Gastric and duodenal ulcers usually cannot be differentiated based on history alone, although some findings may be suggestive. Epigastric pain is the most common symptom of both gastric and duodenal ulcers. It is characterized by a gnawing or burning sensation and occurs after meals—classically, shortly after meals with gastric ulcer and 2-3 hours afterward with duodenal ulcer. In uncomplicated peptic ulcer disease (PUD), the clinical findings are few and nonspecific. "Alarm features" that warrant prompt gastroenterology referral[1] include bleeding, anemia, early satiety, unexplained weight loss, progressive dysphagia or odynophagia, recurrent vomiting, and family history of GI cancer. Patients with perforated PUD usually present with a sudden onset of severe, sharp abdominal pain. In most patients with uncomplicated PUD, routine laboratory tests usually are not helpful; instead, documentation of PUD depends on radiographic and endoscopic confirmation. Testing for H pylori infection is essential in all patients with peptic ulcers. Rapid urease tests are considered the endoscopic diagnostic test of choice. Of noninvasive tests, fecal antigen testing is more accurate than antibody testing and is less expensive than urea breath tests. A fasting serum gastrin level should be obtained in certain cases to screen for Zollinger-Ellison syndrome. Upper GI endoscopy is the preferred diagnostic test in the evaluation of patients with suspected PUD. Endoscopy provides an opportunity to visualize the ulcer, to determine the presence and degree of active bleeding, and to attempt hemostasis by direct measures, if required. Perform endoscopy early in patients older than 45-50 years and in patients with associated so-called alarm features. Most patients with PUD are treated successfully with cure of H pylori infection and/or avoidance of nonsteroidal anti-inflammatory drugs (NSAIDs), along with the appropriate use of antisecretory therapy. In the United States, the recommended primary therapy for H pylori infection is proton pump inhibitor (PPI)--based triple therapy. These regimens result in a cure of infection and ulcer healing in approximately 85-90% of cases. Ulcers can recur in the absence of successful H pylori eradication. In patients with NSAID-associated peptic ulcers, discontinuation of NSAIDs is paramount, if it is clinically feasible. For patients who must continue with their NSAIDs, proton pump inhibitor (PPI) maintenance is recommended to prevent recurrences even after eradication of H pylori. Prophylactic regimens that have been shown to dramatically reduce the risk of NSAID-induced gastric and duodenal ulcers include the use of a prostaglandin analog or a PPI. Maintenance therapy with antisecretory medications (eg, H2 blockers, PPIs) for 1 year is indicated in high-risk patients. Testing for H pylori infection is essential in all patients with peptic ulcers. In most patients with uncomplicated peptic ulcer disease (PUD), routine laboratory tests usually are not helpful. Documentation of PUD depends on radiographic and endoscopic confirmation. If the diagnosis of PUD is suspected, obtaining CBC count, liver function tests (LFTs), amylase, and lipase may be useful. CBC count and iron studies can help detect anemia, which is an alarm signal that mandates early endoscopy to rule out other sources of chronic GI blood loss. H pylori Testing Testing for H pylori infection is essential in all patients with peptic ulcers. Endoscopic or invasive tests for H pylori include a rapid urease test, histopathology, and culture. Rapid urease tests are considered the endoscopic diagnostic test of choice. The presence of H pylori in gastric mucosal biopsy specimens is detected by testing for the bacterial product urease. Fecal antigen testing identifies active H pylori infection by detecting the presence of H pylori antigens in stools. This test is more accurate than antibody testing and is less expensive than urea breath tests. Three kits (ie, CLOtest, Hp-fast, Pyloritek) are commercially available for H pylori testing, and each contains a combination of a urea substrate and a pH sensitive indicator. One or more gastric biopsy specimens are placed in the rapid urease test kit. If H pylori is present, bacterial urease converts urea to ammonia, which changes the pH, resulting in a color change. Urea breath tests detect active H pylori infection by testing for the enzymatic activity of bacterial urease. In the presence of urease produced by H pylori, labeled carbon dioxide (heavy isotope, carbon-13, or radioactive isotope, carbon-14) is produced in the stomach, absorbed into the bloodstream, diffused into the lungs, and exhaled. Obtain histopathology, often considered the criterion standard to establish a diagnosis of H pylori infection , if the rapid urease test result is negative and a high suspicion for H pylori persists (presence of a duodenal ulcer).

• published: 08 Sep 2012
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