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Vaezi and richter studied 20 control subjects, 30 patients with gastroesophageal reflux disease (GERD), and 20 patients with Barrett’s esophagus using both a conventional pH electrode and a recently developed electrode that detects bilirubin (the Bilitec 2000 probe). They found that reflux of acid and duodenal contents (as detected by the bilirubin probe) tended to occur in parallel and were more severe in patients with more severe disease. They conclude that both acid and duodenogastric reflux showed a graded increase in severity across the GERD spectrum and that acid and duodenogastric reflux occur simultaneously in the majority of the reflux episodes.
While acid and pepsin have long been regarded as the most important offensive factors in the pathogenesis of GERD and its complications, several recent studies have sought to invoke bile and other intestinal contents in the etiology of complicated GERD and Barrett’s esophagus, in particular. In animal models, esophageal exposure to bile and intestinal enzymes can induce intestinal metaplasia and even adenocarcinoma, and studies in man have reported abnormal intra-esophageal levels of bile, alkali, and bilirubin. Taken together, these lines of evidence have led to the hypothesis that bile, either alone or in conjunction with acid, may be the central agent in the ominous progression of esophagitis to Barrett’s esophagus and adenocarcinoma. As is often the case, the story has proven more complex. It has become clear that alkaline reflux is simply not a reality except in the patient who has been rendered surgically achlorhydricGERD patients with more "alkaline" reflux always have even more significant acid reflux. The bile hypothesis has proven more difficult to define, given the unreliability of most techniques for the detection and quantitation of bile in the stomach or esophagus. Richter and colleagues have pioneered and validated a novel approach by using a bilirubin-sensitive electrode as a surrogate for bile detection. Using this technique, they demonstrate in this and other studies that such reflux is most prominent among patients with Barrett’s.1-3 What they also demonstrate is that those very same patients have the most severe acid reflux and that bile and acid reflux occur, for the most part, together and in parallel. Bile reflux is not, therefore, a unique event in Barrett’s. What is more likely is that these patients reflux more of everythingacid, bile, bilirubin, etc. This should come as no surprise, given the prevalence of lower esophageal sphincter hypotension in complicated GERD.
What are the clinical implications of these findings? I believe that the most important message is that we should not attempt to address bile reflux as an isolated phenomenon in defining therapeutic strategies for complicated GERD; effective acid suppression with omeprazole, for example, will also decrease bile reflux by reducing gastric volume. In clinical therapy, the emphasis should continue to be on gastroesophageal reflux, not on duodenogastric reflux. While bile and acid may interact to induce mucosal changes, these agents do not act alone.
1. Vaezi MF, et al. Gastroenterol 1995;108:1897-1907.
2. Singh S, et al. Gut 1993;34:309-316.
3. Champion G, et al. Gastroenterol 1994;107:747-754.