| pubmed-article:8769282 | pubmed:abstractText | Long-term H. pylori associated gastritis is recognized as a pathogenic factor in gastric carcinogenesis. In gastric carcinomas the amount and activity of the tissue-type plasminogen activator (t-PA) have been reported to be decreased, whereas those of the urokinase-type plasminogen activator (u-PA) were increased, contributing to the neoplastic and invasive process. The present study was performed to determine t-PA and u-PA levels and activity in gastric mucosa from 102 patients and to investigate whether these levels are influenced by H. pylori infection. The antigen concentration and activity of t-PA and u-PA in corpus mucosa were low (P < 0.001) compared with those in antral mucosa, although for the u-PA activity this did not reach statistical significance. In H. pylori-associated antral gastritis the mucosal t-PA antigen concentration and activity were found to be decreased (P < 0.001) compared with normal mucosa, whereas in H. pylori-associated pangastritis the corpus t-PA levels were not affected. The antigen concentration and activity of u-PA were found to be significantly (P < 0.005) increased, both in H. pylori-associated gastritis of antrum and corpus mucosa. Levels 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-PA and an increase in u-PA, show a similar tendency as the previously found alterations in gastric carcinomas, which provides additional support for the possible involvement of H. pylori-associated gastritis in the pathogenesis of gastric carcinoma. | lld:pubmed |
