Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Mucosa
 The
 Esophagogastric  Junction
 Barrett's
 Esophagus

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OESO©2015
 
Volume: Barrett's Esophagus
Chapter: Short Barrett's esophagus
 

Is there a difference in exposure time to duodenogastroesophageal reflux in patients with short or long segments of intestinal metaplasia?

K.R. DeVault (Jacksonville)

This is a very difficult to answer question. The concept of duodeno-gastroesophageal reflux (DGER) has been reported to be a possible factor in the development of Barrett's esophagus and perhaps even cancer, although the data are stronger in animal compared to human models [1]. It is certainly clear that duodenal contents can produce esophageal injury in animal models and may cause symptoms and mucosal injury in patients with altered gastric anatomy. What is less clear is the role these potentially injurious materials might play in Barrett's esophagus [2].

It is clear that patients with Barrett's esophagus have impaired physiology at the lower esophageal sphincter (LES) and perhaps that impairment in physiology is more severe in long segment Barrett's esophagus (LSBE) compared to short segment Barrett's esophagus (SSBE). Oberg et al. compared lower esophageal sphincter pressure (LESP) and acid exposure in a group of patients with intestinal metaplasia (IM) of the cardia, SSBE and LSBE [3]. They found that the LESP decreased with increasing length of Barrett's esophagus (7.2, 6.4 and 3.8 mm Hg respectively) while the percentage acid exposure increased (5.8, 8.4 and 16.5%). Loughney et al. reported a similar relationship between controls, SSBE and LSBE [4].

Attempts at actually measuring bile exposure in the esophagus have been challenging. The finding of bile stained gastric mucosa is neither specific nor sensitive for DGER. Attempts to document this disorder with biliary scintigraphy have also been less than successful. If bile or the misnamed "alkaline" reflux is to be diagnosed, evaluation of esophageal bile acid using an ambulatory monitor is more accurate than attempting to quantify esophageal alkalinization using a pH probe [5]. While the length of Barrett's esophagus was not directly addressed, Vaezi and Richter compared both acid and bile exposure (measured with the Bilitec™ device) in normal controls, patients with nonerosive disease and in those with esophagitis, uncomplicated Barrett's esophagus and complicated Barrett's esophagus (dysplasia or cancer) [6]. They found that both the acid exposure and the bile exposure increased with worsening esophageal damage. This increase in bile exposure with Barrett's esophagus is almost always associated with a concomitant increase in acid exposure. To my knowledge, there is only one comparisons of bile exposure in SSBE versus LSBE. This study evaluated 20 patients with SSBE, 12 with LSBE and 33 patients with GERD and no Barrett's esophagus [7]. Bile exposure was increased in the patients with LSBE, but not in the patients with LSBE or GERD without Barrett's esophagus.

We are therefore left with insufficient data to completely answer the question. The available data support the suggestion that the physiological defect is worse with LSBE, that acid exposure is greater in LSBE and that bile exposure is greater in complicated Barrett's esophagus. From these studies and the additional single study by Pfaffenbach et al., it is safe to infer that bile exposure should be greater in LSBE when compared to SSBE [7]. A more important question is: does this matter? The answer to that is more complex and will be addressed in other questions in this volume.

References

1. Yamashita Y, Homma K, Kako N, et al. Effect of duodenal components of the refluxate on development of esophageal neoplasia in rats. J Gastrointest Surg 1998;2:350-355.

2. Sears RJ, Champion GL, Richter JE. Characteristics of distal partial gastrectomy patients with esophageal symptoms of duodenogastric reflux. Am J Gastreoenterol 1995;90:211-215.

3. Oberg S, DeMeester TR, Peters JH, et al. The extent of Barrett's esophagus depends on the status of the lower esophageal sphincter and the degree of esophageal acid exposure. J Thorac Cardiovasc Surg 1999;117:572-580.

4. Loughney T, Maydonovitch CL, Wong RKH. Esophageal manometry and ambulatory pH monitoring in patients with short and long segment Barrett's esophagus. Am J Gastroenterol 1998;93:916-919.

5. Mela GS, Savarino V, Vigneri S, et al. Limitations of continuous 24-h intragastric pH monitoring in the diagnosis of duodenogastric reflux. Am J Gastroenterol 1995;90:933-937.

6. Vaezi MF, Richter JE. Role of acid and duodenogastroesophageal reflux in gastroesophageal reflux disease. Gastroenterology 1996;111:1192-1199.

7. Pfaffenbach B, Hullerum J, Orth KH, et al. Bile and acid reflux in long and short segment Barrett's esophagus, and in reflux disease. Zeitschr Gastroenterol 2000;38:565-570.


Publication date: August 2003 OESO©2015