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: Pathophysiology
 

What is the prevalence of alkaline material in Barrett's patients?

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

The term "alkaline gastro-esophageal reflux" is somewhat of a misnomer as the pH in the lower esophagus rarely exceeds 8. By convention, alkaline reflux is said to be present when there is excessive esophageal exposure to a pH > 7. The quantification of this exposure is based on six measurements: the percentage of total. upright and supine time the esophagus has a pH greater than 7, number of episodes that pH of the esophagus exceeds 7, number of episodes lasting longer than 5 min, and the longest episode the pH remained above 7 [1]. Normal values for these six components have been derived from 50 asymptomatic control subjects. The upper limits of normal were established at the 95th percentile. If a patient's values are above this level, he or she is considered abnormal for the component measured. The six components are combined into one expression of the overall esophageal alkaline exposure, by calculating a composite alkaline pH score [2].

The presence of increased esophageal exposure to pH > 7 must be interpreted carefully. Increased exposure in this pH range can be caused by abnormal calibration of the pH recorder, the presence of dental infection which increases salivary pH [3], the presence of esophageal obstruction resulting in static pools of saliva with an increase in pH secondary to bacterial overgrowth [4], or the regurgitation of gastric juice with a pH > 7 into the esophagus. When using a properly calibrated probe, in the absence of dental infections or esophageal obstruction, the percentage of time that the pH is measured above 7 has been shown to correlate with the concentration of bile acids continuously aspirated from the esophagus over a 24-h period [5].

Recently, it has been shown that gastric juice with a pH of 1.5 must contain at least 70% of duodenal juice in order to raise the pH to > 7. Thus, abnormal esophageal exposure to pH > 7 require an excessive amount of duodenogastric reflux. It is important to understand that increased esophageal exposure to pH > 7 only infers increased esophageal exposure to duodenal juice, that is bile and/or pancreatic juice. When present, it represents only the tip of the iceberg of the total time the esophagus is actually exposed to duodenal contents. Newer tests allowing direct measurement of the components of duodenal juice in the esophagus have shown that reflux episodes of duodenal juice can occur when the esophageal pH remains in its normal range of 4-7.

Data from 24-h esophageal aspiration studies indicate that, compared to normal subjects, abnormal amounts of bile are detected in patients with proven acid reflux during the postprandial and supine periods (Figure 1). Studies using a fiberoptic probe which recognizes intraluminal bilirubin as a marker of duodenal juice have shown that bile, and hence duodenal juice, is commonly present in the refluxate independent of its pH and that most reflux consists of a mixture of gastric and duodenal juice. In general, there appears to be a direct relationship between the degree of duodenal juice present in the refluxate and the severity of mucosal injury, that is, refluxing a mixture of duodenal and gastric juice is worse than gastric juice alone. Patients with Barrett's esophagus, for example, had a significantly higher amount of bilirubin in their refluxate than patients with uncomplicated reflux disease. The latter group showed higher amounts of bilirubin than normal subjects (Figure 2). The refluxing of a high percentage of duodenal with gastric juice in Barrett's esophagus is presumably due to excessive duodenogastric reflux present in these patients. When the mixed gastric and duodenal juice is refluxed into the esophagus, there is little

Figure 1. Percentage of subjects with bile on esophageal aspiration during postprandial, upright and supine period in normals and patients with reflux disease (*p < 0.01 versus normals).

Figure 2. Esophageal acid and duodenal juice exposure expressed as percentage total time pH < 4 and percentage total time bilirubin absorption > 0.14 in normals, patients with reflux disease and patients with Barrett's esophagus (* p < 0.03 and ** p < 0.01 versus normals)

change in the esophageal pH and consequently minimal heartburn. Despite the lack of symptoms, mucosal damage still appears, probably from activated pancreatic enzymes.

References

1. DeMeester TR, Wang CI, Wernly JA, et al. Technique, indications, and clinical use of 24 hour esophageal pH monitoring. J Thor Cardiovasc Surg 1980;79:656-667.

2. Jamieson JR, Stein HJ, DeMeester TR, et al. Ambulatory 24-hour esophageal pH monitoring. Am J Gastroenterol 1992;87:1102-1111.

3. Jaervinen V, Meurman JH, Hyvaerinen H, et al. Dental erosion and upper gastrointestinal disorders. Oral Surg Med Pathol 1988;65:298-303.

4. DeVault KR, Georgeson S, Castell DO, et al. Salivary stimulation mimics esophageal exposure to refluxed duodenal contents. Am J Gastroenterol 1993;88:1040-1043.

5. Stein HJ, Feussner H, Kauer WKH, et al. Alkaline gastroesophageal reflux assessment by ambulatory esophageal aspiration and pH monitoring. Am J Surg 1994;167:163-168.


Publication date: August 2003 OESO©2015