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Gastroesophageal Reflux Disease and Peptic Ulcer Disease

Definition and Epidemiology

Gastroesophageal reflux disease (GERD) is defined as symptoms or tissue injury arising from the reflux of gastric contents into the esophagus. Heartburn is the primary symptom of GERD and reflux esophagitis is the primary finding. However, symptoms do not always correlate closely with the degree of esophageal injury. Patients with severe symptoms may have minimal esophagitis whereas patients with severe, erosive esophagitis or with esophagitis complicated by bleeding or stricture heartburn, heart burn, indigestion, peptic ulcer disease, ulcer formation may report minimal heartburn. Furthermore, many patients have atypical symptoms of GERD either in addition to or in the absence of classical symptoms such as heartburn and acid regurgitation. Thus "reflux esophagitis" is an important manifestation of GERD but is not required for the diagnosis of GERD heart burn

Approximately 7% of the U.S. population experience GERD symptoms, especially heartburn, on a daily basis. The incidence of GERD increases with advancing age, particularly after age forty years. Erosive peptic esophagitis is seen in approximately 2% of adults. Therefore, many patients with symptomatic GERD do not have endoscopic evidence of reflux esophagitis. GERD is often a chronic disease. Effective medical therapy is available, but symptoms and esophageal injury frequently recur when therapy is discontinued.

Anti-reflux mechanisms and conditions predisposing to GERD

GERD results from deficiencies in the normal anti-reflux mechanisms. These include the lower esophageal sphincter, the diaphragmatic "pinch" mechanism, and the intra-abdominal location of the lower esophagus (which transmits increases in intra-abdominal pressure to the lower esophagus). When reflux occurs, esophageal clearance of the refluxed material is accomplished by esophageal peristalsis and gravity. Refluxed acid is also neutralized by swallowed saliva and by bicarbonate secretion by esophageal submucosal glands.

Transient lower esophageal sphincter relaxation appears to be a primary mechanism for reflux of gastric contents in patients with symptomatic GERD. The LES normally relaxes briefly during primary peristalsis and regains its tone when the