Helicobacter pylori and peptic ulcer disease

Abstract

The role played by Helicobacter pylori in the pathogenesis of peptic ulcer disease (PUD) is discussed, and the epidemiology, identification, diagnosis, eradication, and treatment of H. pylori infection are reviewed. Isolation of H. pylori from up to 100% of patients with duodenal ulcer and 80% of patients with gastric ulcer establishes a strong association between H. pylori and idiopathic PUD, although other factors also may be essential for the development of PUD. Invasive procedures for diagnosis of H. pylori infection include upper endoscopy and biopsy of gastroduodenal tissues followed by culture or the rapid urea test; noninvasive tests include the urea breath tests and serology. Although H. pylori is susceptible to a number of antimicrobials, eradication (as opposed to suppression) of this organism has been a major challenge. The most important predictive factor for clinical and microbiological efficacy is the pretreatment susceptibility of H. pylori to nitroimidazoles. Triple therapy with bismuth, metronidazole, and either amoxicillin or tetracycline has resulted in better clinical and microbiological outcomes than either monotherapy or dual therapy. Possible adverse effects of this regimen include nausea, vomiting, taste disturbance, and diarrhea. Anti-H. pylori therapy should be reserved for those patients who have recurrent symptomatic or intractable PUD. Currently, the regimen of choice includes bismuth, metronidazole, and either amoxicillin or tetracycline given for at least two weeks.