Barrett's Esophagus

Emerging Evidence for Improved Clinical Practice
 
 
Academic Press
  • 1. Auflage
  • |
  • erschienen am 28. März 2016
  • |
  • 234 Seiten
 
E-Book | ePUB mit Adobe DRM | Systemvoraussetzungen
E-Book | PDF mit Adobe DRM | Systemvoraussetzungen
978-0-12-802649-6 (ISBN)
 

Barrett's Esophagus: Emerging Evidence for Improved Clinical Practice is a comprehensive reference on the treatment and new imaging modalities of Barrett's Esophagus for researchers, clinicians, and scholars. Each chapter is composed from the perspective of investigators who summarize the data as well as the reasoning behind why those studies were conceived.

In addition, the future directions of research are discussed within each chapter, providing insights from the investigators. Research questions are described, and cutting-edge applications are explained. Each chapter contains clinical scenarios to highlight the directions in which the research is, and should be, heading.


  • Provides a perspective into the research behind Barrett's Esophagus
  • Emphasizes the emerging technologies in surveillance and treatment of Barrett's
  • Features clinical scenarios to highlight the directions in which research is, and should be, heading
  • Includes coverage of current guidelines and discussions on where these guidelines fall short


Dr. Pleskow's major research interests have been the study of serologic markers in pancreatic disease, therapeutic pancreaticobiliary endoscopy and endoscopic ultrasound. He pioneered the endoscopic placement of gold markers in patients with pancreaticobiliary malignancy to facilitate Cyberknife therapy. He and his colleagues have worked closely on the endoscopic treatment of Gastroesophageal Reflux Disease (GERD) and Barrett's esophagus. Dr. Pleskow is also an active and influential member of the NPF (National Pancreas Foundation) board and its Executive Committee. He has also previously served as Executive Director and currently presides over the Scientific Advisory Committee and sits on the Grant Review Council. Dr. Pleskow holds board certification from the American Board of Internal Medicine (Gastroenterology).
  • Englisch
  • San Diego
  • |
  • USA
Elsevier Science
  • 6,56 MB
978-0-12-802649-6 (9780128026496)
0128026499 (0128026499)
weitere Ausgaben werden ermittelt
  • Front Cover
  • Barrett's Esophagus
  • Copyright Page
  • Dedication
  • Contents
  • List of Contributors
  • Preface
  • 1 A Disease Entity Is Identified
  • 1.1 Introduction
  • 1.2 Norman Rupert Barrett (1903-1979)
  • 1.3 Philip Rowland Allison (1907-1974)
  • 1.4 History of Barrett's Esophagus
  • References
  • 2 Fluctuating Risk Factors and Epidemiology
  • 2.1 Introduction
  • 2.2 Prevalence
  • 2.2.1 Population-Based Studies/Routine Endoscopy
  • 2.2.2 Patients with Chronic Gastroesophageal Reflux Disease
  • 2.2.3 Autopsy Studies
  • 2.2.4 Geographic Variation
  • 2.3 Incidence
  • 2.4 Risk Factors
  • 2.4.1 Gastroesophageal Reflux Disease
  • 2.4.2 Age
  • 2.4.3 Gender
  • 2.4.4 Race
  • 2.4.5 Family History of Barrett's Esophagus or Esophageal Adenocarcinoma
  • 2.4.6 Visceral Obesity
  • 2.4.7 Smoking
  • 2.4.8 Alcohol
  • 2.4.9 Diet
  • 2.4.10 Diabetes Mellitus
  • 2.4.11 Obstructive Sleep Apnea
  • 2.4.12 Erosive Esophagitis
  • 2.4.13 Hiatal Hernia
  • 2.4.14 Helicobacter pylori
  • 2.5 Future Directions
  • References
  • 3 Metaplasia and Dysplasia in Barrett's Esophagus
  • 3.1 Introduction
  • 3.2 Normal Anatomy and Histology
  • 3.3 Histology of Barrett's Esophagus
  • 3.3.1 Endoscopic Findings
  • 3.3.2 Microscopic Findings
  • 3.3.3 Goblet Cells versus Pseudogoblet Cells
  • 3.4 Intestinal Metaplasia of the EGJ
  • 3.5 Barrett's Esophagus-Related Dysplasia
  • 3.5.1 Negative for Dysplasia
  • 3.5.2 Indefinite for Dysplasia
  • 3.5.3 Positive for Dysplasia
  • 3.6 Low-Grade (Intestinal-Type) Dysplasia
  • 3.7 High-Grade (Intestinal-Type) Dysplasia
  • 3.8 Gastric Foveolar-Type Dysplasia (Nonadenomatous Dysplasia)
  • 3.9 Basal Crypt Dysplasia
  • 3.10 Intramucosal Adenocarcinoma
  • 3.11 Submucosal Adenocarcinoma
  • 3.12 Diagnostic Issues in Barrett's-Related Dysplasia
  • 3.12.1 Sampling Error
  • 3.12.2 Observer Variation in Barrett's Esophagus-Related Dysplasia
  • 3.12.3 Squamous Overgrowth (Buried Barrett's Esophagus)
  • 3.13 Surrogate Biomarkers for Assessing Risk of Esophageal Adenocarcinoma and Future Directions
  • References
  • 4 Genetics and Biomarkers in Barrett's Esophagus and Esophageal Adenocarcinoma
  • 4.1 Introduction
  • 4.2 Genetics of Barrett's Esophagus and Esophageal Adenocarcinoma
  • 4.2.1 Genetic Susceptibility to Barrett's Esophagus and Esophageal Adenocarcinoma
  • 4.2.2 Acquired Molecular Alterations in the Pathogenesis of Barrett's Esophagus
  • 4.2.2.1 Altered Cell Signaling
  • 4.2.2.2 Mechanisms of Genetic Alteration
  • 4.3 Biomarkers in Barrett's Esophagus and Esophageal Adenocarcinoma
  • 4.3.1 Screening Biomarkers
  • 4.3.2 Barrett's Dysplasia
  • 4.3.3 P53
  • 4.3.4 Other Somatic Mutations
  • 4.3.5 MicroRNAs as Biomarkers
  • 4.3.6 Epigenetic Biomarkers
  • 4.3.7 DNA Content Abnormalities
  • 4.3.8 Cell Cycle and Proliferation Markers
  • 4.3.9 Biomarker Panels
  • 4.4 Conclusions
  • 4.5 Future Directions
  • References
  • 5 Diagnosis of Barrett's Esophagus
  • 5.1 Introduction
  • 5.2 Histopathologic Diagnosis of Barrett's
  • 5.2.1 Definition of Intestinal Metaplasia
  • 5.3 Endoscopic Diagnosis of Barrett's
  • 5.3.1 Tissue Sampling
  • 5.4 Advances in Imaging and Diagnosis of Barret's
  • 5.4.1 Magnification Techniques and High-Resolution Endoscopy
  • 5.4.2 Chromoendoscopy
  • 5.4.3 Virtual Chromoendoscopy and Other Novel Imaging
  • 5.5 Future Directions
  • Acknowledgments
  • References
  • 6 Screening and Surveillance of Barrett's Esophagus
  • 6.1 Overview
  • 6.2 Pathogenesis of Barrett's Esophagus
  • 6.3 Risk Factors for Barrett's Esophagus
  • 6.4 Screening for Barrett's Esophagus
  • 6.5 Surveillance of Barrett's Esophagus
  • 6.5.1 Surveillance of Nondysplastic Barrett's Esophagus
  • 6.5.2 Cost-Effectiveness of NDBE Surveillance
  • 6.5.3 Surveillance of Barrett's Esophagus with Low-Grade Dysplasia
  • 6.5.4 Surveillance of Barrett's Esophagus with High-Grade Dysplasia
  • 6.6 Barrett's Esophagus and Its Impact on Quality of Life
  • 6.7 The Future of Screening and Surveillance of Barrett's Esophagus
  • References
  • 7 In Vivo Optical Detection of Dysplasia in Barrett's Esophagus with Endoscopic Light Scattering Spectroscopy
  • 7.1 Introduction
  • 7.2 Light Scattering from Cells
  • 7.3 Light Transport in Superficial Tissues
  • 7.4 Imaging Dysplasia in Barrett's Esophagus with Endoscopic Polarized Light Scattering Spectroscopy
  • 7.5 Future Directions
  • Acknowledgments
  • References
  • 8 Enhanced Imaging of the Esophagus: Optical Coherence Tomography
  • 8.1 Introduction
  • 8.2 Principles of Optical Coherence Tomography
  • 8.2.1 Optical Coherence Tomography Parameters
  • 8.3 History of Optical Coherence Tomography in the Esophagus
  • 8.3.1 First-Generation Esophageal Time-Domain Optical Coherence Tomography
  • 8.3.2 Second-Generation Esophageal Fourier-Domain Optical Coherence Tomography
  • 8.4 Optical Coherence Tomography Images of the Esophagus
  • 8.4.1 Normal Esophageal Squamous Mucosa
  • 8.4.2 Stomach
  • 8.4.3 Barrett's Esophagus
  • 8.4.4 Dysplasia in Barrett's Esophagus
  • 8.4.5 Response to Esophageal Ablation
  • 8.5 New Advances in Volumetric Laser Endomicroscopy
  • 8.5.1 Optical Coherence Tomography Image Guided Biopsy
  • 8.5.2 En Face Visualization in Optical Coherence Tomography
  • 8.5.3 Tethered Capsule Endomicroscopy
  • 8.6 New Optical Coherence Tomography Technology Development
  • 8.6.1 Vasculature Imaging
  • 8.6.2 Polarization-Sensitive Optical Coherence Tomography
  • 8.6.3 Angle-Resolved Low-Coherence Interferometry
  • 8.6.4 Simultaneous Optical Coherence Tomography and Fluorescence Imaging
  • 8.6.5 Optical Coherence Tomography-Guided Ablation
  • 8.6.6 Automated Optical Coherence Tomography Image Analysis
  • 8.7 Future Outlook
  • Disclosures
  • References
  • 9 Enhanced Imaging of the Esophagus: Confocal Laser Endomicroscopy
  • 9.1 Introduction
  • 9.2 Confocal Endomicroscopy Devices
  • 9.3 Confocal Laser Endomicroscopy in Barrett's Esophagus
  • 9.3.1 Confocal Laser Endomicroscopy Features of Barrett's Esophagus
  • 9.3.2 Clinical Trials for Diagnosing Barrett's Esophagus and Barrett's Esophagus-Associated Neoplasia
  • 9.4 Confocal Laser Endomicroscopy in Barrett's Patients
  • 9.5 Perspective
  • References
  • 10 History of Ablative Therapies for Barrett's and Superficial Adenocarcinoma
  • 10.1 Introduction
  • 10.1.1 Background
  • 10.2 Endoscopic Ablation: History and Overview
  • 10.3 Endoscopic Ablation as a Treatment Paradigm
  • 10.3.1 History of Endoscopic Therapy for Patients Without Dysplasia
  • 10.3.2 History of Endoscopic Therapy for Patients with Low-Grade Dysplasia
  • 10.3.3 History of Endoscopic Therapy for Patients with High-Grade Dysplasia or Intramucosal Adenocarcinoma
  • 10.4 Endoscopic Therapies
  • 10.4.1 Photodynamic Therapy
  • 10.4.1.1 Procedure
  • 10.4.1.2 PDT Compounds
  • 10.4.1.3 Efficacy
  • 10.5 Thermal Ablation
  • 10.5.1 Argon Plasma Coagulation
  • 10.5.1.1 Procedure
  • 10.5.1.2 Efficacy
  • 10.5.2 Multipolar Electrocautery
  • 10.5.2.1 Procedure
  • 10.5.2.2 Efficacy
  • 10.5.3 KTP Laser and Nd:Yag Laser
  • 10.5.3.1 Procedure
  • 10.5.3.2 Heat Probe
  • 10.5.3.3 Efficacy
  • 10.6 Intermodality Comparison
  • 10.6.1 PDT Versus APC
  • 10.6.2 MPEC Versus APC
  • 10.6.3 Others
  • 10.7 Conclusion
  • References
  • 11 Radiofrequency Ablation
  • 11.1 Introduction
  • 11.2 Indications for Radiofrequency Ablation
  • 11.2.1 Barrett's Esophagus with Visible Lesions Containing High-Grade Dysplasia or Intramucosal Carcinoma
  • 11.2.2 Barrett's Esophagus with Flat High-Grade Dysplasia
  • 11.2.3 Barrett's Esophagus with Low-Grade Dysplasia
  • 11.2.4 Nondysplastic Barrett's Esophagus
  • 11.3 Technical Aspects
  • 11.3.1 Circumferential Ablation
  • 11.3.2 Follow-Up After Circumferential Ablation
  • 11.3.3 Focal Ablation
  • 11.3.4 New Ablation Devices
  • 11.3.5 Posttreatment Care
  • 11.3.6 Follow-Up Regimen
  • 11.4 Efficacy of Radiofrequency Ablation
  • 11.4.1 Eradication of Nondysplastic Barrett's Mucosa
  • 11.4.2 Effect on Dysplastic BE
  • 11.4.3 Buried Barrett's
  • 11.4.4 Intestinal Metaplasia of the Cardia
  • 11.4.5 Adverse Events
  • 11.5 Directions for Future Research
  • 11.5.1 Technical Improvements
  • 11.5.2 Risk Stratification
  • 11.5.2.1 Optimizing Diagnosis of LGD
  • 11.5.2.2 The Search for Biomarkers
  • References
  • 12 Cryospray Ablation
  • 12.1 Introduction
  • 12.2 Liquid Nitrogen
  • 12.3 Dosimetry
  • 12.4 Limitations
  • 12.5 Adverse Events
  • 12.6 Carbon Dioxide
  • 12.7 Nitrous Oxide
  • 12.8 Surveillance
  • 12.9 Future Directions
  • References
  • 13 Endoscopic Surgical Therapies for Barrett's Esophagus
  • 13.1 Introduction
  • 13.2 Techniques for Performing Endoscopic Mucosal Resection and Endoscopic Submucosal Dissection
  • 13.2.1 Endoscopic Mucosal Resection
  • 13.2.2 Endoscopic Submucosal Dissection
  • 13.3 Prevention and Management of Complications Following Endoscopic Mucosal Resection and Endoscopic Submucosal Dissection
  • 13.4 Indications for Endoscopic Mucosal Resection and Endoscopic Submucosal Dissection in Barrett's Esophagus
  • 13.5 Results of Endoscopic Mucosal Resection and Endoscopic Submucosal Dissection in Barrett's Esophagus
  • 13.6 Indications for Surgery in Barrett's Esophagus
  • 13.7 Techniques of Minimally Invasive Esophagectomy
  • 13.8 Complications from Esophagectomy
  • 13.9 Esophagectomy Versus Endoscopic Therapies for Early Esophageal Neoplasia
  • 13.10 Future Developments in Endolumenal and Translumenal Surgery
  • 13.11 Conclusion
  • References
  • 14 Chemoprevention of Barrett's Esophagus and Adenocarcinoma
  • 14.1 Introduction
  • 14.2 Suggested Targets and Strategies for Chemoprevention to Prevent or Slow Malignant Transformation of Barrett's Esophagus
  • 14.2.1 Gastric Acid and Bile Reflux
  • 14.2.1.1 Chronic Injury and Inflammation
  • 14.2.1.2 Arachidonic Acid Pathway
  • 14.2.1.3 Oxidative Stress
  • 14.2.2 Obesity, Diet, and Lifestyle
  • 14.2.2.1 Disruption of Antireflux Mechanisms
  • 14.2.2.2 Altered Composition of Refluxate and Mucosal Response to Reflux Injury
  • 14.2.2.3 Endocrine Disorders
  • 14.2.3 Hypergastrinemia
  • 14.2.4 Helicobacter pylori Infection
  • 14.2.5 Molecular Alterations
  • 14.3 Chemoprevention of Adenocarcinoma Associated with Barrett's Esophagus
  • 14.3.1 Proton Pump Inhibitors
  • 14.3.2 Aspirin/NSAIDs
  • 14.3.3 Ursodeoxycholic Acid
  • 14.3.4 Statins
  • 14.3.5 Metformin
  • 14.4 Future Directions
  • Acknowledgment
  • References
  • 15 Posttreatment Surveillance, Risk for Recurrence of Barrett's Esophagus, and Adenocarcinoma After Treatment
  • 15.1 Introduction
  • 15.2 Surveillance and Risk for Recurrence After Ablation
  • 15.2.1 Radiofrequency Ablation
  • 15.2.2 Cryoablation
  • 15.3 Surveillance and Risk for Recurrence After Endoscopic Resection
  • 15.3.1 Endoscopic Resection
  • 15.3.2 Submucosal Dissection
  • 15.4 Surveillance and Risk for Recurrence After Combination of Resection and Ablation
  • 15.5 Surveillance and Risk for Recurrence After Esophagectomy
  • 15.6 Summary and Future Directions
  • References
  • Index
  • Back Cover

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