BACKGROUND: Barrett's esophagus (BE) is a major risk factor for esophageal adenocarcinoma. It is believed that BE is caused by chronic gastro-esophageal reflux disease (GERD). Laparoscopic anti-reflux surgery (LARS) restores the competency of the cardia and may thereby change the natural course of BE. We studied the impact of LARS on the histological profile of BE and on the control of GERD. METHODS: We identified all patients with BE who underwent LARS from 1994 to 2007 and contacted them to assess post-operative GERD symptoms via questionnaire. Endoscopy findings, histology, 24 hour pH monitoring, and manometry were also collected using our prospectively maintained database. Histological regression was defined as either loss of dysplasia or disappearance of BE. RESULTS: Two hundred and fifteen patients met the initial inclusion criteria; in 82 of them histology from post-operative endoscopy was available for review. Endoscopy was performed a median of 8 years (range, 1-16 years) after surgery. Regression of BE occurred in 18 (22%) patients while in 6 (7%) BE progressed to dysplasia or cancer. Thirty-six (43%) patients underwent pre- and post-operative manometry. The median lower esophageal sphincter pressure increased from 9 to 17 mmHg in these patients. Thirty-four (41%) patients underwent pre- and post-operative pH studies. The median DeMeester score decreased from 54 to 9. Sixty-seven (82%) of 82 patients completed the post-operative questionnaire; 86% of these patients reported improvement in heartburn and regurgitation. CONCLUSIONS: LARS was associated with both physiologic and symptomatic control of GERD in patients with BE. LARS resulted in regression of BE in 22% of patients and progression in 7%. Thus, continued surveillance of Barrett's is needed after LARS.
BACKGROUND:Barrett's esophagus (BE) is a major risk factor for esophageal adenocarcinoma. It is believed that BE is caused by chronic gastro-esophageal reflux disease (GERD). Laparoscopic anti-reflux surgery (LARS) restores the competency of the cardia and may thereby change the natural course of BE. We studied the impact of LARS on the histological profile of BE and on the control of GERD. METHODS: We identified all patients with BE who underwent LARS from 1994 to 2007 and contacted them to assess post-operative GERD symptoms via questionnaire. Endoscopy findings, histology, 24 hour pH monitoring, and manometry were also collected using our prospectively maintained database. Histological regression was defined as either loss of dysplasia or disappearance of BE. RESULTS: Two hundred and fifteen patients met the initial inclusion criteria; in 82 of them histology from post-operative endoscopy was available for review. Endoscopy was performed a median of 8 years (range, 1-16 years) after surgery. Regression of BE occurred in 18 (22%) patients while in 6 (7%) BE progressed to dysplasia or cancer. Thirty-six (43%) patients underwent pre- and post-operative manometry. The median lower esophageal sphincter pressure increased from 9 to 17 mmHg in these patients. Thirty-four (41%) patients underwent pre- and post-operative pH studies. The median DeMeester score decreased from 54 to 9. Sixty-seven (82%) of 82 patients completed the post-operative questionnaire; 86% of these patients reported improvement in heartburn and regurgitation. CONCLUSIONS: LARS was associated with both physiologic and symptomatic control of GERD in patients with BE. LARS resulted in regression of BE in 22% of patients and progression in 7%. Thus, continued surveillance of Barrett's is needed after LARS.
Authors: Prateek Sharma; Gary W Falk; Allan P Weston; Dean Reker; Mark Johnston; Richard E Sampliner Journal: Clin Gastroenterol Hepatol Date: 2006-04-17 Impact factor: 11.382
Authors: M Sikkema; C W N Looman; E W Steyerberg; M Kerkhof; F Kastelein; H van Dekken; A J van Vuuren; W A Bode; H van der Valk; R J T Ouwendijk; R Giard; W Lesterhuis; R Heinhuis; E C Klinkenberg; G A Meijer; F ter Borg; J W Arends; J J Kolkman; J van Baarlen; R A de Vries; A H Mulder; A J P van Tilburg; G J A Offerhaus; F J W ten Kate; J G Kusters; E J Kuipers; P D Siersema Journal: Am J Gastroenterol Date: 2011-05-17 Impact factor: 10.864
Authors: W L Hofstetter; J H Peters; T R DeMeester; J A Hagen; S R DeMeester; P F Crookes; P Tsai; F Banki; C G Bremner Journal: Ann Surg Date: 2001-10 Impact factor: 12.969
Authors: Wouter L Curvers; Fiebo J ten Kate; Kausilia K Krishnadath; Mike Visser; Brenda Elzer; Lubertus C Baak; Clarisse Bohmer; Rosalie C Mallant-Hent; Arnout van Oijen; Anton H Naber; Pieter Scholten; Olivier R Busch; Harriët G T Blaauwgeers; Gerrit A Meijer; Jacques J G H M Bergman Journal: Am J Gastroenterol Date: 2010-05-11 Impact factor: 10.864
Authors: Frederik Hvid-Jensen; Lars Pedersen; Asbjørn Mohr Drewes; Henrik Toft Sørensen; Peter Funch-Jensen Journal: N Engl J Med Date: 2011-10-13 Impact factor: 91.245
Authors: Eugene Y Chang; Cynthia D Morris; Ann K Seltman; Robert W O'Rourke; Benjamin K Chan; John G Hunter; Blair A Jobe Journal: Ann Surg Date: 2007-07 Impact factor: 12.969
Authors: Rebecca C Fitzgerald; Massimiliano di Pietro; Krish Ragunath; Yeng Ang; Jin-Yong Kang; Peter Watson; Nigel Trudgill; Praful Patel; Philip V Kaye; Scott Sanders; Maria O'Donovan; Elizabeth Bird-Lieberman; Pradeep Bhandari; Janusz A Jankowski; Stephen Attwood; Simon L Parsons; Duncan Loft; Jesper Lagergren; Paul Moayyedi; Georgios Lyratzopoulos; John de Caestecker Journal: Gut Date: 2013-10-28 Impact factor: 23.059
Authors: Sumeet K Mittal; Joe Abdo; Malika P Adrien; Binyam A Bayu; Jay R Kline; Molly M Sullivan; Devendra K Agrawal Journal: J Gastrointest Oncol Date: 2021-08
Authors: Richard P T Evans; Moustafa Mabrouk Mourad; Simon G Fisher; Simon R Bramhall Journal: World J Gastroenterol Date: 2016-12-21 Impact factor: 5.742