Relationship between nonsteroidal anti-inflammatory drug use, Helicobacter pylori, and gastroduodenal mucosal injury.

Abstract

With the realization that Helicobacter pylori is the main etiologic factor for peptic ulcer disease, recent studies have explored a potential relationship between H. pylori and nonsteroidal anti-inflammatory drug (NSAID)-related gastroduodenal mucosal injury. Using serology and/or histology to detect H. pylori, case-control studies have shown no meaningful differences in H. pylori prevalence in both arthritis and nonarthritis NSAID users and controls. Placebo-controlled short-term trials of NSAIDs have also shown no change in the frequency of detection of H. pylori by gastric mucosal biopsy specimens after 7-30 days of NSAID ingestion. A number of studies have shown that the histological gastritis identified in NSAID users is caused by H. pylori infection, whereas the reactive (chemical) gastritis can be caused by NSAID use. Although the overall relationship between H. pylori gastritis and dyspepsia remains controversial, there is no evidence from well-controlled studies using either serology or histology that this gastritis predisposes to NSAID-related dyspepsia. The effect of H. pylori on NSAID-related gastroduodenal mucosal injury may be best established by evaluating the ulcer recurrence rate after H. pylori eradication and rechallenge with NSAIDs. To date, only one such study has examined this question, and in this small study, the ulcer recurrence rate at 6 months was not reduced by H. pylori eradication.