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Peptic ulcer disease

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  • This document is a translation of a document from (suited for healthcare professionals) and intended for demonstration of the product in English

Key facts


  • Peptic ulcers
    • Are defects in the gastric or proximal duodenal mucosa that extend through the muscularis mucosa
  • Peptic ulcer disease
    • Is a relapsing and chronic disease which involves duodenal ulcers and gastric ulcers
  • An infectious disease
    • Peptic ulcer disease is today considered an infectious disease caused by the bacteria Helicobacter pylori (Hp)
    • However, at least 25% of the gastric ulcers and a small number of duodenal ulcers are caused by ulcerogenic drugs like NSAIDs and salicylates
  • Chronic and relapsing disease
    • A patient with a previous detected peptic ulcer, in whom the Hp has not been eradicated, has by definition still a peptic ulcer disease
    • Again, ulcers caused by ulcerogenic drugs are an exception
  • Further reading
    • See separate article about complications in peptic ulcer disease
    • See separate article about Helicobacter pylori


  • Lifetime prevalence
    • About 10% of the population will some time during life develop peptic ulcer disease, although this proportion is decreasing
  • Incidence
    • The incidence of duodenal ulcers has dropped significantly during the last 30 years, while the incidence of gastric ulcers has shown a small increase, mainly caused by the widespread use of NSAIDs
    • The drop in incidence is considered to be a cohort-phenomena independent of the progress in treatment of the disease. The cohort-phenomena is probably explained by improved standards of living which has lowered the incidence of Hp-infections
  • Gender
    • Nowadays peptic ulcer disease is about just as common among women (9,5%) as among men (10,5%)1
  • Age
    • Duodenal ulcers are most frequent among individuals 30 to 55 years of age, while gastric ulcers are more common among individuals 55 to 70 years of age
  • Location
    • Duodenal ulcers occur fime times as frequent as gastric ulcers
  • Hp epidemiology
    • In the general population 20-50% are infected with Hp, the prevalence increases with age
    • It is estimated that only 15-20% of the infected individuals will develop a peptic ulcer2

Etiology and pathology

  • According to American figures Hp-infection (48%) and NSAIDs (24%) are the dominating causes of peptic ulcers3
  • A number of other infections and co-morbidity increase the risk of developing a peptic ulcer, like cytomegalic virus, tuberculosis, Crohn's disease, cirrhosis of the liver, chronic renal failure, sarcoidosis, myeloprolipherative conditions4
  • Critical illness, surgery or hypovolemia can induce splanchnic hypoperfusion and may result in gastroduodenal erosions or ulcers (stressulcers) - such lesions can be asymptomatic and manifest themselves with bleeding and perforation5
  • Increased production of gastric acid and pepsin is of importance in duodenal ulcers
  • Zollinger-Ellison's disease, a gastrin producing tumor, is a very rare cause of an aggressive type of peptic ulcer disease
  • Smoking is an important risk factor for relapse, and it delays the process of healing

Etiology - infection with Helicobacter pylori

  • Hp is recognised as the main causative factor for peptic ulcer disease - it is a Gram negative bacteria
  • Hp-infection and risk of peptic ulcer disease
    • Only 10-15% of Hp-positives will develop peptic ulcer disease6
  • Frequency of Hp-infection
    • More than 95% of all duodenal ulcers and about 75% of gastric ulcers are Hp-positive
    • Except from patients using NSAIDs or salicylates, the prevalence of Hp is close to 100% also in patients with gastric ulcer
  • Additional effects of Hp-infection
    • Patients with Hp-infection have increased resting and meal stimulated levels of gastrin, reduced production of mucus in the stomach and reduced production of bicarbonate in the duodenum - all are factors that contribute to the development of peptic ulcer
  • Effect of Hp-elimination
    • Eradication of H. pylori was in one study found to reduce the relapse rate of duodenal ulcers from 67% to 6% and in gastric ulcers from 59% to 4%7

Etiology - NSAIDs

  • About 25% of gastric ulcers and a small proportion of duodenal ulcers are caused by side-effects from NSAIDs and salicylates
  • NSAIDs is the commonest reason for peptic ulcer in patients without H. pylori-infection8
  • Pathophysiology
    • Locally NSAIDs can cause submucosal erosions. Besides, by inhibition of the cyclooxygenase, NSAIDs hinder the formation of prostaglandins and their protective cyclooxygenase-2-mediated (COX-2) effects
    • COX-2 enhances the protection of the gastric mucosa by stimulation of the production of mucus and bicarbonate, fascilitates the proliferation of epitelial cells and increases the blood flow in the submucosa
    • Infection with H. pylori adds to the risk and extent of NSAID-induced lesion9
  • Ulcer complications
    • The annual risk of lifethreatening ulcer-related complications is 1-4% among patients on longterm treatment with NSAIDs, with the highest risk among the oldest patients10
    • NSAIDs are the cause of approximately half of all perforated ulcers, which occur most frequently among elderly patients who take aspirin or other NSAIDs for protection of cardiovascular disease or artropathia11-12
  • Protective drugs
    • Protonpump inhibitors and misoprostole reduce the ulcerogenic potential from NSAIDs and reduce the relapse rate of NSAIDs-related peptic ulcers

Pathogenesis of ulcer development

  • A defect (an ulcer) occurs in the mucosa of the stomach or duodenum when protective factors are weakened or the mucosa is exposed to large amounts of aggressive luminal factors, like acid and pepsin
  • The ulcer extend trough the muscularis mucosa and is usually more than 5 mm in diameter
  • More than 95% of the duodenal ulcers are located in the bulbar part of the duodenum or in the pyloric region
  • Benign gastric ulcers are usually located in the antrum (60%) or in the transission zone between the antrum and corpus on the minor curve of the stomach (25%)

Risk factors

  • NSAIDs
    • NSAIDs increases the risk 5-7 times of developing a gastric ulcer within the first three months after the start of NSAIDs treatment, later the risk is increased 4 times. Two months after cessation of the treatment the risk is back to normal13
    • There is a clear dose-response relation
    • An additive risk is observed when NSAIDs are combined with SSRI treatment14-15
    • COX-2 reduces the frequency of milder forms of dyspepsia and also lowers the risk of perforation, obstruction and bleeding16
  • Salicylates
    • Relative risk was in one study found to be increased with 2.6 and low dosage reduced the risk (Ia)17
    • In another study the relative risk was 1.6 among patients using 50-162 mg daily and 1.7 among patients using 163-1500 mg daily (Ia)18
  • SSRI
    • Use of SSRI is associated with increased risk (RR = 3.6) of bleeding in the digestive tract14-15
    • This risk is significantly increased if NSAIDs are used at the same time (RR = 12.2)
  • Family history
    • Peptic ulcer disease among parents or siblings increases the risk by 2-2.5
  • Smoking
    • Increases the incidence of peptic ulcer disease with appr. 1.5
  • Rheumatic problems and low socioeconomic status
    • Increase the risk of peptic ulcer disease
  • Psychosocial factors (stress)
    • Is shown to be of importance among Hp-infected individuals and when the disease will manifest itself
  • Dietary factors
    • Do not alter the risk of peptic ulcer disease


  • D85 Duodenal ulcer
  • D86 Other types of peptic ulcers


  • K25 Gastric ulcer
  • K26 Duodenal ulcer
  • K27 Peptic ulcer disease, unspecified location
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