Is there evidence of enhanced duodenogastric reflux in Barrett's esophagus?
R.C. Heading (Edinburgh)
The role of refluxed bile acids and other constituents of duodenal luminal fluid in causing esophageal mucosal damage has long been a topic of controversy. Part of the controversy comes about because of methodological difficulties in detecting and quantitating abnormal duodenogastric reflux. It is now certain that some duodenogastric reflux is physiological and occasional measurements may demonstrate quite substantial reflux in apparently healthy subjects. This has made for difficulties in defining the "normal range".
A substantial body of literature nevertheless points to enhanced duodenogastric reflux in patients with esophageal reflux disease, including those with Barrett's esophagus. This is entirely compatible with pathophysiological concepts, if gastroesophageal reflux disease is regarded primarily as a disorder of upper gastrointestinal motility. It is then understandable that motor dysfunction in the esophagus and its lower sphincter may be accompanied by disordered gastric or pyloroduodenal motor function, but the occurrence of increased duodenogastric reflux in such patients does not prove a causal role for refluxed duodenal content in relation to esophageal mucosal damage.
There is less certainty with respect to the occurrence of enhanced duodenogastric reflux in Barrett's esophagus relative to its occurrence in uncomplicated esophagitis. Recently published data appears to suggest that duodenogastric reflux is little different between them, though some evidence points to significantly increased
duodenogastric reflux in complicated Barrett's esophagus (i.e., Barrett's esophagus accompanied by strictures or ulcers) [1.2]. Comparing uncomplicated Barrett's esophagus with uncomplicated reflux esophagitis, however, studies of bile salt concentrations in upper gastrointestinal aspirates and studies based on dual (intragastric and intraesophageal) pH monitoring are in agreement in showing no abnormality specifically associated with Barrett's esophagus [3-5]. Consequently, although duodenogastric reflux appears to be enhanced in such individuals relative to healthy control subjects, there is no sound experimental basis for suggesting duodenogastric reflux has a major role in the causation of Barrett's metaplasia.
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