORS IN HELICOBACTER-PYLORI INFECTION

Long-term H. pylori associated gastritis is recognized as a pathogenic factor in gastric carcinogenesis. In gastric carcinomas the amount an d activity of the tissue-type plasminogen activator (t-PA) have been r eported to be decreased, whereas those of the urokinase-type plasminog en activator (u-PA) were increased, contributing to the neoplastic and invasive process. The present study was performed to determine t-PA a nd u-PA levels and activity in gastric mucosa from 102 patients and to investigate whether these levels are influenced by H. pylori infectio n, The antigen concentration and activity of t-PA and u-PA in corpus m ucosa were low (P <0.001) compared with those in antral mucosa, althou gh for the u-PA activity this did not reach statistical significance, In H. pylori-associated antral gastritis the mucosal t-PA antigen conc entration and activity were found to be decreased (P <0.001) compared with normal mucosa, whereas in H. pylori-associated pangastritis the c orpus t-PA levels were not affected, The antigen concentration and act ivity of u-PA were found to be significantly (P <0.005) increased, bot h in H. pyloli-associated gastritis of antrum and corpus mucosa. Level s of u-PA in histologically normal corpus mucosa of patients with an H . pylori-associated antral gastritis were also found to be increased ( P <0.05). In conclusion, the alterations in the plasminogen activator profile found in H. pylori-associated gastritis, ie, a decrease in t-P A and an increase in u-PA, show a similar tendency as the previously f ound alterations in gastric carcinomas, which provides additional supp ort for the possible involvement of H. pylori-associated gastritis in the pathogenesis of gastric carcinoma.