Acid and bile reflux in Barrett's esophagus: A tale of two evils

2001 ◽  
Vol 121 (6) ◽  
pp. 1502-1505 ◽  
Author(s):  
George Triadafilopoulos
Keyword(s):  
Barrett’S Esophagus ◽  
Barrett's Esophagus ◽  
Bile Reflux

Bile salts induce or blunt cell proliferation in Barrett's esophagus in an acid-dependent fashion

2000 ◽  
Vol 278 (6) ◽  
pp. G1000-G1009 ◽  
Author(s):  
Baljeet S. Kaur ◽  
Rodica Ouatu-Lascar ◽  
M. Bishr Omary ◽  
George Triadafilopoulos
Keyword(s):  
Cell Proliferation ◽  
Bile Salt ◽  
Barrett’S Esophagus ◽  
Barrett's Esophagus ◽  
Bile Salts ◽  
Bile Reflux ◽  
Salt Mixture ◽  
Complete Obliteration ◽  
Protein Kinase C Inhibitor ◽  
Incorporation Assay

Barrett's esophagus (BE) results from acid and bile reflux and predisposes to cancer. We investigated the effect of bile salts, with or without acid, on cell proliferation in BE and assessed mechanism(s) involved. To mimic physiological conditions, biopsies of esophagus, BE, and duodenum were exposed to a bile salt mixture, either continuously or as a 1-h pulse, and were compared with control media without bile salts (pH 7.4) for ≤24 h. Similar experiments were also performed with acidified media (pH 3.5) combined with the bile salt mixture as a 1-h pulse. Cell proliferation was assessed by a [3H]thymidine incorporation assay with or without bisindolylmaleimide (BIM), a selective protein kinase C inhibitor. Bile salt pulses enhanced cell proliferation in BE without affecting cell proliferation in esophageal or duodenal epithelia. In the presence of BIM, there was complete obliteration of the bile salt-induced BE hyperproliferation. In contrast, 1-h pulses of bile salts in combination with acid significantly inhibited proliferation in BE but had no effect on esophagus or duodenum. We conclude that in BE explants, brief exposure to bile salts, in the absence of acid, increases proliferation, whereas exposure to a combination of bile salts and acid together inhibits proliferation.

scholarly journals Molecular effects of tobacco smoke and bile reflux in Barrett’s esophagus in vitro

2019 ◽  
Vol 2 ◽  
pp. 17-17
Author(s):  
Zachary Pulliam ◽  
Nicholas Harper ◽  
Yan Li ◽  
Russell Farmer ◽  
Robert C. G. Martin
Keyword(s):  
Barrett’S Esophagus ◽  
Tobacco Smoke ◽  
Barrett's Esophagus ◽  
Bile Reflux ◽  
Molecular Effects

204 ENDOSCOPIC EVIDENCE OF BILE REFLUX IS A STRONG INDEPENDENT FACTOR ASSOCIATED WITH THE PRESENCE OF BARRETT’S ESOPHAGUS

2021 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Yugo Iwaya ◽  
Tadanobu Nagaya ◽  
Tomoaki Suga ◽  
Yoshiko Nakayama ◽  
Takeji Umemura
Keyword(s):  
Barrett’S Esophagus ◽  
White Light ◽  
Barrett's Esophagus ◽  
Bile Reflux ◽  
Univariate Analysis ◽  
Japanese Patients ◽  
Gastric Fundus ◽  
Independent Factor ◽  
Surveillance Strategy ◽  
Sliding Hernia

Abstract   Several basic researches have indicated that there is a significant relationship between bile reflux and the pathogenesis of Barrett’s esophagus (BE). However, only few clinical studies have been reported regarding the endoscopic finding of bile reflux and Barrett’s esophagus. Our objective is to evaluate whether the endoscopic evidence of bile reflux is an independent factor associated with the presence of BE. Methods We conducted a retrospective analysis of a prospectively maintained database comprised of consecutive Japanese patients who underwent screening gastroscopy. Endoscopic findings of BE, reflux esophagitis, atrophic gastritis and sliding hernia were recorded. Evaluation of a BE was based on the Prague criteria. Endoscopic evidence of bile reflux was defined as the presence of yellow or green juice observed by white light image or red juice by narrow band image (NBI) in the gastric fundus. Univariate and multivariate analyses were performed to identify factors that differed significantly between patients with or without BE. Results A total of 454 patients were enrolled; 124 (27%) had BE and 126 (28%) had endoscopic evidence of bile reflux. Compared to patients without BE, patients with BE were more likely to be old, male and to have sliding hernia and endoscopic evidence of bile reflux on univariate analysis. On multivariate analysis, endoscopic evidence of bile reflux was a stronger independent factor associated with BE (odds ratio(OR) 11.3, 95% confidence interval(CI) 6.56–19.4) compared to the presence of sliding hernia (OR 3.58, 95%CI 2.14–6.0). Conclusion Endoscopic evidence of bile reflux identified by white light or NBI is a strong independent factor associated with the presence of BE, implying that this finding should be considered as an important parameter to determine the surveillance strategy for gastroesophageal reflux disease patients same as the presence of sliding hernia.

Microscopic Barrett's esophagus: Relationship to acid and bile reflux in man

1998 ◽  
Vol 114 ◽  
pp. A322
Author(s):  
W. Van Vaerenbergh ◽  
J. Tack ◽  
K. Geboes ◽  
A.M. Gevers ◽  
P. Rutgeerts ◽  
...  
Keyword(s):  
Barrett’S Esophagus ◽  
Barrett's Esophagus ◽  
Bile Reflux

Esophagitis and Barrett's esophagus: Acid reflux, bile reflux, or both?

2000 ◽  
Vol 118 (4) ◽  
pp. A224
Author(s):  
Gerardus H. Koek ◽  
Danie Sifrim ◽  
Tony Lerut ◽  
Jozef Janssens ◽  
Jan F. Tack
Keyword(s):  
Barrett’S Esophagus ◽  
Barrett's Esophagus ◽  
Bile Reflux ◽  
Acid Reflux

Acid- and bile-induced PGE2release and hyperproliferation in Barrett's esophagus are COX-2 and PKC-ε dependent

2002 ◽  
Vol 283 (2) ◽  
pp. G327-G334 ◽  
Author(s):  
Baljeet S. Kaur ◽  
George Triadafilopoulos
Keyword(s):  
Bile Salt ◽  
Barrett’S Esophagus ◽  
Barrett's Esophagus ◽  
Bile Salts ◽  
Bile Reflux ◽  
Salt Mixture ◽  
Dramatic Decrease ◽  
Pkc Inhibitor ◽  
Kinase C ◽  
Cox 2

Barrett's esophagus (BE) results from acid and bile reflux and predisposes to cancer. To further understand the mechanisms of acid- and bile-induced hyperproliferation in BE, we investigated the release of PGE2in response to acid or bile salt exposure. Biopsies of esophagus, BE, and duodenum were exposed to a bile salt mixture as a 1-h pulse and compared with exposure to pH 7.4 for up to 24 h, and PGE2release, cyclooxygenase-2 (COX-2), and protein kinase C (PKC) expression were compared. Similar experiments were also performed with acidified media (pH 3.5) alone, in the presence or absence of bisindolylmaleimide (BIM), a selective PKC inhibitor, and NS-398, a COX-2 inhibitor. One-hour pulses of bile salts or acid significantly enhanced proliferation, COX-2 expression, and PGE2release in BE. In contrast, the combination pulse of acid and bile salts had no such effect. Treatment with either BIM or NS-398 led to a dramatic decrease in PGE2release in BE explants and a suppression of proliferation. The acid- or bile salt-mediated hyperproliferation is related to PGE2release. Acid- and bile salt-induced induction of COX-2 and PKC may explain, at least in part, the tumor-promoting effects of acid and bile in BE.

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