Abstract

Infection with Helicobacter pylori is a causal factor in the development of peptic ulcers. There is a strong association between gastritis induced by H. pylori and ulcer development, and peptic ulcer disease seldom develops in the absence of infection. Eradication of H. pylori leads to long-term remission and cure of peptic ulcer disease. The ability of H. pylori to cause ulcers appears to be linked to strain-specific characteristics, such as the presence of the cagA gene. Studies of ulcer patients with healed H. pylori infection suggest that the pathogenesis of peptic ulcers in Japan is comparable to that elsewhere in the world. Smoking, a recognized risk factor for peptic ulcer disease, does not cause ulcers in the absence of infection with H. pylori; by contrast, the presence of H. pylori is not necessary for the development of ulcers associated with non-steroidal anti-inflammatory drugs (NSAIDs). Reinfection after eradication of H. pylori occurs at a rate similar to the infection rate; both are infrequent events in adults living in industrialized countries. Effective and well-tolerated eradication therapies are now available, and represent the most cost-effective treatment for peptic ulcer disease.

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