This article aims to review recent scientific, epidemiological, and clinical publications, and to examine this intricate interrelationship.
Pathophysiological studiesIt is generally thought that H. pylori and NSAIDs damage the mucosa by different mechanisms. H. pylori infection induces mucosal inflammation and stimulates cytokine release, resulting in apoptosis. In contrast, NSAIDs inhibit mucosal prostaglandin (PG) synthesis, leading to weakening of the mucosal barrier and impaired resistance to acid injury. Several factors have been shown to be of importance in the pathogenesis of ulceration, and the effects of H. pylori infection and NSAID constitute a complex interaction.
ApoptosisApoptosis (programmed cell death) is the mechanism of normal cell turnover of the mucosa throughout the gastrointestinal tract and maintains a fine balance with cell proliferation. 2 H. pylori directly induces apoptosis or indirectly by invoking the host inflammatoryimmune response. Zhu et al. 3 found that, individually, both NSAID use and H. pylori infection induced apoptosis. When H. pylori infection and NSAID were combined, NSAIDs actually abrogated the apoptosis induced by H. pylori infection. The latter observation led to the impression that H. pylori might ameliorate the mucosal injury induced by NSAIDs. In contrast, Leung et al. 4 showed that H. pylori-infected patients had a higher apoptotic activity than that in noninfected controls. Apoptosis was further increased in H. pyloriinfected patients after exposure to naproxen. Interestingly, the apoptotic effect of naproxen was significantly alleviated when H. pylori was eradicated prior to the administration of naproxen. 4