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Peptic ulcer disease is a chronic illness manifested by recurrent ulcerations in the stomach and proximal duodenum. Acid and pepsin are thought to be crucial to ulcer development, but the great majority of peptic ulcers are directly related to infection with Helicobacter pylori or NSAID use.1,2 Gastritis is acute or chronic inflammation of the gastric mucosa and has various etiologies. Dyspepsia is continuous or recurrent upper abdominal pain or discomfort with or without associated symptoms (nausea, bloating, etc.).3 Dyspepsia may be caused by a number of diseases or may be functional.


About 500,000 new cases and about 4 million recurrent cases of peptic ulcer disease are diagnosed each year in the U.S.4 Most cases occur between the ages of 25 and 64 years.1 There is a lifetime prevalence of peptic ulcer disease of between 8% and 14%, and an estimated U.S. $10 billion is spent per year in total direct and indirect costs.1,4 H. pylori infection is one of the most prevalent human infections in the world, and approximately 30% to 40% of the U.S. population is affected.5 The prevalence of H. pylori infection is inversely related to socioeconomic status and is particularly related to density of living and household income during childhood.6 The age-adjusted prevalence of H. pylori infection is decreasing in industrialized countries, likely due to an improved standard of living, especially during childhood, as well as spontaneous loss of infection.5,6 This may explain the decreasing incidence of peptic ulcer disease in the U.S., although increased use of proton pump inhibitors (PPIs) may also be a factor.1 In any given 6-month period about 40% of the population describes some upper GI symptoms (including both dyspepsia and heartburn), and investigation of these symptoms accounts for about 50% of a gastroenterologist’s workload.7 The point prevalence of dyspepsia alone is about 25%.3


Hydrochloric acid and pepsin destroy gastric and duodenal mucosa. Mucus and bicarbonate ion secretions protect mucosa. Prostaglandins protect mucosa by enhancing mucus and bicarbonate production and by enhancing mucosal blood flow, thereby supporting metabolism. The balance between these protective and destructive forces determines whether peptic ulcer disease occurs. H. pylori infection or NSAIDs are thought to be the causal agents of peptic ulcer disease in almost all cases.2,8 H. pylori infection is present in about 95% of patients who develop duodenal ulcer and about 70% of those who develop gastric ulcer.9 Although traditional treatment of peptic ulcers by various modalities heals most ulcers, eradication of H. pylori reduces 1-year recurrence rates from 35% to 2% for duodenal ulcers and from 39% to 3% for gastric ulcers.5 H. pylori is a spiral, gram-negative, urease-producing, flagellated bacterium that is found living between the mucous gel and the mucosa. The bacterium’s production of urease, cytotoxins, proteases, and other compounds is thought to disturb the mucous gel and cause tissue injury. In addition, increased gastrin levels and decreased mucus and ...

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