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INTRODUCTION AND EPIDEMIOLOGY

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 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 and may be caused by a number of diseases or may be functional.3 Uncomplicated peptic ulcer disease has an estimated incidence of 0.1% to 0.3% per year, and about 5% to 10% of people living in the Western world will experience a peptic ulcer at some point during their lives.2 H. pylori infection, one of the main risk factors for peptic ulcer disease, is one of the most prevalent human infections in the world, affecting at least 50% of the world’s population.4 The age-adjusted prevalence of H. pylori infection is decreasing in industrialized countries, likely due to an improved standard of living and to the increased use of proton pump inhibitors and antimicrobial therapy.2,3 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 Currently, at least a fifth of peptic ulcer disease cases have been found to be H. pylori–negative, NSAID-negative, and aspirin-negative.2 Certain medical conditions such as Helicobacter heilmannii, cytomegalovirus infections, Behçet’s disease, Zollinger-Ellison syndrome, Crohn’s disease, and cirrhosis with portal hypertension may contribute to the development of peptic ulcers.2 Other risk factors include antiplatelet agents, psychological stress, older age, and African-American ethnicity.2,5

PATHOPHYSIOLOGY

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 has been shown to accelerate healing and decrease both relapse and rebleeding of ulcers that are not associated with the use of NSAIDs.2,6

H. pylori is a spiral, gram-negative, urease-producing, flagellated bacterium that is found living between the mucous gel and the mucosa. The bacterium’s production of urease, cytotoxins, proteases, and other compounds is thought to disturb the mucous gel and cause tissue injury. In addition, increased gastrin levels and decreased mucus and bicarbonate production are associated with H. pylori infection. Chronic active (usually asymptomatic) gastritis is an almost universal finding with H. pylori infection, but only some infected ...

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