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  • History of dyspepsia present in 80–90% of patients with variable relationship to meals.

  • Ulcer symptoms characterized by rhythmicity and periodicity.

  • Ulcer complications present without antecedent symptoms in 10–20% of patients.

  • Most NSAID-induced ulcers are asymptomatic.

  • Upper endoscopy with gastric biopsy for H pylori is the diagnostic procedure of choice in most patients.

  • Gastric ulcer biopsy or documentation of complete healing necessary to exclude gastric malignancy.


Peptic ulcer is a break in the gastric or duodenal mucosa that arises when the normal mucosal defensive factors are impaired or are overwhelmed by aggressive luminal factors such as acid and pepsin. By definition, ulcers extend through the muscularis mucosae and are usually over 5 mm in diameter. In the United States, there are about 500,000 new cases per year of peptic ulcer and 4 million ulcer recurrences; the lifetime prevalence of ulcers in the adult population is approximately 10%. Ulcers occur either in the duodenum, where over 95% are in the bulb or pyloric channel, or in the stomach, where benign ulcers are located most commonly in the antrum (60%) or at the junction of the antrum and body on the lesser curvature (25%).

Although ulcers can occur in any age group, duodenal ulcers most commonly occur in patients between the ages of 30 and 55 years, whereas gastric ulcers are more common in patients between the ages of 55 and 70 years. The incidence of duodenal ulcer disease has been declining dramatically for the past 30 years (due to the eradication of H pylori), but the incidence of gastric ulcers has not been declining (due to the widespread use of NSAIDs and low-dose aspirin).


There are two major causes of peptic ulcer disease: NSAIDs and chronic H pylori infection. Evidence of H pylori infection or NSAID ingestion should be sought in all patients with peptic ulcer. Alcohol, dietary factors, and stress do not appear to cause ulcer disease. Less than 5–10% of ulcers are caused by other conditions, including acid hypersecretory states (such as Zollinger-Ellison syndrome or systemic mastocytosis), CMV (especially in transplant recipients), Crohn disease, lymphoma, medications (eg, alendronate), or chronic medical illness (cirrhosis or chronic kidney disease), or are idiopathic. NSAID-induced and H pylori–associated ulcers will be presented in this section; Zollinger-Ellison syndrome will be discussed subsequently.

A. H pylori–Associated Ulcers

H pylori infection with associated gastritis appears to be a necessary cofactor for the majority of duodenal and gastric ulcers not associated with NSAIDs. Ulcer disease will develop in an estimated 10% of infected patients. The prevalence of H pylori infection in duodenal ulcer patients is 70–90%. Infection with cag-A positive strains of H pylori is associated with an 18-fold and 2.9-fold increased risk of duodenal and gastric ulcer, respectively. Most H pylori–infected duodenal ulcer patients have infection predominantly ...

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