Peptic ulcer disease and Helicobacter pylori infection

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Abstract
Two major treatment studies of triple-antibacterial therapy, including bismuth for 4 weeks for duodenal ulcer, have achieved high rates of healing and eradication of Helicobacter pylori infection. When H. pylori infection was eradicated, follow-up for 1 or 2 years showed no duodenal ulcer relapse, but a high relapse rate was observed when the infection was not eradicated. Thus, this therapy is now the treatment of choice for chronic duodenal ulcer. Treatment with nonsteroidal anti-inflammatory drugs (NSAID) reduced the frequency of duodenal ulcer in H. pylori infection, but gastric ulcer was more frequent. The infrequency of gastric metaplasia and genetic factors probably explain why only a few people develop duodenal ulcer among those with H. pylori gastritis. A pathogenetic cascade for the development of duodenal ulcer from H. pylori gastritis is illustrated. A range of papers on the pathogenesis of duodenal ulcer and antibacterial therapy were reviewed. H. pylori infection probably acts as a promoter in the earliest stages of gastric cancer; its eradication in patients with intestinal metaplasia may reduce the risk of gastric cancer.

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