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Upon completion of the chapter, the reader will be able to:

  1. Recognize differences between ulcers induced by Helicobacter pylori, nonsteroidal anti-inflammatory drugs (NSAIDs), and stress-related mucosal damage (SRMD) in terms of risk factors, pathogenesis, signs and symptoms, clinical course, and prognosis.

  2. Identify desired therapeutic outcomes for patients with H. pylori–associated ulcers and NSAID-induced ulcers.

  3. Identify factors that guide selection of an H. pylori eradication regimen and improve adherence with these regimens.

  4. Determine the appropriate management for a patient taking a nonselective NSAID who is at high risk for ulcer-related GI complications (e.g., GI bleed) or who develops an ulcer.

  5. Devise an algorithm for the evaluation and treatment of a patient with signs and symptoms suggestive of an H. pylori–associated or NSAID-induced ulcer.

  6. Given patient-specific information and the prescribed drug treatment regimen, formulate a monitoring plan for a patient who is receiving drug therapy either to eradicate H. pylori or to treat an active NSAID-induced ulcer or GI complication.




  • Image not available. Patients with peptic ulcer disease (PUD) should avoid exposure to factors known to worsen the disease, exacerbate symptoms, or lead to ulcer recurrence (e.g., NSAID use, alcohol consumption, or cigarette smoking).

  • Image not available. Reliance on conventional antiulcer drug therapy as an alternative to Helicobacter pylori eradication is inappropriate because it is associated with a higher incidence of ulcer recurrence and ulcer-related complications.

  • Image not available. Eradication therapy with a proton pump inhibitor (PPI)–based three-drug regimen should be considered for all patients who test positive for H. pylori and have an active ulcer or a documented history of either an ulcer or ulcer-related complication. Different antibiotics should be used if a second course of H. pylori eradication therapy is required.

  • Image not available. In patients at risk for NSAID-induced ulcers, PPIs at standard doses reduce the risk of both gastric and duodenal ulcers as effectively as misoprostol and more effectively than histamine2-receptor antagonists (H2RAs).

  • Image not available. Selective cyclooxygenase (COX)-2 inhibitors are no more effective than the combination of a PPI and a nonselective NSAID in reducing the incidence of ulcers and are associated with a greater incidence of cardiovascular (CV) events (e.g., ischemic stroke).

  • Image not available. Indications for stress ulcer prophylaxis include major trauma or surgery, severe head trauma, multiple organ failure, burns covering more than 25% to 30% of body, severe sepsis, shock, mechanical ventilation, coagulopathy, and high-dose corticosteroid use.

  • Image not available. Low-dose maintenance therapy with a PPI or H2RA is only indicated in patients with severe complications secondary to PUD such as gastric outlet obstruction or patients who need to be on long-term NSAIDs or high-dose corticosteroids and are at high risk for bleeding.




Peptic ulcer disease (PUD) refers to a defect in the gastric or duodenal mucosal wall that extends through the muscularis mucosa into the deeper layers of the submucosa.1 PUD is a significant cause of morbidity and is associated with substantial healthcare costs. Over ...

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