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A definitive diagnosis of peptic ulcer disease cannot be made on clinical grounds alone. Uncomplicated peptic ulcer disease can be strongly suspected in the presence of a "classic" history, including epigastric burning pain; relief of pain with ingestion of milk, food, or antacids; and night pain accompanied by "benign" physical examination findings, including normal vital signs with or without mild epigastric tenderness. The differential diagnosis of epigastric pain is extensive and, in addition to peptic ulcer disease, includes gastritis, gastroesophageal reflux disease, cholelithiasis, pancreatitis, hepatitis, abdominal aortic aneurysm, gastroparesis, and functional dyspepsia. Careful history taking may elicit features that point away from peptic ulcer disease: burning pain radiating into the chest, water brash, and belching may suggest gastroesophageal reflux disease; more severe pain radiating to the right upper quadrant and around the right or left side suggests cholelithiasis; radiation through to the back indicates pancreatitis or abdominal aortic aneurysm; chronic pain, anorexia, or weight loss may indicate gastric cancer. Myocardial ischemic pain may also present as epigastric pain and should be strongly considered in the appropriate clinical setting.
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Physical examination findings may suggest other diagnoses: right upper quadrant tenderness points to cholelithiasis or hepatitis, an epigastric mass to pancreatitis (pseudocyst) or pancreatic or gastric neoplasm, a pulsatile mass to abdominal aortic aneurysm, jaundice to hepatitis, and peritoneal findings to an acute abdomen.
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Ancillary tests may help exclude peptic ulcer disease complications and narrow the differential diagnosis. Normal results for CBC rule out anemia from chronic GI bleeding due to peptic ulcer disease, gastritis, or cancer (but do not rule out acute blood loss). Elevated liver function test results may indicate hepatitis, and an elevated lipase level may indicate pancreatitis. An acute abdominal series may show free air associated with perforation. A limited ED US examination may show gallstones or an abdominal aortic aneurysm. An ECG and cardiac enzyme determination are indicated if there is a suspicion of myocardial ischemic pain.
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The gold standard for diagnosis of peptic ulcer disease is visualization of an ulcer by upper GI endoscopy.2,4 Although not all patients with undiagnosed dyspepsia require endoscopy, those with "alarm features" do3,4 (Table 78-1). Alarm features raise the index of suspicion for gastric or esophageal cancer, as well as other potentially serious conditions, but the features are not specific.3
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Because most peptic ulcers are caused by H. pylori infection and eradication of H. pylori dramatically decreases the ulcer recurrence rate, it is important to know how to diagnose infection. H. pylori infection can be diagnosed by endoscopic tests, including the rapid urease test, histologic study, and culture, all of which rely on a biopsy of the gastric mucosa.1,7,11 Noninvasive tests include serologic tests, urea breath tests, and stool antigen tests.1,7,11
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The rapid urease test detects the presence of urease in a biopsy specimen (presumptive evidence of H. pylori infection) with >90% sensitivity and >95% specificity.7 Histologic studies allow direct assessment of H. pylori infection and culture of the organism, but these tests require highly trained technicians and appropriate facilities and are not widely available.7,11 The major disadvantage of all the aforementioned tests is the cost in time, dollars, and potential complications of endoscopy.
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Serologic studies detect immunoglobulin G antibodies to H. pylori and are readily available, but the sensitivity and specificity are not very good (85% and 79%, respectively).7,11 Serologic studies are not useful as a test of cure, because antibodies remain for several months to years after eradication of infection.
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The urea breath test relies on the presence of urease produced by H. pylori. Urea labeled with carbon-13 or carbon-14 instead of carbon-12 is ingested and, in the presence of bacterial urease, is broken down into labeled carbon dioxide and ammonia. The labeled carbon dioxide is detected in the breath later. Sensitivity and specificity are >95%.7,11 The urea breath test can be used to determine the presence of infection after eradication therapy.11
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H. pylori antigens can be detected in the stool with >90% sensitivity and specificity.1,7 Testing performed ≥4 weeks after completion of H. pylori eradication therapy is useful as a test of cure. The sensitivity of all tests that rely on active infection with H. pylori is decreased significantly by recent treatment with PPIs, histamine-2 (H2) antagonists, antibiotics, and bismuth compounds.7,11