The majority of patients with duodenal ulcer (DU) are infected with Helicobacter pylori (H. pylori). However, in multicenter trials, H. pylori was absent in almost 30 percent of patients with an endoscopically documented duodenal ulcer . Studies that have investigated these patients found that they have generally had a shorter duration of symptoms and that many had regularly used nonsteroidal antiinflammatory drugs (NSAIDs) [2-4]. Such patients have a significantly worse outcome, especially if treated empirically for H. pylori infection. Thus, H. pylori status should be determined in all ulcer patients before initiating treatment . High acid output may be a cause of recurrent DU in patients in whom H. pylori has been eradicated . A variety of other causes are responsible for the remaining cases. (See "Unusual causes of peptic ulcer disease".)
The link between H. pylori and DU will be reviewed here. The pathophysiology of H. pylori infection as it relates to gastrointestinal disease in general is discussed separately. (See "Pathophysiology of and immune response to Helicobacter pylori infection".)
EVIDENCE LINKING HELICOBACTER PYLORI TO DUODENAL ULCERS
There are several lines of evidence that implicate H. pylori as a major etiologic factor in duodenal ulcers (DU):
- H. pylori is present in most patients who have a DU that is not related to NSAID use
- H. pylori infection is detectable before the occurrence of DU and appears to be a risk factor for the disorder
- Eradication of H. pylori prevents DU recurrence
Incidence of H. pylori in patients with duodenal ulcer — Early studies noted a high incidence of H. pylori infection (then called Campylobacter pylori) in patients with DU ; subsequent reviews confirmed that H. pylori is detectable in 80 to 95 percent of these patients [2,7]. These data were supported by reports which found that the prevalence of H. pylori is negligible in populations in which ulcer disease is rare .