Duodenal ulcer in the context of Non-steroidal anti-inflammatory drug


Duodenal ulcer in the context of Non-steroidal anti-inflammatory drug

⭐ Core Definition: Duodenal ulcer

Peptic ulcer disease refers to damage of the inner part of the stomach's gastric mucosa (lining of the stomach), the first part of the small intestine, or sometimes the lower esophagus. An ulcer in the stomach is called a gastric ulcer, while one in the first part of the intestines is a duodenal ulcer. The most common symptoms of a duodenal ulcer are waking at night with upper abdominal pain, and upper abdominal pain that improves with eating. With a gastric ulcer, the pain may worsen with eating. The pain is often described as a burning or dull ache. Other symptoms include belching, vomiting, weight loss, or poor appetite. About a third of older people with peptic ulcers have no symptoms. Complications may include bleeding, perforation, and blockage of the stomach. Bleeding occurs in as many as 15% of cases.

Common causes include infection with Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). Other, less common causes include tobacco smoking, stress as a result of other serious health conditions, Behçet's disease, Zollinger–Ellison syndrome, Crohn's disease, and liver cirrhosis. Older people are more sensitive to the ulcer-causing effects of NSAIDs. The diagnosis is typically suspected due to the presenting symptoms with confirmation by either endoscopy or barium swallow. H. pylori can be diagnosed by testing the blood for antibodies, a urea breath test, testing the stool for signs of the bacteria, or a biopsy of the stomach. Other conditions that produce similar symptoms include stomach cancer, coronary heart disease, and inflammation of the stomach lining or gallbladder inflammation.

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Duodenal ulcer in the context of Helicobacter pylori

Helicobacter pylori, previously known as Campylobacter pylori, is a gram-negative, flagellated, helical bacterium. Mutants can have a rod or curved rod shape that exhibits less virulence. Its helical body (from which the genus name Helicobacter derives) is thought to have evolved to penetrate the mucous lining of the stomach, helped by its flagella, and thereby establish infection. While many earlier reports of an association between bacteria and the ulcers had existed, such as the works of John Lykoudis, it was only in 1983 when the bacterium was formally described for the first time in the English-language Western literature as the causal agent of gastric ulcers by Australian physician-scientists Barry Marshall and Robin Warren. In 2005, the pair was awarded the Nobel Prize in Physiology or Medicine for their discovery.

Infection of the stomach with H. pylori does not necessarily cause illness: over half of the global population is infected, but most individuals are asymptomatic. Persistent colonization with more virulent strains can induce a number of gastric and non-gastric disorders. Gastric disorders due to infection begin with gastritis, or inflammation of the stomach lining. When infection is persistent, the prolonged inflammation will become chronic gastritis. Initially, this will be non-atrophic gastritis, but the damage caused to the stomach lining can bring about the development of atrophic gastritis and ulcers within the stomach itself or the duodenum (the nearest part of the intestine). At this stage, the risk of developing gastric cancer is high. However, the development of a duodenal ulcer confers a comparatively lower risk of cancer. Helicobacter pylori are class 1 carcinogenic bacteria, and potential cancers include gastric MALT lymphoma and gastric cancer. Infection with H. pylori is responsible for an estimated 89% of all gastric cancers and is linked to the development of 5.5% of all cases cancers worldwide. H. pylori is the only bacterium known to cause cancer.

View the full Wikipedia page for Helicobacter pylori
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