Abstract
Both infection with
Helicobacter pylori and use of nonsteroidal anti-inflammatory drugs (NSAIDs) can result in gastritis and ulcers.
H. pylori has been identified as a major etiologic factor in the development of peptic ulcer disease; however, its relationship to NSAID-associated toxicity is less well characterized. Several studies have suggested that NSAID use does not increase susceptibility to
H. pylori, and the converse has also been suggested, namely, that
H. pylori does not exacerbate NSAID-associated injury.
H. pylori itself may stimulate production of gastric prostaglandins, which may have a role in ulcer healing. More carefully controlled studies may be better able to elucidate the individual and synergistic mechanisms involved in ulceration induced by
H. pylori and NSAIDs. Recent studies have suggested that elimination of
H. pylori before NSAID treatment decreases ulcer occurrence. Therefore, at this time, eradication of
H. pylori should be considered only in certain high-risk patients, i.e., those with a history of gastroduodenal ulcers.