Clinical presentation
History. The classic symptoms of peptic ulcer disease – epigastric burning pain on an empty stomach that is relieved by food or antacids – are familiar to most physicians and lay people. Sometimes the pain radiates to the back, suggesting an ulcer of the posterior aspect of the duodenal bulb that may have penetrated into the pancreas. However, many patients with peptic disease experience nonspecific abdominal discomfort, which broadens the differential diagnostic considerations to include gastroesophageal reflux disease, gallbladder disease; pancreatic disorders; cancer of the stomach, pancreas, or biliary system; mesenteric vascular insufficiency; and irritable bowel syndrome. A minority of patients has gastrointestinal bleeding, weight loss, or vomiting; the vomiting may be caused by partial or complete gastric outlet obstruction.
Over the past three decades, the yearly incidence of discrete peptic ulcer disease appears to have decreased, but peptic disease of other types, such as gastritis and duodenitis, sometimes related to ingestion of aspirin, nonsteroidal antiinflammatory drugs, corticosteroids, or ethanol have increased in incidence. Thus, important historical information includes a record of drug and alcohol use and a history of smoking, and previous diagnosis of peptic disease.
Physical examination. The physical examination of a patient with peptic disease may be normal. Some patients have upper abdominal tenderness and guarding. Rigidity of the abdomen and absent bowel sounds suggests perforation. Stool should be tested for occult blood.
Diagnostic studies
Most patients with dyspepsia or uncomplicated peptic disease may initially require no diagnostic study. It may be sufficient to begin empiric treatment H2 blockers or proton-pump inhibitors to control acid secretion. Patients also should be advised regarding diet, smoking, and lifestyle, as described in section III. If they do not respond to treatment within a reasonable time, usually 2 to 4 weeks, endoscopy should be considered, during which biopsies can be obtained to test for H. pylori and, in the case of a gastric ulcer, to evaluate for a cancerous lesion.
Patients with potential complications
A minority of patients present initially with signs or symptoms that should act as «red flags» to alert the physician to the increased possibility of complications of peptic disease or cancer. These warnings are clinically significant weight loss, evidence of gastrointestinal bleeding, repeated vomiting, and intractable abdominal pain. If one of these circumstances is present, prompt diagnostic evaluation rather than empiric therapy is recommended. The diagnostic procedure preferred is upper gastrointestinal endoscopy because of its superior diagnostic accuracy over upper gastrointestinal series. The upper gastrointestinal series is often ambiguous or nondiagnostic and patients have to undergo subsequent endoscopy to clarify the questions that remain. In general, judicious use of endoscopy as the initial diagnostic study in selected patients with peptic complaints probably is the most cost-effective approach.
Laboratory studies
Most patients with uncomplicated peptic disease require no laboratory studies except for the determination of H. pylori status by serologic testing. However, a complete blood count and serum electrolytes are indicated in the evaluation of patients who have bleeding or vomiting. A serum amylase is helpful in evaluating patients with persistent pain that radiates to the back. If peptic disease is persistent or there is a strong family history of peptic disease, the patient should be evaluated for a hypersecretory syndrome (see section C).
Serum gastrin levels may be elevated in conditions in which gastric acid secretion is very low or absent or in conditions in which there is gastric acid hypersecretion. Because acid is the major inhibitory influence on antral gastrin release, hypo- or achlorhydric conditions predispose to hypergastrinemia. However, in these conditions there is no known adverse consequence of the hypergastrinemia because the major end organ for gastrin, the parietal cell mass, is absent.
In hypersecretory conditions associated with hypergastrinemia, the source of gastrin either is independent of normal physiologic control (e.g., Zollinger-Ellison syndrome and retained antrum syndrome), is an unusual physiologic variant that results in too many G cells (antral G-cell hyperplasia), is a consequence of antral stimulation (e.g., gastric outlet obstruction), is a result of unopposed action of gastrin (e.g., hypersecretion after small-bowel resection), or develops because of poor renal excretion of gastrin caused by renal disease.
Serum for gastrin determination should be drawn in the fasting state. Because some patients with Zollinger-Ellison syndrome may have intermittent secretion of gastrin, repeated fasting serum gastrin determinations may be indicated.
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The secretin stimulation test takes advantage of the peculiar response of gastrinomas to secretin. Normally, intravenous secretin inhibits the release of gastrin from antral G cells, and serum gastrin either falls or remains unchanged after secretin injection. In patients with a gastrinoma, however, secretin stimulates release of gastrin from the tumor, causing a prompt rise in serum gastrin.
To perform the test, give secretin-kabi 2 U/kg of body weight by rapid intravenous push. Draw blood for serum gastrin 15 minutes and 1 minute before the secretin injection, and at 2, 5, 10, 20, and 30 minutes after injection. In patients with gastrinoma, the serum gastrin levels should rise rapidly within 5 to 10 minutes of secretin administration. The increase usually is greater than 400 pg/mL. With other causes of hypergastrinemia that are associated with hypersecretion of gastric acid, such as the retained antrum syndrome (observed occasionally after an antrectomy and gastrojejunostomy), gastric outlet obstruction, small-bowel resection, and renal insufficiency, the serum gastrin level should decline or remain unchanged.
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