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What is the effect of gastric juice on Barrett's mucosa?
RM. Bremner, T.R. DeMeester (Los Angeles)
Continued erosion of the lower esophageal mucosa by gastroesophageal reflux can result in replacement of the squamous epithelium with columnar cells. This appears to occur because the columnar cells are more resistant to acid. Evidence of this is seen at endoscopy where erosive esophagitis occurs in the squamous epithelium above a quiescent Barrett's lining. In effect, the columnar change is an attempt to protect the esophagus from further acid injury. Complications such as ulceration, stricture, dysplasia and carcinoma that can occur in the metaplastic Barrett's mucosa are likely, due to the composition of the refluxed material. Reflux of duodenal contents has long been suspected to cause gastric mucosal injury and has been causally implicated in the development of gastric carcinoma [1,2]. There is growing evidence that a similar process is involved in the columnar lined esophagus. Experimental animal models have shown that bile and various enzymes can cause significant esophageal injury. A similar process is thought to occur in humans,
although it remains to be shown which specific components of the refluxed juice are important [3,4]. We have recently found that there was a close relationship between esophageal injury and increased esophageal exposure to pH < 2 and to pH > 7, suggesting that alkaline components of refluxed gastric juice contribute to esophageal injury in humans [5]. Many studies have shown that duodenal contents can reflux through the stomach and into the esophagus. Cowen reported on 42 patients with hypochlorhydria who had prominent gastric bile pool on endoscopy and histological evidence of gastritis, as well as esophagitis with heartburn unrelieved by antacids. An increase in gastric bile salts in patients with reflux esophagitis and strictures has also been reported [6,7]. Bremner supported his early hypothesis that bile reflux may be related to Barrett's ulceration by reports of increased bile acids in the stomachs of some Barrett's patients and later, in the gastric juice of Barrett's patients with stricture [8-10]. This was independently supported by Gillen who showed that postprandial gastric bile concentrations in patients with complicated Barrett's was greater than that of patients with uncomplicated Barrett's [11].
Attwood et al. used 24-h pH monitoring to compare patients with uncomplicated to complicated Barrett's disease. They used esophageal exposure to pH > 7 as an indirect indicator of entero-gastroesophageal reflux. They adhered to the use of glass combined electrodes and dilated all patients with strictures prior to pH monitoring. They found a similar acid exposure and a definite increase in the alkaline esophageal exposure in the patients with complicated disease (Fig. 1) [12], More recently, Stein and colleagues used esophageal aspirate studies to quantitate duodenal contents in the esophagus, and found an increase in bile acids in the esophagus of patients with
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