Duodenogastroesophageal reflux and methods to monitor nonacidic reflux
Section snippets
Animal studies
The role of duodenal contents, specifically bile acids and the pancreatic enzyme trypsin, in the development of esophageal mucosal injury is controversial and the subject of many in vitro animal studies.1 Early studies2 suggested a role for bile and its constituents, namely bile acids, in esophageal mucosal damage. Using a dog model with biliary diversion and a jejunal conduit anastomosing directly to the esophagus, Moffat and Berkas3 showed that canine bile was capable of producing various
Methods for measuring duodenogastroesophageal reflux
Prior methodologies employed for measuring DGER, including endoscopy, aspiration studies (both gastric and esophageal), scintigraphy, and ambulatory pH monitoring, have technical difficulties and do not accurately measure DGER. Currently, the most commonly used means of assessing DGER is ambulatory esophageal bilirubin monitoring. Table 1 lists currently available tests and summarizes their strengths and shortcomings.
The observation of bile in the esophagus or stomach is a poor indicator of
Role of duodenal contents in human studies
Despite its limitations, Bilitec is an important advancement in the assessment of DGER in the clinical arena. Several studies using this new device have provided important insight into the role of DGER in causing esophageal mucosal injury in humans. These studies show a significant but graded increase in both acid and DGER from controls to patients with esophagitis, with the highest values in patients with Barrett’s esophagus (Figure 3). Furthermore, it appears that DGER occurs more commonly
Medical and surgical treatment of duodenogastroesophageal reflux
Recent studies37, 38, 39 in patients with severe GERD found that aggressive acid suppression with omeprazole (20 mg twice daily) dramatically decreased both acid and DGER (Figure 4). For example, esophageal acid and DGER were both significantly reduced (P <0.02) after 28 days of treatment with pantoprazole (40 mg once daily) compared with pretreatment values in 7 patients with endoscopic evidence of GERD.38 Similarly, esophageal and gastric bile reflux was evaluated in 23 patients with
Conclusions
Both animal and human studies strongly suggest that acid is the key factor in causing esophageal injury and Barrett’s esophagus in patients with GERD. Studies using advanced techniques to identify DGER spectrophotometrically and independent of pH (Bilitec), however, suggest that duodenal contents often are present in the esophageal refluxate. The degree of esophageal exposure to acid and DGER shows a graded and similar increase from controls to patients with esophagitis, with the highest value
References (46)
- et al.
Role of acid and duodenogastric reflux in esophageal mucosal injurya review of animal and human studies
Gastroenterology
(1995) - et al.
Intercellular junctions of oral epithelium, IIultrastructural changes in rat buccal epithelium induced by trypsin digestion
J Ultrastruct Res.
(1977) - et al.
Rabbit esophageal cells show regulatory volume decreaseionic basis and effect of pH
Gastroenterology
(1993) - et al.
Do bile acids reflux into the esophagus? A study in normal subjects and patients with gastroesophageal reflux disease
Gastroenterology
(1987) - et al.
Alkaline gastroesophageal reflux
Am J Surg.
(1978) - et al.
Duodenogastroesophageal refluxrelationship to pH and importance in Barrett’s esophagus
Gastroenterology
(1994) - et al.
Role of acid and duodenogastroesophageal reflux in gastroesophageal reflux disease
Gastroenterology
(1996) - et al.
Duodenogastroesophageal reflux and esophageal mucosal injury in mechanically ventilated patients
Gastroenterology
(1999) - et al.
Duodenogastroesophageal refluxrelationship to pH and importance in Barrett’s esophagus
Gastroenterology
(1994) - et al.
Differentiation and proliferation in Barrett’s esophagus and the effects of acid suppression
Gastroenterology
(1999)