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Gastric fluid bile concentrations and risk of Barrett's esophagus

^a Department of Surgery, University of Washington, Seattle, WA, USA
^b Department of Epidemiology, University of Washington, Seattle, WA, USA
^c Department of Gastroenterology, University of Washington, Seattle, WA, USA
^d Cleveland Clinic Foundation, Cleveland, OH, USA
^e Group Health Cooperative, Seattle, WA, USA

*Corresponding author. Department of Cardiothoracic Surgery, University of Wisconsin, Madison, 600 Highland Ave, H3/466 Madison, WI 53792-3236, USA. Tel.: +1-608-220-3401; fax: +1-608-263-0547.

E-mail address: ks.nason{at}hosp.wisc.edu (K.S. Nason).

Patients with Barrett's esophagus are at high risk of progression to adenocarcinoma. A growing, but conflicting body of evidence implicates bile reflux as a contributor to Barrett's esophagus. To investigate whether duodenogastric reflux was associated with an increased risk of Barrett's esophagus, a case-control study of incident Barrett's esophagus was performed. Cases (n=72) were identified by new histologically-confirmed diagnosis of specialized intestinal metaplasia (indicative of Barrett's esophagus) following upper endoscopy for refractory gastroesophageal reflux between October 1997 and September 2000. Cases were compared to gastroesophageal reflux patients without specialized intestinal metaplasia (controls; n=72). There was no difference in total bile acid concentrations between cases and controls. Risk of Barrett's esophagus did not significantly vary with increasing concentrations of total or free bile acids, respectively (OR 0.35 (95% CI 0.12, 1.02) and 0.60 (95% CI 0.22, 1.66)). Low gastric fluid pH (toxic range 3–5), was associated with a non-significant increase in the risk of Barrett's esophagus. In conclusion, no significant association between Barrett's esophagus and total or free bile acids in gastric refluxate was found. Patients with low gastric fluid pH (3–5) may represent a subset of patients at high risk of developing Barrett's esophagus.

Key Words: Barrett's esophagus; Metaplasia; Esophageal neoplasms; Gastroesophageal reflux; Bile acids and salts