Bile reflux index after therapeutic biliary procedures

Sedef Kuran, Erkan Parlak, Gulden Aydog, Sabite Kacar, Nurgul Sasmaz, Ali Ozden, Burhan Sahin, Sedef Kuran, Erkan Parlak, Gulden Aydog, Sabite Kacar, Nurgul Sasmaz, Ali Ozden, Burhan Sahin

Abstract

Background: Therapeutic biliary procedures disrupt the function of the sphincter of Oddi. Patients are potential "bile refluxers". The aim of this study was to assess how these procedures affect the histology-based bile reflux index (BRI), which can be used to reflect duodenogastric reflux (DGR).

Methods: Gastric antrum and corpus biopsies were collected from 131 subjects (56 men, 75 women; mean age, 55.9 +/- 15.6 years). Group 1 (Biliary group-BG; n = 66) had undergone endoscopic sphincterotomy, endoscopic stenting, or choledochoduodenostomy for benign pathology; Group 2 (n = 20) had undergone cholecystectomy alone; and Group 3 (n = 6) Billroth II gastroenterostomy. Group 4 (no cholecystectomy; n = 39) had upper endoscopy with normal findings and served as controls. BRI > 14 indicated DGR (BRI [+]). To eliminate confounding effects of Helicobacter pylori (Hp) infection, comparisons were made according to Hp colonization.

Results: Fifty-nine subjects (45%) were Hp (+). The frequencies of BRI (+) status in antrum and corpus specimens from Hp (-) BG patients were 74.3% and 71.4%, respectively (85.7% for both antrum and corpus for choledochoduodenostomy). Corresponding results were 60% and 60% for Group 2, 100% (only corpus) for Group 3, and 57.1% and 38.1% for controls (BG, Group 2, and Group 3 vs controls - p > 0.05 antrum, p < 0.05 corpus). Fifty-four BG patients had previously undergone cholecystectomy. Excluding those, the rates of BRI (+) in Hp (-) BG patients were 75% antrum and 62.5% corpus (p > 0.05 for both vs. Group 2).

Conclusion: Patients who had undergone biliary procedures showed similar bile-related histological changes in both corpus and antrum biopsies, but the changes seen in controls were more prominent in the antrum than corpus. Therapeutic biliary procedures increase the rate of BRI (+) especially in the case of choledochoduodenostomy. Therapeutic biliary procedures without cholecystectomy also increase the rate of BRI (+) similar to that observed in patients with cholecystectomy.

References

    1. Malagelada JR, Phillips SP, Shorter RG, Higgins JA, Magrina C, van Heerden JA, Adson MA. Postoperative reflux gastritis: pathophysiology and long term outcome after Roux-en-Y diversion. Ann Int Med. 1985;103:173–183.
    1. Cooperman AM. Postoperative alkaline reflux gastritis. Surg Clin North Am. 1976;56:1445–59.
    1. Stein HJ, Kauer WKH, Feussner H, Siewert JR. Bile acids as components of the duodenogastric refluxate: detection, relationship to bilirubin, mechanism of injury and clinical relevance. Hepatogastroenterology. 1999;46:66–73.
    1. Koek GH, Vos R, Sifrim D, Cuomo R, Janssens J, Tack J. Mechanisms underlying duodeno-gastric reflux in man. Neurogastroenterol Motil. 2005;17:191–199. doi: 10.1111/j.1365-2982.2004.00633.x.
    1. Sobala GM, O'Connor HJ, Dewar EP, King RF, Axon AT, Dixon MF. Bile reflux and intestinal metaplasia in gastric mucosa. J Clin Pathol. 1993;46:235–240. doi: 10.1136/jcp.46.3.235.
    1. Mackie C, Hulks G, Cuschieri A. Enterogastric reflux and gastric clearance of refluxate in normal subjects and in patients with or without bile vomiting following peptic ulcer surgery. Ann Surg. 1986;204:537–542. doi: 10.1097/00000658-198611000-00005.
    1. King PM, Pryde A, Heading RC. Transpyloric fluid movement and antroduodenal motility in patients with gastroesophageal reflux. Gut. 1987;28:545–548. doi: 10.1136/gut.28.5.545.
    1. Schindlbeck NE, Heinrich C, Stellaard F, Paumgartner G, Müller-Lissner SA. Healthy controls have as much bile reflux as gastric ulcer patients. Gut. 1987;28:1577–83. doi: 10.1136/gut.28.12.1577.
    1. Fiorucci S, Distrutti E, Di Matteo F, Brunori P, Santucci L, Mallozzi E, Bigazzi U, Morelli A. Circadian variations in gastric acid and pepsin secretion and intragastric bile acid in patients with reflux esophagitis and in healthy controls. Am J Gastroenterol. 1995;90:270–276.
    1. Offerhaus GJ, Rieu PN, Jansen JB, Joosten HJ, Lamers CB. Prospective comparative study of the influence of postoperative bile reflux on gastric mucosal histology and Campylobacter pylori infection. Gut. 1989;30:1552–1557. doi: 10.1136/gut.30.11.1552.
    1. Ritchie W. Alkaline reflux gastritis: a critical reappraisal. Gut. 1984;25:975–987. doi: 10.1136/gut.25.9.975.
    1. Muller-Lissner SA, Schindlbeck NE, Heinrich C. Bile salt reflux after cholecystectomy. Scand J Gastroenterol Suppl. 1987;139:20–24. doi: 10.3109/00365528709089770.
    1. Brown TH, Walton G, Cheadle WG, Larson GM. The alkaline shift in gastric pH after cholecystectomy. Am J Surg. 1989;157:58–65. doi: 10.1016/0002-9610(89)90420-0.
    1. Brough WA, Taylor TV, Torrance HB. The surgical factors influencing duodenogastric reflux. Br J Surg. 1984;71:770–773. doi: 10.1002/bjs.1800711011.
    1. Kalima T, Sjoberg J. Bile reflux after cholecystectomy. Scand J Gastroenterol Suppl. 1981;67:153–156.
    1. Byrne JP, Attwood SEA. Duodenogastric reflux and cancer. Hepatogastroenterology. 1999;46:74–85.
    1. Dixon MF, Neville PM, Mapstone NP, Moayyedi P, Axon AT. Bile reflux gastritis and Barrett's oesophagus: further evidence of a role for duodenogastro-oesophageal reflux? Gut. 2001;49:359–363. doi: 10.1136/gut.49.3.359.
    1. Dixon MF, Mapstone NP, Neville PM, Moayyedi P, Axon AT. Bile reflux gastritis and intestinal metaplasia at the cardia. Gut. 2002;51:351–355. doi: 10.1136/gut.51.3.351.
    1. Mason RC. Duodenogastric reflux in rat gastric carcinoma. Br J Surg. 1986;73:801–803. doi: 10.1002/bjs.1800731014.
    1. Miwa K, Hattori T, Miyazaki I. Duodenogastric reflux and foregut carcinogenesis. Cancer. 1995;75:1426–1432. doi: 10.1002/1097-0142(19950315)75:6+<1426::AID-CNCR2820751506>;2-#.
    1. Miwa K, Segawa M, Takano Y, Matsumoto H, Sahara H, Yagi M, Miyazaki I, Hattori T. Introduction of oesophageal and forestomach carcinomas in rats by reflux of duodenal contents. Br J Cancer. 1994;70:185–189.
    1. Champion G, Richter JE, Vaezi MF, Singh S, Alexander R. Duodenogastroesophageal reflux: relationship to pH and importance in Barrett's esophagus. Gastroenterol. 1994;108:747–754.
    1. Vaezi MF, Richter JE. Synergism of acid and duodenogastroesophageal reflux in complicated Barrett's esophagus. Surgery. 1995;117:699–704. doi: 10.1016/S0039-6060(95)80015-8.
    1. Fountos A, Chrysos E, Tsiaoussis J, Karkavitsas N, Zoras OJ, Katsamouris A, Xynos E. Duodenogastric reflux after biliary surgery: scintigraphic quantification and improvement with erythromycin. ANZ J Surg. 2003;73:400–3. doi: 10.1046/j.1445-2197.2003.t01-1-02654.x.
    1. Tritapepe R, Piro D, Damilano I. Long-term effects in bilio-digestive shunts. Ital J Gastroenterol. 1993;25:425–428.
    1. Di Vita G, Siragusa G, Asaro M, Costa R, Salerno V, Di Pace G. Br-IDA in the evaluation of papillo-sphincterotomy and choledochoduodenostomy. Minerva Chir. 1991;46:175–178.
    1. Stein HJ, Smyrk TC, Demeester TR, Rouse J, Hinder RA. Clinical value of endoscopy and the histology in the diagnosis of duodenogastric reflux disease. Surgery. 1992;112:796–804.
    1. Tibbling Grahn L, Blackadder L, Kullman E. Gastric bile monitoring: an in vivo and in vitro study of Bilitec reliability. Scand J Gastroenterol. 2002;37:1334–1337. doi: 10.1080/003655202761020632.
    1. Bechi P, Cianchi F. Technical aspects and clinical indications of 24-hour intragastric bile monitoring. Hepatogastoenterology. 1999;46:54–59.
    1. Fuchs K-H, Fein M, Maroske J, Heimbucher J, Freys SM. The role of 24-hr gastric pH-monitoring in the interpretation of 24-hr gastric bile monitoring for duodenogastric reflux. Hepatogastroenterology. 1999;46:60–65.
    1. Bollschweiler E, Wolfgarten E, Putz B, Gutschow C, Holscher AH. Bile reflux in to the stomach and esophagus for volunteers older than 40 years. Digestion. 2005;71:65–71. doi: 10.1159/000084521.
    1. Byrne JP, Romagnoli R, Bechi P, Attwood SE, Fuchs KH, Collard JM. Duodenogastric reflux of bile in health: the normal range. Physiol Meas. 1999;20:149–158. doi: 10.1088/0967-3334/20/2/304.

Source: PubMed

Sponsors en medewerkers

Medische omstandigheden

Geneesmiddelinterventies

3
Abonneren