Chapter 32-14: Peptic Ulcer Disease (PUD)

TEXTBOOK PRESENTATION

The pain of PUD is classically described as a dull or hunger-like pain in the epigastrium that is either exacerbated or improved by food intake. The pain is often worse on waking and may radiate to the back. Symptomatic periods often last for several weeks. Nausea and early satiety may be seen.

DISEASE HIGHLIGHTS

1. 250,000 cases per year in the United States

2. Etiology: In the United States, most ulcers are secondary to NSAID use, Helicobacter pylori infection or both. The prevalence of H pylori varies widely depending on the region.

   1. H pylori infection

      1. Present in 50% of the world’s population

      2. Asymptomatic in the majority of patients

      3. Peptic ulcers (in the stomach or duodenum) develop in 1–10% of infected patients.

      4. H pylori may also cause atrophic gastritis, intestinal metaplasia, and rarely, gastric cancer (0.1–3% of infected patients).

   2. NSAIDs

      1. Virtually all NSAIDs increase the risk of PUD, including over-the-counter NSAIDs and low-dose aspirin. The risk is lower with cyclooxygenase (COX)-2 inhibitors.

      2. Ulcer disease develops in 25% of persons who take NSAIDs regularly.

      3. PUD-related bleeding or perforation is present in 2–4% of persons who take NSAIDs regularly.

      4. Results in 100,000 NSAID-associated hospitalizations in the United States annually, with 7000–10,000 deaths.

      5. Gastric ulcers are 5 times more common than duodenal ulcers.

      6. Ulcers are most likely to occur in the first 1–3 months of NSAID use.

      7. Risk factors for NSAID-associated PUD include the following:

         1. History of prior PUD

         2. Age > 65 years

         3. High-dose NSAID therapy

         4. Concomitant use of aspirin (low or high dose), corticosteroids, or anticoagulants.

         5. Concurrent H pylori infection

      8. NSAIDs may be nonselective, inhibiting both COX-1 and COX-2, or selective, inhibiting only COX-2.

         1. Selective COX-2 inhibitors have less GI toxicity.

         2. However, several selective COX-2 inhibitors increase the risk of myocardial infarction and several have been withdrawn from the market. Celecoxib is still available.

         3. Alternate strategies to decrease the risk of NSAID-related PUD include concurrent use of proton pump inhibitors (PPIs) or misoprostol.

   3. Zollinger-Ellison syndrome is a rare cause of PUD that results from a tumor secreting gastrin, leading to hypersecretion of HCL in the stomach.

3. Complications

   1. Bleeding, which can vary from massive hemorrhage (with hematemesis and melena or hematochezia) to occult, chronic, subtle bleeding with iron deficiency anemia (see Chapter 19-11: Peptic Ulcer Disease).

   2. Perforation

   3. Weight loss

EVIDENCE-BASED DIAGNOSIS

1. History and physical exam

   1. Pain is not a good predictor of PUD.

      1. Ulcers are often asymptomatic and symptoms are more likely with non–NSAID-associated ulcers.

         1. 60% of NSAID-associated ulcers are asymptomatic.

         2. 25% of non-NSAID ulcers are asymptomatic.

      2. Pain often reflects nonulcer dyspepsia rather than PUD.

         1. Less than one-third of patients with epigastric discomfort have PUD.

         2. Among patients undergoing endoscopy, patients with nonulcer dyspepsia have more severe and numerous symptoms than patients with PUD.

      3. Surprisingly, several clinical predictors are not good at discriminating ulcer from nonulcer dyspepsia including:

         1. Response to antisecretory therapy

         2. Epigastric tenderness

         3. The quality of the pain

   2. Best predictors ...