Accurate estimates require endoscopic studies because symptoms are insensitive and non-specific indicators of peptic ulcer. One systematic review of the literature reported an 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]

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.[4] Both sexes are similarly affected.

The epidemiology of peptic ulcer disease largely reflects the epidemiology of the two major aetiologic factors, Helicobacter pylori infection and use of non-steroidal 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.[5] Most studies report that peptic ulcers are decreasing in prevalence over time.[4][6][7][8]

Nevertheless they remain a problem, especially in the developing world where H pylori infection is highly prevalent.[9]

Risk factors

H pylori is known to have a role in the aetiology of peptic ulcer disease. If those taking non-steroidal anti-inflammatory drugs (NSAIDs) are excluded, about 90% of patients with duodenal ulcers and more than 70% with gastric ulcers have H pylori infection.[13][14] Infection increases the lifetime risk of peptic ulcers.[9]

The likely mechanisms are through gastrin and acid hyper-secretion (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 non-users.[15] 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.[16][17]

NSAIDs more commonly cause gastric ulcers than duodenal ulcers and do so by impairing mucosal defences, mainly mediated through cyclo-oxygenase (COX)-1. Selective cyclo-oxygenase-2 (COX-2) inhibitors are less likely to cause peptic ulcers.[18]

In patients using NSAIDs, peptic ulcer disease is more common in H pylori-positive than in H pylori-negative patients.[19]

Stopping NSAID use (and treating H pylori, if present) reduces ulcer recurrence. If NSAID use cannot be stopped, coprescription with a proton-pump inhibitor reduces recurrence.

Smoking is a risk factor for peptic ulcers. One population-based study found that the prevalence of ulcer disease in current and former smokers (11.4% and 11.5%) is nearly double that of people who have never smoked (6.0%).[20] The mechanisms are likely multifactorial.[21]

The incidence of peptic ulcers and associated complications increase with age.

Mainly through persistent unrecognised Helicobacter pylori infection.

Family history of peptic ulcer is a risk factor for peptic ulcer disease.[22][23] Risk may be present in families with low Helicobacter pylori prevalence.[24]

Only clinically significant for patients on mechanical ventilation or with coagulopathy.[25] The risk lessens as patient status improves.

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