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

J. M. Götz, J. W. Ravensbergen, H. W. Verspaget, I. Biemond, C. F M Sier, G. J A Offerhaus, C. B H W Lamers, R. A. Veenendaal

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)85-89
Number of pages5
JournalFibrinolysis
Volume10
Issue numberSUPPL. 2
StatePublished - 1996
Externally publishedYes

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Plasminogen Activators
Helicobacter Infections
Helicobacter pylori
Stomach
Urokinase-Type Plasminogen Activator
Gastritis
Therapeutics
Antigens
Mucous Membrane
Clarithromycin
Metronidazole
Carcinoma
Ranitidine
Omeprazole
Tissue Plasminogen Activator
Infection
Carcinogenesis
Enzyme-Linked Immunosorbent Assay

ASJC Scopus subject areas

  • Hematology

Cite this

Götz, J. M., Ravensbergen, J. W., Verspaget, H. W., Biemond, I., Sier, C. F. M., Offerhaus, G. J. A., ... Veenendaal, R. A. (1996). The effect of treatment of Helicobacter pylori infection on gastric mucosal plasminogen activators. Fibrinolysis, 10(SUPPL. 2), 85-89.

The effect of treatment of Helicobacter pylori infection on gastric mucosal plasminogen activators. / Götz, J. M.; Ravensbergen, J. W.; Verspaget, H. W.; Biemond, I.; Sier, C. F M; Offerhaus, G. J A; Lamers, C. B H W; Veenendaal, R. A.

In: Fibrinolysis, Vol. 10, No. SUPPL. 2, 1996, p. 85-89.

Research output: Contribution to journalArticle

Götz, JM, Ravensbergen, JW, Verspaget, HW, Biemond, I, Sier, CFM, Offerhaus, GJA, Lamers, CBHW & Veenendaal, RA 1996, 'The effect of treatment of Helicobacter pylori infection on gastric mucosal plasminogen activators', Fibrinolysis, vol. 10, no. SUPPL. 2, pp. 85-89.
Götz JM, Ravensbergen JW, Verspaget HW, Biemond I, Sier CFM, Offerhaus GJA et al. The effect of treatment of Helicobacter pylori infection on gastric mucosal plasminogen activators. Fibrinolysis. 1996;10(SUPPL. 2):85-89.
Götz, J. M. ; Ravensbergen, J. W. ; Verspaget, H. W. ; Biemond, I. ; Sier, C. F M ; Offerhaus, G. J A ; Lamers, C. B H W ; Veenendaal, R. A. / The effect of treatment of Helicobacter pylori infection on gastric mucosal plasminogen activators. In: Fibrinolysis. 1996 ; Vol. 10, No. SUPPL. 2. pp. 85-89.
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abstract = "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.",
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T1 - The effect of treatment of Helicobacter pylori infection on gastric mucosal plasminogen activators

AU - Götz, J. M.

AU - Ravensbergen, J. W.

AU - Verspaget, H. W.

AU - Biemond, I.

AU - Sier, C. F M

AU - Offerhaus, G. J A

AU - Lamers, C. B H W

AU - Veenendaal, R. A.

PY - 1996

Y1 - 1996

N2 - 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.

AB - 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.

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