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Gastritis and Peptic Ulcer Disease: Overview and Risk Factors

Gastritis and peptic ulcers affect up to 50% of adult populations in Westernized countries. Gastritis is a superficial erosion and inflammation of the gastric mucosa. Peptic ulcers are deeper erosions and ulcerations that extend through the muscularis layer of the gastric or duodenal mucosa.

These disorders result from a disrupted balance between formation of caustic gastric acid and maintenance of the protective mucosal barrier that depends on secretion of bicarbonate, prostaglandins, and mucosal growth factors. In general, gastritis and gastric ulcers are associated with insufficient mucosal protection, whereas duodenal ulcers are associated with excess acid secretion.

Helicobacter pylori infection may be responsible for up to 95% of duodenal ulcers and 85% of gastric ulcers, worldwide. The bacteria disrupt the mucosal protective barrier, making it more vulnerable to acid damage and inciting an inflammatory response. In the United States, H pylori is a less prevalent cause of ulcers; nonsteroidal anti-inflammatory drugs (NSAIDs) are the most common cause of gastric ulcers in the United States. Other etiologies include irritants such as aspirin and steroids; severe physiologic stress, including burns, sepsis, trauma, and major surgery; local trauma, such as nasogastric tube placement; and hypersensitivity and autoimmune reactions.

These disorders are often asymptomatic. When symptoms occur, they may include:

  • Gnawing epigastric or right-upper-quadrant abdominal pain that may radiate to the back.
  • Nausea and vomiting.
  • Weight loss/anorexia.
  • Dyspepsia.
  • Gastrointestinal bleeding that may present as hematemesis, melena, guiac-positive stools, and/or anemia.

Whereas eating exacerbates the pain of gastritis and gastric ulcers, duodenal ulcer pain is relieved by eating, but increases 2 to 3 hours after meals.

The sudden onset of severe pain (or significant worsening of existing pain), or peritoneal signs (abdominal rigidity, guarding, rebound tenderness) may signify a perforation, which is a surgical emergency.

Risk Factors

Increasing age. Gastric ulcers typically occur in patients over 40 years old, and the incidence of duodenal ulcers peaks at around age 60.

H pylori infection. One in six patients exposed to H pylori will develop an ulcer. Ulcers recur much less often when H pylori is eradicated.

NSAIDS. NSAIDs suppress prostaglandin formation in the mucosa, which is normally a part of the protective mechanism of the mucosal barrier.

Tobacco use. Nicotine increases acid secretion and reduces mucosal blood flow in the stomach and duodenum.

Alcohol use. Alcohol can cause gastritis by stimulating acid secretion and damaging the mucosal barrier. However, no evidence for a role in ulcer formation has been found.

Major surgery or severe illness. Prophylaxis for gastritis and ulcers may be administered in hospitalized patients, especially those on mechanical ventilation or those undergoing major surgery. Although some reports have argued for prophylaxis in all hospitalized patients, this claim is not backed by rigorous data.

Family history. More than 25% of ulcer patients have a family history of ulcers, compared with 5% of nonulcer patients.


Gastritis and Peptic Ulcer Disease: Diagnosis and Treatement >>