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A systematic search of the medical literature was conducted in January 2008. Databases used in this search were PubMed, UpToDate®, National Guideline Clearinghouse, and SUMSearch. The search was limited to humans and journals published in the English language. Information included in this chapter is current as of January 2008.

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Peptic ulcer disease (PUD) is characterized by excoriation of the mucosal layer of the stomach (gastric ulcer) or duodenum (duodenal ulcer). Ulcers should be differentiated from erosions in that ulcers extend deep into the muscular mucosae, whereas erosions tend to be superficial and less deep. Patients with peptic ulcers typically present with dyspepsia. However, several gastrointestinal (GI) disorders other than peptic ulcers can cause dyspepsia. Thus, the diagnosis of gastroesophageal reflux disease (GERD, Chapter 10), function dyspepsia (indigestion), and acid-hypersecretory states such as Zollinger–Ellison syndrome need to be considered in patients presenting with upper GI symptoms. Our understanding of the role of Helicobacter pylori in the development of peptic ulcers has increased significantly and has had a tremendous impact on the treatment of PUD. Unfortunately, advances in the treatment of peptic ulcers have not altered the rate of complications associated with PUD.1

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Approximately 25 million Americans have had PUD during their lifetime.2 PUD causes an estimated 1 million hospitalizations and 6500 deaths per year.2 The incidence of complications secondary to peptic ulcer increases with age, possibly due to increased risk for bleeding associated with nonsteroidal anti-inflammatory drug (NSAID) use. The burden of PUD on our healthcare system—although frequently overlooked—is quite substantial. Excluding medication costs, estimated expenditures are $5.65 billion annually.3

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Traditionally, the major risk factors for peptic ulcer were thought to be acid hypersecretion, diet, and stress. However, it is now known that causative factors such as infection with H. pylori and NSAID use are the primary mechanisms of ulceration.

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Helicobacter-Pylori-Induced Peptic Ulcer

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H. pylori may induce ulcer formation by several mechanisms.4 First, the pathogen produces urease, which catalyzes urea to ammonia. Ammonia, which is necessary for the organism to survive the acidic environment of the stomach, is very caustic to the GI mucosa and can lead to epithelial damage. H. pylori also secretes various mucolytic enzymes that degrade the protective mucosal layer, exposing the epithelium and increasing the risk for acid-related damage. Finally, the cytokines and other inflammatory factors that are released in response to infection may play a role in ulcer formation.

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NSAID-Induced Peptic Ulcer

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NSAIDs exert both topical and systemic effects that contribute to the development of PUD.4 Topically, NSAIDs diffuse across the mucosal layer and into epithelial cells where damage to the cells may occur. Systemically, NSAIDs inhibit the production of prostaglandins that protect epithelial cells in the GI tract from acid-related damage.

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Classic symptoms of PUD include epigastric pain or discomfort, often described as a ...

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