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Journal of Digestive Diseases 2015; 16; 55–57
doi: 10.1111/1751-2980.12224
Leading article
Reflections on esophageal columnar metaplasia (Barrett)-ANNO 2015 Guido NJ TYTGAT Academic Medical Center, Amsterdam, The Netherlands
Esophageal columnar metaplasia (ECM) (Barrett’s esophogus) continues to generate clinical and basic attention. Yet many questions remain unanswered and global consensus on important issues is often still KEY WORDS:
lacking. This article discusses a selection of certain recent findings and reflects on some remaining uncertainties of this intriguing disease.
ablation techniques, adenocarcinoma, Barrett esophagus, dysplasia, endoscopic resection.
PREVALENCE AND PATHOGENESIS
SCREENING AND SURVEILLANCE
It seems that the prevalence of esophageal columnar metaplasia (ECM) is slowing down in the West but is continuing to rise in the East. The environmental factors that are responsible for this varying incidence are poorly understood: do they lie in the rising frequency of gastroesophageal reflux disease, nutritional patterns, obesity, smoking and dysbiosis? There are few preventive strategies, except perhaps for long-term therapy with proton pump inhibitors (PPI) in erosive reflux disease.
The main reason for the interest in ECM is its propensity for neoplastic changes. The magnitude of the risk remains debatable, but overall the annual conversion of ECM to esophageal adenocarcinoma (EAC) fluctuates at around 0.3%.1,2 Invasive cancer is the final stage in the progression from early neoplasia (dysplasia) to more advanced neoplasia. The goal of screening and surveillance is the early detection of neoplasia at a still curable state. The practice of screening and surveillance is widespread, despite the lack of randomized controlled trial evidence to demonstrate its true efficacy. Even a recent large case-control study failed to demonstrate significant differences in mortality between EAC detected through endoscopic surveillance versus non-surveillance,3 contrasting with a population-based cohort study4 showing that mortality from EAC was reduced when individuals participated in a surveillance program. What seems clear, however, is that cancers discovered during surveillance are often at a relatively early stage of malignancy, but most ECM are not recognized and such patients are therefore never candidates for screening and surveillance. Justification for screening and surveillance may perhaps be enhanced by tailoring the individual risk profile, that is, individuals at lower risk (shorter segment, cardia-like mucosa) and those at higher risk (longer segment, intestinal metaplasia, dysplasia,
Excessive acid–peptic–bile reflux, particularly when combined with sluggish clearance of the refluxate, appears to be the dominant mechanism for the injury of the squamous epithelium, with subsequent upregulation of CDX2 leading to columnar metaplasia, usually of the intestinal type, especially in the more proximal segments, and occasionally of cardia-like mucosa, especially more distally.
Correspondence to: Guido NJ TYTGAT, Academic medical Center Amsterdam, The Netherlands. Email: [email protected] © 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
55
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obesity, obstructive sleep apnea, family history and so on). Ideally, additional chemoprevention should be attempted, but whether all ECM patients, both symptomatic and asymptomatic, should be treated with long-term PPI remains a moot point, despite metaanalysis-based evidence supporting such a strategy.5 The results of a recent large population-based study showing that prolonged PPI therapy does not prevent advanced neoplasia is certainly sobering.6 Summarizing the views mentioned above, it would appear that at present there is no consensus on the effectiveness of screening and surveillance of patients with ECM. This issue is further complicated by the fact that the proportion of all-cause mortality due to EAC is rather small, that EAC generally afflicts patients relatively late in life and that the endoscopic procedures involved have known shortcomings. IMAGING MODALITIES Endoscopy remains the prime imaging modality used to detect metaplasia, and several novel imaging modalities have been explored such as fluorescence, spectral modulation with narrow-band imaging (Olympus), FICE (Fujinon) or iSCAN (Pentax), to facilitate the detection of foci of neoplasia.7 Advanced imaging technology may increase the diagnostic yield by 34% compared with white light endoscopy (WLE), but interobserver variability is high. Experience with confocal laser endomicroscopy (CLE), both endoscope-based (eCLE) and probe-based (pCLE), is increasing, suggesting a sensitivity of at least 70% and a specificity of at least 90% for the detection of neoplasia, including flat high-grade dysplasia (HGDys). A recent meta-analysis revealed a pooled sensitivity of 86% and a specificity of 88% for CLE compared to four-quadrant non-targeted biopsies.8 When eCLE was combined with high-definition WLE in the detection of neoplasia a sensitivity of 95% and a specificity of 92% was reached.9 Such methodologies are probably most useful during the endoscopic training phase. Proving their utility for experienced endoscopists using standard high-resolution/highdefinition endoscopy is increasingly difficult as the level of expertise rises. The matter is further complicated and utterly confused by the repetitive introduction of different classification schemes which makes engaging in novel imaging technology challenging. Consensus on diagnostic criteria, terminology and grading is essential for uniform diagnosis and adequate comparison of various worldwide studies. The selection of novel grading systems should be restricted to a consortium of world-renowned experts
Journal of Digestive Diseases 2015; 16; 55–57 in the field and internationally validated. It seems sensible to conclude that currently no real clinical indications exist to encourage the enhanced methodologies name above to be implemented in daily routine practice.10 Whether non-endoscopic screening measures such as the use of capsule endoscopy, cytosponges or tethered capsules will allow widespread cost-effective screening and surveillance needs further evaluation.11 HISTOPATHOLOGY Ideally, targeted biopsies should be obtained because traditional untargeted four-quadrant biopsies have a rather poor positive predictive value of around 35% and may miss adjacent occult HG-Dys or early EAC. It is now clear that experienced pathologists are essential for the adequate histological detection and grading of neoplasia. Low-grade dysplasia (LG-Dys) is often overdiagnosed by non-expert pathologists. Over 73% of community-based diagnosis can be downstaged to non-dysplasia or indefinite dysplasia. To reduce overstaging due to reactive and regenerative mucosal changes, high-dose PPI therapy prior to biopsy is often advised but there has been so far no evidence to support this recommendation. Of correctly diagnosed LG-Dys patients, 9.1% were shown to progress to HG-Dys/EAC after 39 months compared to 0.6% in non-dysplastic and 0.9% in indefinite per patientyear.12 Only LG-Dys diagnosed by expert pathologists is an important predictor of risk for malignant progression. THERAPEUTIC POSSIBILITIES There is widespread agreement that HG-Dys and mucosal EAC (m-EAC) should be removed whenever possible via endoscopic resection, making the expert examination of resected specimen possible. Whether resection therapy is also needed for incipient submucosal invasion remains debatable. Endoscopic removal requires the careful delineation of the suspicious focus, often using chromoscopy or other advanced imaging modalities. Cap-assisted or rubber band-assisted endoscopic resection is the dominant therapeutic modality and usually obviates the need for endoscopic submucosal dissection, which is more challenging in the esophagus and upper cardia. The adjacent, truly flat, non-suspicious metaplastic mucosa, which rarely bears deep infiltrating cancer, is currently most often ablated with radiofrequency ablation (RFA).13 RFA, which has been shown to be superior to endoscopic surveillance, seems also to be
© 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
Journal of Digestive Diseases 2015; 16; 55–57 indicated for consensus-based LG-Dys, especially when it is persistent and multifocal.14 Tissue ablation with argon plasma coagulation should be restricted because of incomplete ablation and the risk of buried ECM glands. Both the early and long-term outcomes of endoscopic resection combined with RFA are gratifying and durable.15 However, further surveillance remains indicated as long-term recurrence of ECM and neoplasia remains possible.16 Whether also non-dysplastic metaplasia should be routinely ablated with RFA remains highly debated, and the arguments for and against have been nicely summarized in a recent debate.17,18 This unsolved question will require careful multicenter evaluation with long-term follow-up before final advice can be given. Currently, our ability to predict which patient with no dysplasia or LG-Dys is at risk of progression to HG-Dys/m-EAC is limited. Various candidate biomarkers are being explored in addition to dysplasia, including aneuploidy, abnormal p53 expression, upregulated cyclin A, lectins, wheat germ agglutinin, Lewis antigen and McMT.19 Expectations are rising, as shown by the high accuracy of a combination of autofluorescence endoscopy and molecular biomarkers.20 CONCLUDING REMARKS ECM will remain for a considerable length of time one of the most challenging gastrointestinal diseases, not only because of its clinical impact but also because it is an ideal model both for unravelling the mysteries of metaplastic tissue transdifferentiation and for evaluating all novel diagnostic and therapeutic endoscopic modalities. Many lessons remain to be learned. REFERENCES 1 di Pietro M, Alzoubaidi D, Fitzgerald RC. Barrett’s esophagus and cancer risk: how research advances can impact clinical practice. Gut Liver 2014; 8: 356–70. 2 Fitzgerald RC, di Pietro M, Ragunath K et al.; British Society of Gastroenterology. British society of Gastroenterology guidelines on the diagnosis and management of Barrett’s oesophagus. Gut 2014; 63: 7–42. 3 Corley DA, Mehtani K, Quesenberry C, Zhao W, de Boer J, Weiss NS. Impact of endoscopic surveillance on mortality from Barrett’s esophagus-associated esophageal adenocarcinomas. Gastroenterolgy 2013; 145: 312–9. 4 Verbeek RE, Leenders M, ten Kate FJ et al. Surveillance of Barrett’s esophagus and mortality from esophageal adenocarcinoma: a population-based cohort study. Am J Gastroenterol 2014; 109: 1215–22.
Barrett anno 2015
57
5 Aydin Y, Akin H. Letter: proton pump inhibitor usage still seems to reduce the risk of high-grade dysplasia and/or oesophageal adenocarcinoma in Barrett’s oesophagus. Aliment Pharmacol Ther 2014; 40: 859–60. 6 Hvid-Jensen F, Pedersen L, Funch-Jensen P, Drewes AM. Proton pump inhibitor use may not prevent high-grade dysplasia and oesophageal adenocarcinoma in Barrett’s oesophagus: a nationwide study of 9883 patients. Aliment Pharmacol Ther 2014; 39: 984–91. 7 Qumseya BJ, Wang H, Badie N et al. Advanced imaging technologies increase detection of dysplasia and neoplasia in patients with Barrett’s esophagus: a meta-analysis and systematic review. Clin Gastroenterol Hepatol 2013; 11: 1562–70. e1–2. 8 Gupta A, Attar BM, Koduru P, Murali AR, Go BT, Agarwal R. Utility of confocal laser endomicroscopy in identifying high-grade dysplasia and adenocarcinoma in Barrett’s esophagus: a systematic review and meta-analysis. Eur J Gastroenterol Hepatol 2014; 26: 369–77. 9 Canto MI, Anandasabapathy S, Brugge W et al.; Confocal Endomicroscopy for Barrett’s Esophagus or Confocal Endomicroscopy for Barrett’s Esophagus (CEBE) Trial Group. In vivo endomicroscopy improve detection of Barrett’s esophagus-related neoplasia: a multicenter international randomized controlled trial (with video). Gastrointest Endosc 2014; 79: 211–21. 10 Boerwinkel DF, Swager A, Curvers WL, Bergman JJ. The clinical consequences of advanced imaging techniques in Barrett’s esophagus. Gastroenterology 2014; 146: 622–9.e4. 11 Gerson LB. Is it time to consider other options for Barrett’s esophagus screening? Gastrointest Endosc 2014; 80: 783–5. 12 Duits LC, Phoa KN, Curvers WL et al. Barrett’s oesophagus patients with low-grade dysplasia can be accurately risk-stratified after histological review by an expert pathology panel. Gut 2014 Jul 17. pii: gutjnl-2014-307278. doi: 10.1136/gutjnl-2014-307278. [Epub ahead of print]. 13 Phoa KN, Pouw RE, van Vilsteren FG et al. Remission of Barrett’s esophagus with early neoplasia 5 years after radiofrequency ablation with endoscopic resection: a Netherlands cohort study. Gastroenterology 2013; 145: 96–104. 14 Phoa KN, van Vilsteren FG, Weusten BL et al. Radiofrequency ablation vs endocopic surveillance for patients with Barrett esophagus and low-grade dysplasia: a randomized clinical trial. JAMA 2014; 311: 1209–17. 15 Pech O, May A, Manner H et al. Long-term efficacy and safety of endoscopic resection for patients with mucosal adenocarcinoma of the esophagus. Gastroenterology 2014; 146: 652–60.e1. 16 Anders M, Bähr C, El-Masry MA et al. Long-term recurrence of neoplasia and Barrett’s epithelium after complete endoscopic resection. Gut 2014; 63: 1535–43. 17 Ganz RA, Mitlyng B, Leon S. The case for ablating nondysplastic Barrett’s esophagus. Gastrointest Endosc 2014; 80: 866–72. 18 Lightdale CJ. Radiofrequency ablation for nondysplastic Barrett’s eosphagus: certainly not for all. Gastrointest Endosc 2014; 80: 873–6. 19 Timmer MR, Sun G, Gorospe EC et al. Predictive biomarkers for Barrett’s esophagus: so near and yet so far. Dis Esophagus 2013; 26: 574–81. 20 di Pietro M, Boerwinkel DF, Shariff MK et al. The combination of autofluorescence endoscopy and molecular biomarkers is a novel diagnostic tool for dysplasia in Barrett’s oesophagus. Gut 2015; 64: 49–56.
© 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
Copyright of Journal of Digestive Diseases is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Journal of Digestive Diseases 2015; 16; 55–57
doi: 10.1111/1751-2980.12224
Leading article
Reflections on esophageal columnar metaplasia (Barrett)-ANNO 2015 Guido NJ TYTGAT Academic Medical Center, Amsterdam, The Netherlands
Esophageal columnar metaplasia (ECM) (Barrett’s esophogus) continues to generate clinical and basic attention. Yet many questions remain unanswered and global consensus on important issues is often still KEY WORDS:
lacking. This article discusses a selection of certain recent findings and reflects on some remaining uncertainties of this intriguing disease.
ablation techniques, adenocarcinoma, Barrett esophagus, dysplasia, endoscopic resection.
PREVALENCE AND PATHOGENESIS
SCREENING AND SURVEILLANCE
It seems that the prevalence of esophageal columnar metaplasia (ECM) is slowing down in the West but is continuing to rise in the East. The environmental factors that are responsible for this varying incidence are poorly understood: do they lie in the rising frequency of gastroesophageal reflux disease, nutritional patterns, obesity, smoking and dysbiosis? There are few preventive strategies, except perhaps for long-term therapy with proton pump inhibitors (PPI) in erosive reflux disease.
The main reason for the interest in ECM is its propensity for neoplastic changes. The magnitude of the risk remains debatable, but overall the annual conversion of ECM to esophageal adenocarcinoma (EAC) fluctuates at around 0.3%.1,2 Invasive cancer is the final stage in the progression from early neoplasia (dysplasia) to more advanced neoplasia. The goal of screening and surveillance is the early detection of neoplasia at a still curable state. The practice of screening and surveillance is widespread, despite the lack of randomized controlled trial evidence to demonstrate its true efficacy. Even a recent large case-control study failed to demonstrate significant differences in mortality between EAC detected through endoscopic surveillance versus non-surveillance,3 contrasting with a population-based cohort study4 showing that mortality from EAC was reduced when individuals participated in a surveillance program. What seems clear, however, is that cancers discovered during surveillance are often at a relatively early stage of malignancy, but most ECM are not recognized and such patients are therefore never candidates for screening and surveillance. Justification for screening and surveillance may perhaps be enhanced by tailoring the individual risk profile, that is, individuals at lower risk (shorter segment, cardia-like mucosa) and those at higher risk (longer segment, intestinal metaplasia, dysplasia,
Excessive acid–peptic–bile reflux, particularly when combined with sluggish clearance of the refluxate, appears to be the dominant mechanism for the injury of the squamous epithelium, with subsequent upregulation of CDX2 leading to columnar metaplasia, usually of the intestinal type, especially in the more proximal segments, and occasionally of cardia-like mucosa, especially more distally.
Correspondence to: Guido NJ TYTGAT, Academic medical Center Amsterdam, The Netherlands. Email: [email protected] © 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
55
56
GNJ Tytgat
obesity, obstructive sleep apnea, family history and so on). Ideally, additional chemoprevention should be attempted, but whether all ECM patients, both symptomatic and asymptomatic, should be treated with long-term PPI remains a moot point, despite metaanalysis-based evidence supporting such a strategy.5 The results of a recent large population-based study showing that prolonged PPI therapy does not prevent advanced neoplasia is certainly sobering.6 Summarizing the views mentioned above, it would appear that at present there is no consensus on the effectiveness of screening and surveillance of patients with ECM. This issue is further complicated by the fact that the proportion of all-cause mortality due to EAC is rather small, that EAC generally afflicts patients relatively late in life and that the endoscopic procedures involved have known shortcomings. IMAGING MODALITIES Endoscopy remains the prime imaging modality used to detect metaplasia, and several novel imaging modalities have been explored such as fluorescence, spectral modulation with narrow-band imaging (Olympus), FICE (Fujinon) or iSCAN (Pentax), to facilitate the detection of foci of neoplasia.7 Advanced imaging technology may increase the diagnostic yield by 34% compared with white light endoscopy (WLE), but interobserver variability is high. Experience with confocal laser endomicroscopy (CLE), both endoscope-based (eCLE) and probe-based (pCLE), is increasing, suggesting a sensitivity of at least 70% and a specificity of at least 90% for the detection of neoplasia, including flat high-grade dysplasia (HGDys). A recent meta-analysis revealed a pooled sensitivity of 86% and a specificity of 88% for CLE compared to four-quadrant non-targeted biopsies.8 When eCLE was combined with high-definition WLE in the detection of neoplasia a sensitivity of 95% and a specificity of 92% was reached.9 Such methodologies are probably most useful during the endoscopic training phase. Proving their utility for experienced endoscopists using standard high-resolution/highdefinition endoscopy is increasingly difficult as the level of expertise rises. The matter is further complicated and utterly confused by the repetitive introduction of different classification schemes which makes engaging in novel imaging technology challenging. Consensus on diagnostic criteria, terminology and grading is essential for uniform diagnosis and adequate comparison of various worldwide studies. The selection of novel grading systems should be restricted to a consortium of world-renowned experts
Journal of Digestive Diseases 2015; 16; 55–57 in the field and internationally validated. It seems sensible to conclude that currently no real clinical indications exist to encourage the enhanced methodologies name above to be implemented in daily routine practice.10 Whether non-endoscopic screening measures such as the use of capsule endoscopy, cytosponges or tethered capsules will allow widespread cost-effective screening and surveillance needs further evaluation.11 HISTOPATHOLOGY Ideally, targeted biopsies should be obtained because traditional untargeted four-quadrant biopsies have a rather poor positive predictive value of around 35% and may miss adjacent occult HG-Dys or early EAC. It is now clear that experienced pathologists are essential for the adequate histological detection and grading of neoplasia. Low-grade dysplasia (LG-Dys) is often overdiagnosed by non-expert pathologists. Over 73% of community-based diagnosis can be downstaged to non-dysplasia or indefinite dysplasia. To reduce overstaging due to reactive and regenerative mucosal changes, high-dose PPI therapy prior to biopsy is often advised but there has been so far no evidence to support this recommendation. Of correctly diagnosed LG-Dys patients, 9.1% were shown to progress to HG-Dys/EAC after 39 months compared to 0.6% in non-dysplastic and 0.9% in indefinite per patientyear.12 Only LG-Dys diagnosed by expert pathologists is an important predictor of risk for malignant progression. THERAPEUTIC POSSIBILITIES There is widespread agreement that HG-Dys and mucosal EAC (m-EAC) should be removed whenever possible via endoscopic resection, making the expert examination of resected specimen possible. Whether resection therapy is also needed for incipient submucosal invasion remains debatable. Endoscopic removal requires the careful delineation of the suspicious focus, often using chromoscopy or other advanced imaging modalities. Cap-assisted or rubber band-assisted endoscopic resection is the dominant therapeutic modality and usually obviates the need for endoscopic submucosal dissection, which is more challenging in the esophagus and upper cardia. The adjacent, truly flat, non-suspicious metaplastic mucosa, which rarely bears deep infiltrating cancer, is currently most often ablated with radiofrequency ablation (RFA).13 RFA, which has been shown to be superior to endoscopic surveillance, seems also to be
© 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
Journal of Digestive Diseases 2015; 16; 55–57 indicated for consensus-based LG-Dys, especially when it is persistent and multifocal.14 Tissue ablation with argon plasma coagulation should be restricted because of incomplete ablation and the risk of buried ECM glands. Both the early and long-term outcomes of endoscopic resection combined with RFA are gratifying and durable.15 However, further surveillance remains indicated as long-term recurrence of ECM and neoplasia remains possible.16 Whether also non-dysplastic metaplasia should be routinely ablated with RFA remains highly debated, and the arguments for and against have been nicely summarized in a recent debate.17,18 This unsolved question will require careful multicenter evaluation with long-term follow-up before final advice can be given. Currently, our ability to predict which patient with no dysplasia or LG-Dys is at risk of progression to HG-Dys/m-EAC is limited. Various candidate biomarkers are being explored in addition to dysplasia, including aneuploidy, abnormal p53 expression, upregulated cyclin A, lectins, wheat germ agglutinin, Lewis antigen and McMT.19 Expectations are rising, as shown by the high accuracy of a combination of autofluorescence endoscopy and molecular biomarkers.20 CONCLUDING REMARKS ECM will remain for a considerable length of time one of the most challenging gastrointestinal diseases, not only because of its clinical impact but also because it is an ideal model both for unravelling the mysteries of metaplastic tissue transdifferentiation and for evaluating all novel diagnostic and therapeutic endoscopic modalities. Many lessons remain to be learned. REFERENCES 1 di Pietro M, Alzoubaidi D, Fitzgerald RC. Barrett’s esophagus and cancer risk: how research advances can impact clinical practice. Gut Liver 2014; 8: 356–70. 2 Fitzgerald RC, di Pietro M, Ragunath K et al.; British Society of Gastroenterology. British society of Gastroenterology guidelines on the diagnosis and management of Barrett’s oesophagus. Gut 2014; 63: 7–42. 3 Corley DA, Mehtani K, Quesenberry C, Zhao W, de Boer J, Weiss NS. Impact of endoscopic surveillance on mortality from Barrett’s esophagus-associated esophageal adenocarcinomas. Gastroenterolgy 2013; 145: 312–9. 4 Verbeek RE, Leenders M, ten Kate FJ et al. Surveillance of Barrett’s esophagus and mortality from esophageal adenocarcinoma: a population-based cohort study. Am J Gastroenterol 2014; 109: 1215–22.
Barrett anno 2015
57
5 Aydin Y, Akin H. Letter: proton pump inhibitor usage still seems to reduce the risk of high-grade dysplasia and/or oesophageal adenocarcinoma in Barrett’s oesophagus. Aliment Pharmacol Ther 2014; 40: 859–60. 6 Hvid-Jensen F, Pedersen L, Funch-Jensen P, Drewes AM. Proton pump inhibitor use may not prevent high-grade dysplasia and oesophageal adenocarcinoma in Barrett’s oesophagus: a nationwide study of 9883 patients. Aliment Pharmacol Ther 2014; 39: 984–91. 7 Qumseya BJ, Wang H, Badie N et al. Advanced imaging technologies increase detection of dysplasia and neoplasia in patients with Barrett’s esophagus: a meta-analysis and systematic review. Clin Gastroenterol Hepatol 2013; 11: 1562–70. e1–2. 8 Gupta A, Attar BM, Koduru P, Murali AR, Go BT, Agarwal R. Utility of confocal laser endomicroscopy in identifying high-grade dysplasia and adenocarcinoma in Barrett’s esophagus: a systematic review and meta-analysis. Eur J Gastroenterol Hepatol 2014; 26: 369–77. 9 Canto MI, Anandasabapathy S, Brugge W et al.; Confocal Endomicroscopy for Barrett’s Esophagus or Confocal Endomicroscopy for Barrett’s Esophagus (CEBE) Trial Group. In vivo endomicroscopy improve detection of Barrett’s esophagus-related neoplasia: a multicenter international randomized controlled trial (with video). Gastrointest Endosc 2014; 79: 211–21. 10 Boerwinkel DF, Swager A, Curvers WL, Bergman JJ. The clinical consequences of advanced imaging techniques in Barrett’s esophagus. Gastroenterology 2014; 146: 622–9.e4. 11 Gerson LB. Is it time to consider other options for Barrett’s esophagus screening? Gastrointest Endosc 2014; 80: 783–5. 12 Duits LC, Phoa KN, Curvers WL et al. Barrett’s oesophagus patients with low-grade dysplasia can be accurately risk-stratified after histological review by an expert pathology panel. Gut 2014 Jul 17. pii: gutjnl-2014-307278. doi: 10.1136/gutjnl-2014-307278. [Epub ahead of print]. 13 Phoa KN, Pouw RE, van Vilsteren FG et al. Remission of Barrett’s esophagus with early neoplasia 5 years after radiofrequency ablation with endoscopic resection: a Netherlands cohort study. Gastroenterology 2013; 145: 96–104. 14 Phoa KN, van Vilsteren FG, Weusten BL et al. Radiofrequency ablation vs endocopic surveillance for patients with Barrett esophagus and low-grade dysplasia: a randomized clinical trial. JAMA 2014; 311: 1209–17. 15 Pech O, May A, Manner H et al. Long-term efficacy and safety of endoscopic resection for patients with mucosal adenocarcinoma of the esophagus. Gastroenterology 2014; 146: 652–60.e1. 16 Anders M, Bähr C, El-Masry MA et al. Long-term recurrence of neoplasia and Barrett’s epithelium after complete endoscopic resection. Gut 2014; 63: 1535–43. 17 Ganz RA, Mitlyng B, Leon S. The case for ablating nondysplastic Barrett’s esophagus. Gastrointest Endosc 2014; 80: 866–72. 18 Lightdale CJ. Radiofrequency ablation for nondysplastic Barrett’s eosphagus: certainly not for all. Gastrointest Endosc 2014; 80: 873–6. 19 Timmer MR, Sun G, Gorospe EC et al. Predictive biomarkers for Barrett’s esophagus: so near and yet so far. Dis Esophagus 2013; 26: 574–81. 20 di Pietro M, Boerwinkel DF, Shariff MK et al. The combination of autofluorescence endoscopy and molecular biomarkers is a novel diagnostic tool for dysplasia in Barrett’s oesophagus. Gut 2015; 64: 49–56.
© 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
Copyright of Journal of Digestive Diseases is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
