Helicobacter pylori, gastric ulcer, and agents noxious to the gastric mucosa

Conclusions regarding the interaction of H. pylori infection with noxious agents such as NSAIDs, alcohol, and smoking in the development of histologic gastritis and gross gastric injury are limited by the paucity of well-performed studies specifically addressing this problem. At present, we can conclude that H. pylori prevalence is not affected by NSAIDs, alcohol, or smoking. On the other hand, reflux of duodenal contents may play a role in eradication of H. pylori after gastroenterostomy. Although NSAIDs and alcohol do cause gross gastric injury they do not appear to induce changes in the inflammatory cell infiltrate of the gastric mucosa. Rather, the histologic gastritis sometimes attributed to NSAIDs or alcohol seems to be related to the underlying presence of H. pylori. Furthermore, HP does not clearly influence the development of gross injury by NSAIDs or alcohol, and these noxious agents do not influence the H. pylori-associated histologic gastritis. Patients with NSAID-associated gastric ulcers have an H. pylori prevalence similar to that of NSAID users without gastric ulcers and lower than that of patients with gastric ulcers who do not take NSAIDs. These findings suggest that NSAIDs induce ulcers through a mechanism that does not require H. pylori and histologic gastritis. Because NSAIDs are much more likely to cause gastric than duodenal ulcers, this information may explain why patients with gastric ulcers are more commonly H. pylori negative than are patients with duodenal ulcers.