Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Esophagogastric  Junction

  Browse by Author
  Browse by Movies
Volume: Barrett's Esophagus
Chapter: Pathophysiology

Are there specific abnormalities in esophageal function existing in Barrett's patients?

H.J. Stein, W.K.H. Kauer, J.R. Siewert (München)

On functional assessment, Barrett's esophagus is associated with end stage reflux disease characterized by a markedly increased esophageal exposure to gastric juice. Compared with patients with increased esophageal acid exposure but no columnar metaplasia, both the quality and quantity of the refluxate appear to be different in patients with Barrett's esophagus. On ambulatory, 24-hour, esophageal pH monitoring, this is reflected in a markedly increased frequency and duration of reflux episodes as compared with reflux patients with no columnar metaplasia [1, 2].

The increased esophageal acid exposure in patients with Barrett's esophagus appears to be primarily due to a marked loss of lower esophageal sphincter (LES) resistance [3, 4]. When LES pressures are measured with radially oriented pressure transducers, a mechanically defective sphincter can be documented in over 95% of patients with Barrett's esophagus [5]. Abnormally high plasma levels of vasoactive intestinal polypeptide may be responsible for this loss of LES resistance [6].

In the presence of an incompetent LES, ineffective clearance function of the esophageal body further prolongs esophageal exposure to gastric contents. Simultaneous fluoroscopy and manometry has shown that propulsion of a bolus in the distal esophagus, and, consequently, clearance of refluxed gastric contents, depends on peristaltic contractions with a minimum amplitude of 30-40 mmHg [7]. Both standard and ambulatory 24-hour manometry of the esophageal body show an increased prevalence of ineffective esophageal contractions, i.e. nonperistaltic and low amplitude contractions, in patients with Barrett's mucosa. On combined ambulatory 24-hour esophageal pH and motility monitoring, ineffective contractions in the esophageal body correlate with the prolonged duration of individual reflux episodes. The development of Barrett's esophagus in patients with severely compromised esophageal body function, i.e. patients with scleroderma or after myotomy for achalasia, further supports the critical role of esophageal clearance function [8].

Increased gastric acid secretion may also contribute to the development of columnar metaplasia by exposing the esophageal mucosa to a higher degree of acidity. In patients with Barrett's esophagus, ambulatory, 24 hour esophageal pH monitoring shows an increased esophageal exposure not only to pH < 4 but also to more caustic gastric acid, i.e., pH < 3 and pH < 2 (Figure 1) [2]. Increased basal and stimulated gastric acid secretion has been reported in Barrett's esophagus [9], and columnar cell metaplasia has been described in patients with Zollinger-Ellison syndrome. Using appropriate control subjects, the role of acid hypersecretion in the pathogenesis of Barrett's esophagus has, however, recently been questioned. Compared with patients with uncomplicated Barrett's esophagus, the quality of the refluxate appears to be different in those Barrett's patients with complications, i.e., strictures, ulcers, and dysplasia. In addition to a markedly increased acid exposure, patients with complications of Barrett's esophagus also have an increased esophageal exposure to alkalinity, as indicated by the time pH > 7 on esophageal pH monitoring [4].

Figure 1. EsophageaI exposure time to pH < 2. pH < 3. pH < 4. and pH > 7 in normal volunteers patients with esophagitis, and patients with Barrett's esophagus. *p < 0.01 versus patients with esophagitis. (From Stein et al. with permission.)

The alkaline component of the refluxate appears to result from a contamination of the refluxed gastric juice with excessive duodenogastric reflux [4]. The functional abnormalities, their prevalence, and their consequences in patients with Barrett's esophagus are summarized in Table I.

Table I. Functional abnormalities and their consequences in patients with Barrett's esophagus.


1. Gillen P, Keeling P, Byrne PJ, et al. Barrett's esophagus:pH profile. Br J Surg 1987;74:774-776.

2. Stein HJ, Hoeft S, DeMeester TR, et al. Reflux and motility pattern in Barrett's esophagus. Dis Esoph 1992;5:21-28.

3. Iascone C, DeMeester TR, Little AG, et al. Barrett's esophagus: functional assessment, proposed pathogenesis, and surgical therapy. Arch Surg 1983;118:543-549.

4. Stein HJ, Barlow AP, DeMeester TR, et al. Complications in gastroesophageal reflux disease. Ann Surg 1992;216:3543.

5. Stein HJ, DeMeester TR, Naspetti R, et al. The three-dimensional lower esophageal sphincter pressure profile in gastroesophageal reflux disease. Ann Surg 1991;214:374-384.

6. Rositter A, Guelrud M, Souney PF, et al. High vasoactive intestinal polypeptide plasma levels in patients with Barrett's esophagus. Scand J Gastroenterol 1991;26:572-576.

7. Kahrilas PJ, Dodds WJ, Hogan WJ. Effect of peristaltic dysfunction on esophageal volume clearance. Gastroenterology 1988;94:73-80.

8. Cameron AJ, Payne WS. Barrett's esophagus occurring as a complication of scleroderma. Mayo Clinic Proc 1987;53:612-615.

9. Collen MJ, Johnson DA. Correlation between basal acid output and daily ranitidine dose required for therapy in Barrett's esophagus. Dig Dis Sci 1989;34:1329-1335.

Publication date: August 2003 OESO©2015