ESSENTIALS OF DIAGNOSIS
Peptic ulcers are mucosal defects in the stomach or small intestine.
Helicobacter pylori infection, nonsteroidal anti-inflammatory drugs (NSAIDs), and aspirin use are the most common causes.
Patients may have epigastric pain or complications such as gastrointestinal (GI) bleeding, perforation, and obstruction.
Diagnosis is often made by endoscopy or radiologic studies.
Peptic ulcers are defects or breaks in the gastric or small intestinal mucosa that have depth and extend through the muscularis mucosae. In contrast to erosions, which are small and superficial mucosal lesions, peptic ulcers can vary in size from 5 mm to several centimeters and may lead to complications such as GI bleeding, obstruction, penetration, and perforation.
The pathogenesis of peptic ulcers is multifactorial and arises from an imbalance of protective and aggressive factors such as when GI mucosal defense mechanisms are impaired in the presence of gastric acid and pepsin. Peptic ulcer disease was long considered as an idiopathic and lifelong disorder. This paradigm changed dramatically in 1984 when Marshall and Warren reported that a curved bacillus, initially named Campylobacter pyloridis and subsequently classified as H pylori, was linked to ulcers. Multiple studies have since shown that eradication of H pylori significantly reduces the rate of ulcer recurrence. Another major risk factor for peptic ulcers is the use of NSAIDs and aspirin. These medications generally exert their therapeutic and toxic effects by inhibiting the enzymes cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), which, in turn, impair mucosal protection and promote ulcers. The treatment of ulcer patients has been revolutionized since the development of the acid-suppressive medications such as the histamine-2 (H2)-receptor blockers and proton pump inhibitors (PPIs), the synthetic prostaglandin misoprostol, and the selective COX-2 inhibitors. Only a small fraction of ulcers are associated with neoplasia or caused by acid hypersecretory states such as Zollinger-Ellison syndrome and other rare disorders.
The incidence of both gastric and duodenal ulcers in developed countries rapidly increased throughout the 19th century and peaked during the first half of the 20th century. Since the 1950s, however, the incidence and prevalence of both ulcers have steadily declined. There has also been a decrease in the prevalence of H pylori over recent decades, attributed to improved hygiene and widespread use of antibiotics in developed countries. Hospital discharge data for the general US population showed that the age-adjusted hospitalization rate for peptic ulcer disease and H pylori was highest among adults of age 65 years and older and decreased with each subsequent age group. These trends are thought to reflect an underlying birth cohort effect with a decrease in H pylori incidence among younger generations.
A systematic review of the literature on the epidemiology of peptic ulcer disease estimated an annual incidence ranging from 0.10% to 0.19% for physician-diagnosed peptic ulcers and from 0.03% to 0.17% for peptic ulcers diagnosed during hospitalization. In the ...