Helicobacter pylori and the pathogenesis of gastroduodenal disease: Implications for the management of peptic ulcer disease.

The discovery of Helicobacter pylori has changed our understanding of the pathophysiology of peptic ulcer disease. An estimated one billion people harbour the organism worldwide but the highest prevalence is found in developing countries with up to 80% of people infected. The most favoured modes of transmission are faeco-oral and oral-oral. The mechanisms of H pylori-induced gastroduodenal disease include the provocation of local inflammatory reaction with the release of toxic cytokines, elevation of gastrin concentration and cytotoxic epithelial injury from the activity of urease and other enzymes produced by the bacterium. However, a large proportion of infected persons have no disease or are asymptomatic thereby suggesting that there may be other factors apart from H pylori infection necessary for ulcer formation. The simple finger prick test, a variant of serology and the newly developed ELISA-based Faecal Antigen Test hold the ace for large-scale epidemiological studies. The eradication of H pylori is now a very important goal of treatment of gastric and duodenal ulcers. Most H pylori eradication regimens combine anti-secretory agent, usually a proton pump inhibitor or H2-receptor antagonist and two antibiotics (usually, Clarithromycin and Amoxycillin or Metronidazole). Emergence of antibiotic resistance is worrisome but a quadruple therapy that incorporates bismuth may be used if the triple therapy fails.