Peptic ulcer disease is caused by defects in the gastrointestinal mucosa extending into the muscularis mucosa secondary to gastric acid and/or pepsin. Recent advances have provided a better understanding of peptic ulcer pathophysiology. The propensity for peptic ulcers is caused by the imbalance between digestive and protective factors. Since the discovery of the bacterium Helicobacter pylori, the medical management of peptic ulcer disease has changed dramatically. Most peptic ulcers fall into two etiologies: nonsteroidal anti-inflammatory drugs (NSAIDS) or H. pylori.

The clinical presentation of peptic ulcer disease is variable. Some patients with peptic ulcer disease have classic symptoms, while other patients may have ulcer symptoms and no identifiable ulcers (non-ulcer dyspepsia). Many patients with peptic ulcer disease have no symptoms.

Epidemiology

The annual incidence of peptic ulcer disease ranges from 0.1% to 0.3%. Several studies have shown the incidence of peptic ulcer disease in H. pylori-infected individuals to be about 1% per year, which is six to tenfold higher than H. pylori-negative individuals. Since the mid 1970s, the incidence of duodenal ulcer seems to be declining in the USA reflected by decreasing rate of hospitalization, surgery, and death. Rates of hospitalization for ulcer hemorrhage decreased slightly for duodenal ulcers but have increased for gastric ulcers. Death rates from peptic ulcer disease seem to be declining for younger men and increasing for the elderly. Estimates of ulcer prevalence must take into account the H. pylori status of the patient.