GERD -  Parakrama T. Chandrasoma,  Tom R. DeMeester

GERD (eBook)

Reflux to Esophageal Adenocarcinoma
eBook Download: EPUB
2010 | 1. Auflage
464 Seiten
Elsevier Science (Verlag)
978-0-08-046474-9 (ISBN)
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102,93 inkl. MwSt
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Gastroesophageal Reflux Disease (GERD) is one of the most common maladies of mankind. Approximately 40% of the adult population of the USA suffers from significant heartburn and the numerous antacids advertised incessantly on national television represents a $8 billion per year drug market. The ability to control acid secretion with the increasingly effective acid-suppressive agents such as the H2 blockers (pepcid, zantac) and proton pump inhibitors (nexium, prevacid) has given physicians an excellent method of treating the symptoms of acid reflux.
Unfortunately, this has not eradicated reflux disease. It has just changed its nature. While heartburn, ulceration and strictures have become rare, reflux-induced adenocarcinoma of the esophagus is becoming increasingly common. Adenocarcinoma of the esophagus and gastric cardia is now the most rapidly increasing cancer type in the Western world.
The increasing incidence of esophageal adenocarcinoma has created an enormous interest and stimulus for research in this area. GERD brings together a vast amount of disparate literature and presents the entire pathogenesis of reflux disease in one place. In addition to providing a new concept of how gastroesophageal reflux causes cellular changes in the esophagus, GERD also offers a complete solution to a problem that has confused physicians for over a century. Both clinical and pathological information about reflux disease and its treatment are presented. GERD is meant to be used as a comprehensive reference for gastroenterologists, esophageal surgeons, and pathologists alike.
*Outlines how gastroesophageal reflux causes cellular changes in the esophagus
*Brings together the pathogenesis of the disease in one source and applies it toward clinical treatment
*Tom DeMeester is THE leading international expert on reflux disease; Parakrama Chandrasoma is one of the leading pathologists in the area
*Book contains approximately 350 illustrations
*Ancillary web site features color illustrations: www.chandrasoma.com

Dr. Parakrama Chandrasoma was born in Sri Lanka and received his medical education and initial pathology training in the Medical School of the University of Sri Lanka. He has postgraduate degrees in internal medicine, including the M.D. (Sri Lanka) and Membership of the Royal College of Physicians (UK). He immigrated to the United States in 1978. Upon completing his pathology residency, he assumed duties as Chief of Surgical Pathology at the Los Angeles County + University of Southern California Medical Center He has held this position since. After an initial interest in neuropathology, Dr. Chandrasoma joined Dr. Tom DeMeester's Foregut Surgery team as pathologist in 1991. This led to a productive study of gastroesophageal reflux disease spanning 16 years and resulting in the development of numerous original concepts relating to the pathogenesis of gastroesophageal reflux disease. Dr. Chandrasoma has written over 140 peer reviewed papers and 6 previous pathology textbooks, including a general text on Gastrointestinal Pathology and a text on Gastroesophageal Reflux Disease, and is a Professor of Pathology at the Keck School of Medicine at the University of Southern California. He is married with three children and lives in Pasadena, California.
Gastroesophageal Reflux Disease (GERD) is one of the most common maladies of mankind. Approximately 40% of the adult population of the USA suffers from significant heartburn and the numerous antacids advertised incessantly on national television represents a $8 billion per year drug market. The ability to control acid secretion with the increasingly effective acid-suppressive agents such as the H2 blockers (pepcid, zantac) and proton pump inhibitors (nexium, prevacid) has given physicians an excellent method of treating the symptoms of acid reflux.Unfortunately, this has not eradicated reflux disease. It has just changed its nature. While heartburn, ulceration and strictures have become rare, reflux-induced adenocarcinoma of the esophagus is becoming increasingly common. Adenocarcinoma of the esophagus and gastric cardia is now the most rapidly increasing cancer type in the Western world.The increasing incidence of esophageal adenocarcinoma has created an enormous interest and stimulus for research in this area. GERD brings together a vast amount of disparate literature and presents the entire pathogenesis of reflux disease in one place. In addition to providing a new concept of how gastroesophageal reflux causes cellular changes in the esophagus, GERD also offers a complete solution to a problem that has confused physicians for over a century. Both clinical and pathological information about reflux disease and its treatment are presented. GERD is meant to be used as a comprehensive reference for gastroenterologists, esophageal surgeons, and pathologists alike. - Outlines how gastroesophageal reflux causes cellular changes in the esophagus- Brings together the pathogenesis of the disease in one source and applies it toward clinical treatment- Tom DeMeester is THE leading international expert on reflux disease; Parakrama Chandrasoma is one of the leading pathologists in the area- Book contains approximately 350 illustrations- Ancillary web site features color illustrations: www.chandrasoma.com

Front cover 1
Title page 5
Copyright page 6
Table of contents 9
Preface 17
CHAPTER 1: Overview of Gastroesophageal Reflux Disease 19
PHYSIOLOGICAL VERSUS PATHOLOGICAL REFLUX 21
PREVALENCE OF GASTROESOPHAGEAL REFLUX DISEASE 21
HISTOLOGIC DEFINITION OF GASTROESOPHAGEAL REFLUX DISEASE 23
PREVALENCE OF BARRETT ESOPHAGUS 24
MANAGEMENT OF BARRETT ESOPHAGUS 24
PREVALENCE OF REFLUX-INDUCED ADENOCARCINOMA 24
CHAPTER 2: The Past, Present, and Future of Columnar-Lined (Barrett) Esophagus 29
THE HISTORY OF COLUMNAR-LINED ESOPHAGUS 30
THE REASONS FOR CONFUSION 45
HISTORICAL EVOLUTION OF COLUMNAR-LINED (BARRETT) ESOPHAGUS 49
THE STATE OF THE ART AND TODAY’S PROBLEMS 53
SOLUTIONS TO THE PROBLEM AND WHAT WE HOPE TO SHOW 54
CHAPTER 3: Fetal Development of the Esophagus and Stomach 59
THE STUDY OF EMBRYOLOGY OF THE FOREGUT 60
EARLY DEVELOPMENT OF THE GASTROINTESTINAL TRACT 61
EARLY DEVELOPMENT OF THE FOREGUT 63
EPITHELIAL DEVELOPMENT IN THE FETAL ESOPHAGUS 63
EPITHELIAL DEVELOPMENT IN THE FETAL STOMACH 67
EPITHELIAL DEVELOPMENT IN THE FETAL GASTROESOPHAGEAL JUNCTION 69
SUMMARY OF EPITHELIAL DEVELOPMENT OF THE ESOPHAGUS 77
CONTROL OF FOREGUT EPITHELIAL DEVELOPMENT 77
CHAPTER 4: Normal Anatomy Present Definition of the Gastroesophageal Junction
ANATOMY AND PHYSIOLOGY 83
ENDOSCOPIC/GROSS LANDMARKS 90
THE MEANING OF ENDOSCOPIC/GROSS LANDMARKS 92
PRESENT DEFINITION OF THE GASTROESOPHAGEAL JUNCTION 93
WHAT IS THE CARDIA? LET’S REMOVE THIS TERM FROM OUR VOCABULARY 101
THE LOGICAL CONCLUSION THAT SHOULD BE TESTED 104
CHAPTER 5: Histologic Definitions and Diagnosis of Epithelial Types 107
DEFINITIONS 107
PROBLEMS WITH THE DEFINITIONS 116
DIAGNOSIS OF DIFFERENT EPITHELIAL TYPES 119
CHAPTER 6: Cardiac Mucosa 125
WHAT IS CARDIAC MUCOSA? 125
WHERE IS CARDIAC MUCOSA LOCATED? 129
IS CARDIAC MUCOSA PRESENT IN EVERYONE? 135
WHAT IS OXYNTOCARDIAC MUCOSA, AND WHERE IS IT? 142
HOW MUCH CARDIAC AND OXYNTOCARDIAC MUCOSA ARE PRESENT? 145
WHAT DOES THE PRESENCE/ABSENCE AND AMOUNT OF CARDIAC MUCOSA MEAN? 146
WHAT DOES INCREASING LENGTH OF CARDIAC MUCOSA MEAN? 148
A HUMAN EXPERIMENT 149
SUMMARY STATEMENT REGARDING CARDIAC MUCOSA 150
CHAPTER 7: New Histologic Definitions of Esophagus, Stomach, and Gastroesophageal Junction 153
LET US ESTABLISH COMMON GROUND IN HISTOLOGY 153
LET US UNDERSTAND THE PROBLEM 159
NORMAL HISTOLOGY OF THE ESOPHAGUS AND STOMACH: A STATEMENT OF FACT AND NEW HISTOLOGIC DEFINITIONS 160
APPLICATION OF THESE DEFINITIONS TO PRACTICE 161
CHAPTER 8: Pathology of Reflux Disease at a Cellular Level: Part 1—Damage to Squamous Epithelium and Transformation into Cardiac Mucosa 165
REFLUX-INDUCED DAMAGE OF THE SQUAMOUS EPITHELIUM 167
COLUMNAR METAPLASIA OF THE SQUAMOUS EPITHELIUM 177
SUMMARY 185
CHAPTER 9: The Pathology of Reflux Disease at a Cellular Level: Part 2—Evolution of Cardiac Mucosa to Oxyntocardiac Mucosa and Intestinal Metaplasia 187
HISTOLOGIC COMPOSITION OF COLUMNAR-LINED ESOPHAGUS 187
CARDIAC TO OXYNTOCARDIAC MUCOSA: THE BENIGN GENETIC SWITCH 194
CARDIAC MUCOSA TO INTESTINAL METAPLASIA: THE SECOND GENETIC SWITCH 197
CHAPTER 10: Pathology of Reflux Disease at a Cellular Level: Part 3—Intestinal (Barrett) Metaplasia to Carcinoma 219
CARCINOGENESIS IN INTESTINAL METAPLASIA 219
DOES ADENOCARCINOMA ARISE IN ESOPHAGUS WITHOUT INTESTINAL (BARRETT) METAPLASIA? 220
NATURAL HISTORY OF DYSPLASIA: SURVEILLANCE FOR BARRETT ESOPHAGUS 225
DOES DYSPLASIA REVERSE? 236
THEORETICAL CONSIDERATIONS RELATING TO ADENOCARCINOMA DISTRIBUTION IN THE COLUMNAR-LINED ESOPHAGUS 236
ASSESSMENT OF CANCER RISK IN BARRETT ESOPHAGUS 239
CLINICALLY USEFUL MOLECULAR TESTS 244
CAUSE OF CARCINOGENESIS IN BARRETT ESOPHAGUS 249
CHAPTER 11: Pathology of Reflux Disease at an Anatomic Level 255
IDENTIFICATION AND VALIDATION OF THE TRUE GASTROESOPHAGEAL JUNCTION 259
THE ANATOMIC CHANGES ASSOCIATED WITH SLIDING HIATAL HERNIA 264
STAGES BETWEEN NORMAL AND SLIDING HIATAL HERNIA: THE REFLUX-DAMAGED DISTAL ESOPHAGUS—DEFINING THE END-STAGE ESOPHAGUS 265
RELATIONSHIP OF THE DILATED END-STAGE ESOPHAGUS TO COLUMNAR-LINED ESOPHAGUS 277
THE DISCREPANCY HAS NOW DISAPPEARED 279
ANATOMY AND HISTOLOGY OF A SLIDING HIATAL HERNIA 279
THE GREAT HISTORICAL MISUNDERSTANDING CONTINUES TO THE PRESENT 280
CHAPTER 12: Reflux Disease Limited to the Dilated End-Stage Esophagus: The Pathologic Basis of NERD 285
GASTROESOPHAGEAL REFLUX VERSUS REFLUX DISEASE 285
REFLUX DISEASE LIMITED TO THE DILATED END-STAGE ESOPHAGUS 286
A NEW LOOK AT INTESTINAL METAPLASIA OF THE GASTRIC CARDIA 300
A NEW LOOK AT ADENOCARCINOMA OF THE GASTRIC CARDIA 308
CHAPTER 13: Definition of Gastroesophageal Reflux Disease and Barrett Esophagus 315
PRESENTLY USED CRITERIA FOR DEFINING GASTROESOPHAGEAL REFLUX DISEASE 315
DEFINITIONS BASED ON QUANTITATING GASTROESOPHAGEAL REFLUX 320
PROPOSED NEW CRITERION FOR DEFINING GASTROESOPHAGEAL REFLUX DISEASE 323
REFLUX CARDITIS: A NEW ENTITY THAT DEFINES GASTROESOPHAGEAL REFLUX DISEASE WITH PERFECTION 325
A NEW DEFINITION OF BARRETT ESOPHAGUS 342
CHAPTER 14: Diagnosis of Gastroesophageal Reflux Disease, Barrett Esophagus, and Dysplasia 349
A NEW DIAGNOSTIC METHOD FOR REFLUX DISEASE 352
THE DIAGNOSIS OF REFLUX CARDITIS AND BARRETT ESOPHAGUS 359
THE DIAGNOSIS OF DYSPLASIA IN BARRETT ESOPHAGUS 361
CHAPTER 15: Research Strategies for Preventing Reflux-Induced Adenocarcinoma 375
MECHANISMS OF CELLULAR CHANGES IN REFLUX DISEASE 375
THE MECHANISM OF METAPLASIA: EPITHELIA DO NOT “MOVE” 377
THE REFLUX-ADENOCARCINOMA SEQUENCE 378
RECOGNITION OF DIFFERENT RISK LEVELS IN THE EPITHELIA OF COLUMNAR-LINED ESOPHAGUS 382
THE STATE OF PRESENT PHARMACEUTICAL INTERVENTION IN REFLUX DISEASE 384
ACID SUPPRESSIVE DRUGS PROMOTE ESOPHAGEAL ADENOCARCINOMA 385
PROPOSED NEW PHARMACEUTICAL RESEARCH TARGETS AIMED AT PREVENTING ADENOCARCINOMA 387
RESEARCH INTO SURGICAL METHODS OF PREVENTING ADENOCARCINOMA 390
IDENTIFYING FACTORS IN GASTRIC JUICE RESPONSIBLE FOR MOLECULAR EVENTS 391
MOLECULAR RESEARCH INTO CARCINOGENESIS 396
CHAPTER 16: Rationale for Treatment of Reflux Disease and Barrett Esophagus 399
THE PRESENT RATIONALE FOR TREATMENT OF REFLUX DISEASE 399
ACID SUPPRESSION WITH DRUGS AS TREATMENT FOR REFLUX DISEASE 400
DOES ACID SUPPRESSIVE DRUG THERAPY INCREASE THE RISK OF ADENOCARCINOMA? 409
ANTIREFLUX SURGERY AS TREATMENT FOR REFLUX DISEASE 411
ABLATION AS TREATMENT FOR BARRETT ESOPHAGUS 426
CHAPTER 17: Treatment Strategies for Preventing Reflux-Induced Adenocarcinoma 429
ASYMPTOMATIC VERSUS SYMPTOMATIC PATIENTS 430
PRESENT TREATMENT OF REFLUX DISEASE 430
OUTCOME OF PRESENT TREATMENT REGIMENS 435
REFLUX DISEASE IS THE PREMALIGNANT PHASE OF CANCER 435
ANTIREFLUX SURGERY CAN PREVENT PROGRESSION IN THE REFLUX TO ADENOCARCINOMA SEQUENCE CANCER CAN BE PREVENTED
DEFINITION OF THE BIOPSY PROTOCOL FOR INDEX DIAGNOSIS 439
CLASSIFICATION OF RISK BASED ON BIOPSY RESULTS 441
RECOMMENDATIONS FOR TREATMENT OF BIOPSY-DEFINED GROUPS 441
RECOMMENDED CHANGES IN THE TREATMENT OF DEFINED PATIENT GROUPS 444
COST OF ANTIREFLUX SURGERY 452
RESOURCES NEEDED TO IMPLEMENT RECOMMENDED CHANGES 453
SUMMARY OF RECOMMENDED CHANGES 454
Index 457
Color plate 467

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