esophagitis is a disorder of the defense mechanisms at the esophagealjunction, which is caused by regurgitation of the gastric contents, especially of gastric acid. GERD is associated with decreased gastric emptying and/or increased incidence of transient lower esoph-ageal relaxation (T-LESR). Smoking and obesity are factors that increase the incidence cf GERD-like symptoms such as heartburn, belching, and bloating. Reflux has been observed in humans and dogs but not in rodents.
can be subdivided into T-LESR. free reflux, and stress reflux. H. pylori infection does not necessarily correlate with GERD, although a reduction in acid secretion reduces the chances of reflux. The effectiveness cf PPIs is reduced in the absence of H. pylori infection; therefore the majority of patients with GERD require >20 mg/day to provide symptom relief and to heal the esophagitis produced by gastric acid reflux. This dose is much higher than that required to inhibit acid secretion associated with DU disease. If PPI therapy is stopped, then GERD patients appear to produce greater amounts of gastric acid and their reflux is potentiated. 11 has been reported that if the prevalence of H. pylori continues to decline, then PPI consumption will continue to increase for GERD (29). Ideally, future therapy for GERD should be independent of H. pylori status and additionally be devoid of the acid-rebound effect produced with PPI therapy.
GERD causes significant discomfort but is not in itself life threatening. The incidence of adenocarcinoma of the esophagus is increasing in the United States (30), with almost 100% of cases occurring in patients with Barrett's esophagus, a condition in which mucin-secreting, metaplastic, columnar epithelium replaces the normal squamous epithelium of the esophagus (31). There is substantial evidence that GERD may increase the incidence of Barrett's esophagus. Fass reported that the length of Barrett's esophagus tissue correlated with the duration of esophageal acid exposure (32). The use of antireflux medication in patients with GERD leads to an improvement or alleviation of symptoms and healing of mucosal inflammation. Antisecre-
tory agents have been used to reduce the exposure of the esophagus to acid in Barrett's esophagus. However, even high doses of PPIs have not resulted in regression of Barrett's mucosa. Not all GERD patients develop Barrett's esophagus and the causative agents for this progression to a precancerous state have not been fully determined. The age of onset, duration of symptoms, and complications of GERD are markers of an increased risk of Barrett's esophagus. In additon, the longer the region of Barrett's mucosa, the higher the risk for the development of dysplasia (33).
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