Epidemiology
Accurate estimates require endoscopic studies because symptoms are insensitive and nonspecific indicators of peptic ulcer. One systematic review of the literature reported a global annual incidence of 0.10% to 0.19% for physician-diagnosed peptic ulcer disease and a 1-year prevalence of 0.12% to 1.50%.[1] The prevalence of gastric ulcer varies significantly worldwide: 4.1% in Sweden and 6.1% in China.[2][3] In the US, peptic ulcer disease is reported to affect 1% of the population, with approximately 54,000 patients admitted for bleeding peptic ulcers annually.[4]
The incidence of peptic ulcer increases with age; gastric ulcers peak in the fifth to seventh decades and duodenal ulcers 10 to 20 years earlier.[5] Both sexes are similarly affected.
The epidemiology of peptic ulcer disease largely reflects the epidemiology of the two major etiologic factors, Helicobacter pylori infection and use of nonsteroidal anti-inflammatory drugs (NSAIDs). In the developed world, H pylori incidence has been slowly declining over the past 50 years and NSAID use has increased. Most studies report that peptic ulcers are decreasing in prevalence over time.[6][7][8][9][10]
Nevertheless, peptic ulcers remain a problem, especially in the developing world where H pylori infection is highly prevalent.[11] A 2019 literature review of the epidemiology of peptic ulcer disease in Africa found heterogeneity in the prevalence and incidence of peptic ulcer disease across the continent. However, most of the tertiary-center studies found a higher prevalence of peptic ulcer disease in Africa when compared with similar studies in western countries.[12]
Risk factors
H pylori is known to have a role in the etiology of peptic ulcer disease. If those taking nonsteroidal anti-inflammatory drugs (NSAIDs) are excluded, about 90% of patients with duodenal ulcers and more than 70% with gastric ulcers have H pylori infection.[19][21] Infection increases the lifetime risk of peptic ulcers.[11]
The likely mechanisms are through gastrin and acid hypersecretion (duodenal ulcers) and local mucosal damage (gastric ulcers).
Eradication of infection prevents recurrence of both peptic ulcer disease and bleeding.
The incidence of ulcers in chronic NSAID users is about 20% compared with about 5% in nonusers.[22] Low-dose aspirin use is also likely to increase the risk, but high-quality trials are lacking.
The risk of NSAID-induced ulcers increases with increasing age (>60 years); a history of peptic ulcer; high doses of NSAIDs and longer duration of use; Helicobacter pylori infection; and concurrent use of corticosteroids, other antithrombotic drugs, and bisphosphonates.[14][23][24][25][26][27]
NSAIDs more commonly cause gastric ulcers than duodenal ulcers and do so by impairing mucosal defenses, mainly mediated through cyclo-oxygenase (COX)-1. Selective COX-2 inhibitors are less likely to cause peptic ulcers.[28]
In patients using NSAIDs, peptic ulcer disease is more common in H pylori-positive than in H pylori-negative patients.[29]
Stopping NSAID use (and treating H pylori, if present) reduces ulcer recurrence. If NSAID use cannot be stopped, coprescription with a proton-pump inhibitor (PPI) reduces recurrence.
The incidence of peptic ulcers and associated complications increase with age.
Mainly through persistent unrecognized Helicobacter pylori infection.
Prophylactic use of a proton-pump inhibitor (PPI) is appropriate for patients in intensive care, who are deemed at high risk of gastrointestinal bleeding due to comorbidities such as chronic liver disease, or have coexisting conditions such as coagulopathy or shock.[35][36] The risk lessens as patient status improves.
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