Box 1. Non-Helicobacter pylori or NSAID aetiologies of peptic ulcer disease | ||||
• Infection:— HSV.— CMV.— Other rare infections: TB, syphilis, mucormycosis. |
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Figure 2. Macroscopic image of the gastric wall showing a peptic ulcer with bloody contents. The gastric mucosa can be seen to the right of the ulcer.
potentially peptic ulcer disease and gastric cancer. 4 Most people with H. pylori colonisation are asymptomatic
and about 10 % develop peptic ulcer disease. 5 Infection is associated with 40-70 % of duodenal ulcers and 25-50 % of gastric ulcers. 6 H. pylori distorts gastrointestinal physiology including gastric acid secretion and mucosal defence mechanisms, which
Samir Grover / CC BY-SA / bit. ly / 3RK1zDE
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• Post-surgical:— Antral exclusion.— Post-gastric bypass.
• Infiltrating disease:— Sarcoidosis.— Crohn’ s disease.
• Radiotherapy
• Others:— Associated with acute illness.— Stress ICU ulcers.— Renal failure.
• Idiopathic
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leads to the development of peptic | ||||
ulcer disease. Furthermore, H. pylori |
infection directly induces mucosal |
infected with H. pylori; however, there |
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cytotoxicity through the release of |
are significant differences between |
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toxins, including cytotoxin-associated |
countries. Based on studies conducted |
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gene A. Most patients infected with H. |
between 1988 and 2006, the overall |
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pylori develop pangastritis via direct |
prevalence of H. pylori infection in |
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cytotoxicity, which, conversely, leads |
asymptomatic non-Indigenous Aus- |
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to a reduction in gastric acid secretion. |
tralians ranged from 15.4 to 30.6 %. 19 |
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However, 10-15 % of patients develop |
Interestingly, the incidence of |
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an antral predominant gastritis that |
peptic ulcer disease has been trend- |
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occurs because of decreased antral |
ing downwards over the past several |
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somatostatin secretion, leading to |
decades. As a result, sharp reductions |
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antral acid hypersecretion. 7 The use of NSAIDs inhibits mucosal gastroprotective prosta- |
in hospital admissions and mortality have been observed. 20 This is likely attributed to widespread H. pylori |
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glandin production, which leads to |
awareness, testing and eradication. In |
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mucosal inflammation and ulceration. Decreased prostaglandin production leads to increased gastric acid generation, reduced mucosal barrier integrity, decreased bicarbonate secretion and impaired mucosal blood flow. |
Figure 3. Endoscopic image of a posterior wall duodenal ulcer with clean base, seen in a patient who presented with upper gastrointestinal haemorrhage. |
developed countries, the prevalence of peptic ulcer disease has declined, particularly in young people. In contrast, NSAID-related ulcers in older adults have increased because of both an increased life expectancy and fre- |
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Compared with non-users, the risk of complications, including upper gastrointestinal bleeding, perforation and pyloric obstruction, are increased fourfold by NSAID use and twofold by aspirin use. 8 In addition, concomitant use of NSAIDs or aspirin with corticosteroids, anticoagulants, SSRIs and |
Smoking is an independent risk factor for the condition, with risk increasing in parallel with increasing pack-years of smoking. 10 In addition, the risk of peptic ulcer disease-related complications, including perforated ulcer, is increased threefold in those who |
complications of peptic ulcer are more prevalent during periods of natural disaster or societal upheaval. Increased psychological stress increases the incidence of peptic ulcer disease by influencing risky health-related behaviours including smoking and may also |
EPIDEMIOLOGY
THE lifetime prevalence of peptic ulcer disease in the general population is 5-10 %, with complications arising in 10-20 % of these patients. 16 In large population studies, the pooled incidence of peptic
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quent use of aspirin and NSAIDs. 2
CLINICAL PRESENTATION
PEPTIC ulcer disease often presents
with dyspeptic symptoms, including postprandial fullness, epigastric pain or early satiety. However, these
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aldosterone receptor antagonists sig- |
smoke more than 15 cigarettes per day. |
increase acid secretion. 13 |
ulcer disease was one case per 1000 |
symptoms may vary depending on |
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nificantly increases the risk of upper |
Smoking-related ulcers also appear to |
The evidence surrounding dietary |
person-years in the general popula- |
patient demographic and character- |
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gastrointestinal bleeding. 9
About 20 % of cases of peptic ulcer disease are H. pylori and / or NSAID negative( see box 1). These may be caused
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be more difficult to treat and are associated with higher rates of recurrence. 11 Another important risk factor is alcohol consumption; this damages the |
intake as a cofactor in peptic ulcer disease is controversial. There is currently no convincing evidence that any foods increase the risk of peptic ulcer disease. |
tion and the incidence of ulcer complications was 0.7 cases per 1000 person-years. 17 The incidence and prevalence varies based on the pres- |
istics, and the natural history of the disease. 21 Atypical presentations are not uncommon and up to two-thirds of older patients with peptic ulcer |
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by a gastrinoma( Zollinger-Ellison syn- |
gastric mucosal barrier and promotes |
Evidence to support dietary restrictions |
ence of H. pylori. Peptic ulcer disease |
disease are asymptomatic. 22 |
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drome), gastric adenocarcinoma, carcinoid syndrome or viral infections. 2
Apart from the above causes of peptic ulcer disease, there are multiple synergistic risk factors that may contribute to the development of the disease— most notably, smoking and alcohol are important cofactors.
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gastric acid secretion. Heavy drinking( more than 42 standard drinks per week) increased the risk of bleeding ulcers fourfold compared with drinking less than one drink per week. 12
Stress, depression and anxiety may be associated with the condition. Several studies have established that the
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to prevent the disorder is lacking. Certain food such as spices and coffee may lead to increased symptoms of dyspepsia, but this does not translate to an increased risk of disease. 14 High consumption of fruits, vegetables, dietary fibre and vitamin A is associated with reduced peptic ulcer disease. 15 |
incidence increases with age for both duodenal and gastric ulcers and both have a male predominance. 18
The incidence of peptic ulcer disease is 1 % per year in those with H. pylori, which is 6-10-fold higher than uninfected individuals. 5 It is estimated that 50 % of the world’ s population is
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Abdominal pain and associated symptoms
Burning epigastric pain, a hallmark
manifestation, commonly emerges when the stomach is empty, such as between meals or during the night. This discomfort can fluctuate in
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