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Helicobacter pylori ‐eradication therapy decreases the level of neutrophil‐derived oxidants in the ulcerous mucosa of the human stomach: Relationship between ulcer stage and mucosal oxidant level
Author(s) -
Suzuki Masayuki,
Suzuki Hidekazu,
Kitahora Tetsuji,
Nagahashi Shoichi,
Masaoka Tatsuhiro,
Tanaka Shin,
Suzuki Kouichi,
Ishii Hiromasa
Publication year - 2003
Publication title -
digestive endoscopy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.5
H-Index - 56
eISSN - 1443-1661
pISSN - 0915-5635
DOI - 10.1046/j.1443-1661.2003.00260.x
Subject(s) - medicine , helicobacter pylori , gastroenterology , gastric mucosa , stomach , scars , antrum , biopsy , gastritis , inflammation , stage (stratigraphy) , pathology , paleontology , biology
Background: The purpose of the present study was to determine the effect of Helicobacter pylori eradication on the intensity of inflammation in the ulcerous mucosa by measuring the level of neutrophil‐associated oxidants and to understand the role of mucosal inflammation in ulcer relapse from the viewpoints of the scarring stage and the H. pylori ‐infection status. The level of inflammation in the gastric mucosa after the eradication of H. pylori was examined using biopsy samples obtained from patients with gastric ulcers. Methods: Gastric mucosal specimens were endoscopically obtained before and after H. pylori ‐eradication therapy from 39 patients with gastric ulcers and a positive H. pylori ‐infection status. The level of neutrophil‐derived oxidants was then measured in each sample using a luminol‐dependent chemiluminescence (ChL) assay. Results: Chemiluminescence activity in the ulcer portion and the background gastric mucosa (antrum and corpus) was significantly reduced 3 months after successful therapy ( n = 32). The ChL activity was further decreased 9 months after successful therapy, but the activity in the ulcer portion remained unchanged. In patients who did not respond to the H. pylori ‐eradication therapy ( n = 7), the ChL activities were not altered in any mucosal portion after the therapy. Before the H. pylori ‐eradication therapy, a higher ChL activity was observed in open ulcer tissue than in scarred tissue. The ChL activity in the scarred tissue was reduced 3 months after the successful eradication of H. pylori ; however, the ChL activity in the red scars was significantly higher than that in the white scars. The ChL level in the white scars was almost equivalent to that in the background mucosa 9 months after the completion of the H. pylori ‐eradication therapy. Conclusion: The eradication of H. pylori may reduce the level of oxidant production in gastric ulcers, promoting the prevention of ulcer recurrence. Furthermore, the presence of a red scar may indicate unstable healing, even after the successful eradication of H. pylori .