Changes in the intragastric distribution of Helicobacter pylori during treatment with omeprazole.

Abstract

MethodsPatients attending for routine diagnostic gastroscopy and likely to need omeprazole were invited to take part in, and give written consent to this study, which was approved by the Parkside Ethical Committee. Patients with previous gastric surgery, known bleeding diathesis, taking oral anticoagulants, or who had been treated with bismuth compounds, omeprazole, or antibiotics known to be active against H pylori within the previous two months, were excluded. To determine H pylori status biopsy specimens were taken from the antrum (within 2 cm of the pylorus, two for histology and two for microbiology), corpus (half way along greater curvature, two for histology), and fundus (two for histology).After each examination the endoscopes were disinfected by an automatic washing machine (Olympus EW20)13 and the biopsy forceps were sterilised by autoclaving.

Gastric corpus IL‐8 concentration and neutrophil infiltration in duodenal ulcer patients

“…Although the in¯uence of omeprazole on the mucosa of the body of the stomach was transient, those who underwent subsequent maintenance treatment with H 2 -blockers showed a persistent increase in neutrophil in®ltration in the body of the stomach. These results corresponded with those reported by Logan et al 23 and Solcia et al 24 who investigated changes in H. pylori-related fundal or corpus gastritis using omeprazole, and reported that omeprazole improves antral H. pylori gastritis and worsens the fundal or corporal gastritis, and suggested that even H 2 -blockers, a weaker acid secretion inhibitor, Figure 6. The effect of acid secretion inhibitors on the amount of H. pylori, IL-8 content and neutrophil in®ltration in the body of the stomach in DU patients.…”

H2‐receptor antagonists and antacids have an aggravating effect on Helicobacter pylori gastritis in duodenal ulcer patients

“…19 Hence, we speculate that the reduction in H. pylori gastritis in the antrum after treatment with omeprazole is associated with a direct antibacterial activity of omeprazole against H. pylori that reduces its density in the antrum, 20,21 or alternatively, the shift in the distribution of H. pylori gastritis towards the corpus correlates with the respective drug's ef®cacy in increasing the pH. This means that a proton pump inhibitor may reduce the acid output to such an extent that H. pylori can only survive in the corpus close to the acidproducing parietal cells where the pH value remains low enough for its survival, 9 whereas ranitidine or antacids increase the pH enough to allow an increase in H. pylori gastritis in the corpus, but not to suppress H. pylori gastritis in the antrum. That the increase in the in¯ammation in the corpus is pH-related rather than being a direct toxic effect of the respective drug is also supported by studies showing similar results after proximal selective vagotomy.…”

The burden of Helicobacter pylori infection in Europe

“…The commonest scenario is where patients undergo endoscopy and biopsies while on continued therapy with proton pump inhibitors or antibiotics. 41 A false-negative histology result can also occur where there is extensive gastric atrophy and intestinal metaplasia.…”