The American journal of gastroenterology · 1995
Increase of Helicobacter pylori-associated corpus gastritis during acid suppressive therapy: implications for long-term safety.
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Kuipers E J, Uyterlinde A M, Peña A S, Hazenberg H J, Bloemena E, Lindeman J, Klinkenberg-Knol E C, Meuwissen S G
Аннотация
OBJECTIVES: Helicobacter pylori causes chronic active gastritis with predominant localization in the gastric antrum. This predisposes to development of mucosal atrophy, intestinal metaplasia, and eventually, gastric cancer. The effects of acid suppression on H. pylori infection and associated gastritis are unclear. However rapid development of atrophic gastritis has been consistently observed in a number of studies during low acid output. We therefore studied the histological features of antrum and corpus of the stomach before and during acid suppressive therapy.
METHODS: Fifty patients with either reflux esophagitis (n = 21), benign gastric ulcer (six patients), gastric erosions (three patients), or duodenal ulcer (20 patients) were treated for 8 wk with omeprazole 40 mg o.d. Esophagogastroduodenoscopy was performed pre-entry and at 8 wk. Biopsy specimens were sampled from the antrum and corpus for histology and cultures.
RESULTS: Seventeen H. pylori-negative patients had no histological signs of active gastritis, before or after therapy. Thirty-three H. pylori-positive patients showed predominant colonization and associated inflammation in the antrum before therapy. After therapy, however, the infection predominantly affected the corpus. The inflammation and bacterial colonization in the antrum significantly decreased, leading to negative antral cultures in 61% (20 of 33 patients). In contrast, the inflammation of the corpus mucosa significantly increased despite stable bacterial counts.
CONCLUSIONS: We conclude 1) that H. pylori testing in patients on profound acid suppressive therapy should be performed on combined corpus and antral specimens, and 2) that omeprazole therapy leads to a strong increase in corpus gastritis, which may explain the observed development of corpus atrophy in a substantial number of patients after several years of continuous acid suppressive treatment. Therefore, we suggest that patients in need of long-term acid suppressive therapy should receive bacterial eradication therapy if they are H. pylori positive.
METHODS: Fifty patients with either reflux esophagitis (n = 21), benign gastric ulcer (six patients), gastric erosions (three patients), or duodenal ulcer (20 patients) were treated for 8 wk with omeprazole 40 mg o.d. Esophagogastroduodenoscopy was performed pre-entry and at 8 wk. Biopsy specimens were sampled from the antrum and corpus for histology and cultures.
RESULTS: Seventeen H. pylori-negative patients had no histological signs of active gastritis, before or after therapy. Thirty-three H. pylori-positive patients showed predominant colonization and associated inflammation in the antrum before therapy. After therapy, however, the infection predominantly affected the corpus. The inflammation and bacterial colonization in the antrum significantly decreased, leading to negative antral cultures in 61% (20 of 33 patients). In contrast, the inflammation of the corpus mucosa significantly increased despite stable bacterial counts.
CONCLUSIONS: We conclude 1) that H. pylori testing in patients on profound acid suppressive therapy should be performed on combined corpus and antral specimens, and 2) that omeprazole therapy leads to a strong increase in corpus gastritis, which may explain the observed development of corpus atrophy in a substantial number of patients after several years of continuous acid suppressive treatment. Therefore, we suggest that patients in need of long-term acid suppressive therapy should receive bacterial eradication therapy if they are H. pylori positive.