Peptic ulcer disease is a chronic illness manifested by recurrent ulcerations in the stomach and proximal duodenum. Acid and pepsin are thought to be crucial to ulcer development, but the great majority of peptic ulcers are directly related to infection with Helicobacter pylori or nonsteroidal anti-inflammatory drug (NSAID) use.1,2 Gastritis is acute or chronic inflammation of the gastric mucosa and has various etiologies. Dyspepsia is continuous or recurrent upper abdominal pain or discomfort with or without associated symptoms (e.g., nausea, bloating).3 Dyspepsia may be caused by a number of diseases or may be functional.
Uncomplicated peptic ulcer disease has an incidence of more than 5 cases per 1000 persons per year, and about 10% of people living in the Western world will experience a peptic ulcer at some point during their lives.4,5 In the United States, peptic ulcer disease costs an estimated $5.65 billion per year in total direct and indirect costs.6 H. pylori infection, one of the main risk factors of peptic ulcer disease, is one of the most prevalent human infections in the world, affecting at least 50% of the world's population.7 The age-adjusted prevalence of H. pylori infection is decreasing in industrialized countries, likely due to an improved standard of living7 and the increased use of proton pump inhibitors (PPIs) and antimicrobial therapy.2,8 This may explain the decreasing incidence of peptic ulcer disease in the United States, but this may be partially offset by the widespread use of low-dose aspirin and NSAIDs.2,9 Over 70 million prescriptions for NSAIDs are written, and over 30 billion tablets are sold over the counter annually in the United States.10 Risk factors for ulcers not due to H. pylori or NSAIDs include antiplatelet agents, stress, Helicobacter heilmannii, cytomegalovirus infections, Behçet's disease, Zollinger-Ellison syndrome, Crohn's disease, cirrhosis with portal hypertension, older age, and African American ethnicity.2
Dyspepsia affects 20% to 40% of the world's population.3 There is no consistent association with sex, age, socioeconomic status, smoking, or alcohol use; however, it is more common in people infected with H. pylori and who take NSAIDs, as well as some other medications.3
Hydrochloric acid and pepsin destroy gastric and duodenal mucosa. Mucus and bicarbonate ion secretions protect mucosa. Prostaglandins protect mucosa by enhancing mucus and bicarbonate production and by enhancing mucosal blood flow, thereby supporting metabolism. The balance between these protective and destructive forces determines whether peptic ulcer disease occurs. H. pylori bacteria or NSAIDs are thought to be the causal agents of peptic ulcer disease in most cases.1,2 Although traditional treatment of peptic ulcers by various modalities heals most ulcers, eradication of H. pylori cures peptic ulcers in over 80% of patients whose ulcers are not associated with the use of NSAIDs.7,11
H. pylori is a spiral, gram-negative, urease-producing, flagellated ...