Peptic ulcer disease: Genetic, environmental, and psychological risk factors and pathogenesis

INTRODUCTION

Peptic ulcers are defects in the gastrointestinal mucosa that extend through the muscularis mucosae. They persist as a function of the acid or peptic activity in gastric juice. Peptic ulcer disease (PUD) is an important cause of morbidity and health care costs. The natural history of peptic ulcer ranges from resolution without intervention to the development of complications with the potential for significant morbidity and mortality, such as bleeding and perforation. (See "Overview of the natural history and treatment of peptic ulcer disease" and "Overview of the complications of peptic ulcer disease".)

This topic review will summarize the pathogenesis and risk factors of PUD. A review of its epidemiology and major causes is presented separately. (See "Epidemiology and etiology of peptic ulcer disease".)

PATHOPHYSIOLOGY

Considering the acid-peptic environment of the stomach and the noxious agents that are ingested, ulcers are surprisingly uncommon, illustrating the importance of protective mechanisms that govern gastric mucosal function and repair. Primary malfunction of these secretory, defense, or repair mechanisms is a very uncommon cause of ulcer, if it occurs at all. Most ulcers occur when the normal mechanisms are disrupted by superimposed processes such as Helicobacter pylori infection and the ingestion of nonsteroidal antiinflammatory drugs (NSAIDs).

The decreasing prevalence of H. pylori infection has had a significant impact on the burden of ulcer disease in both developed and developing countries. In developed countries such as the United States, the prevalence of ulcer disease in young people has declined, while NSAID-related ulcers in older adults have increased due both to the increasing in life expectancy and the use of aspirin and NSAIDs [1-4].

Helicobacter pylori — Helicobacter pylori affects a number of aspects of intestinal and mucosal physiology including gastric acid secretion, gastric metaplasia, immune responses, and mucosal defense mechanisms. (See "Association between Helicobacter pylori infection and duodenal ulcer".)

                  

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Literature review current through: Sep 2014. | This topic last updated: Dec 20, 2012.
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