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Diagnosing and Treating GERD from the Viewpoint of the LES
Gastroesophageal reflux disease (GERD) affects 30% of persons in the USA. It is caused by a failure of the lower esophageal sphincter mechanism that prevents reflux of gastric contents into the esophagus.
Despite this knowledge, GERD is treated primarily with acid suppressive drug therapy. While this controls symptoms of GERD, it does not reverse or prevent progression of lower esophageal sphincter (LES) damage. It does not decrease reflux. In a significant minority of patients, LES damage progresses despite acid suppression, to cause severe GERD. This leads to failure to control symptoms and complications like Barrett esophagus that lead to cancer. Esophageal adenocarcinoma resulting from GERD has increased 7-fold from 1975 and continues to increase. In 2017, it will result in the death of more than 15,000 people in the USA. Present medical treatment does nothing to address this issue.
A new method of diagnosing and treating GERD from the viewpoint of the LES, defining its normal state and understanding how it is damaged is urgently needed. It develops new pathologic criteria for measuring LES damage and predicting its future progression. New algorithms permit predicting, at any point in a person’s life, who will never develop GERD, who will develop GERD and remain controlled with medical therapy, and who will progress to severe GERD with treatment failure and risk of cancer. Identification of the last group at an early stage allow implementation of measures that are aimed at preventing future failure of medical treatment, Barrett esophagus and esophageal adenocarcinoma.
The new method of assessment of abdominal LES damage by pathology provides a new way to assess GERD. Existing evidence show a strong correlation between manometric abdominal LES length with cellular damage. These provide a theoretical basis for extrapolating abdominal LES damage (which is inversely related to manometric abdominal LES length) with cellular changes.
Everyone today mistakes early damage of gastroesophageal reflux disease as the proximal stomach. Recognizing this allows a new method of understanding the pathogenesis of GERD and its diagnosis.
These figures show the three errors made by physicians today: (a) They mistake the dilated distal esophagus that is lined by cardiac epithelium as part of the anatomical proximal stomach. (b) They mistake metaplastic cardiac epithelium of the damaged distal esophagus as normal proximal gastric epithelium. (c) They define the end of the esophagus (the gastroesophageal junction) as the end of the tube, 10 mm proximal to the true GE junction.
When the abdominal LES is damaged beyond its reserve capacity, it fails, first in the postprandial phase when it is subjected to the stress of gastric over-distension. From this onset of reflux and clinical GERD, the severity of reflux and cellular changes in the thoracic esophagus increases as LES damage progresses to complete destruction of the
entire abdominal LES.
Fig 16.3a and b shows the normal state as a drawing (a) and a diagrammatic representation (b). The abdominal segment of the lower esophageal sphincter is 35 mm long and the entire abdominal esophagus s a tube lined by squamous epithelium (gray in the drawing and blue in the diagram). It transitions to gastric oxyntic epithelium (blue in the drawing; white in the diagram) at the gastroesophageal junction.
Fig 16.6a and b shows the early damage to the lower esophageal sphincter. The abdominal length of the sphincter is now 25 mm with 10 mm being damaged. The 10 mm of the damaged sphincter is lined by metaplastic cardiac epithelium (green and purple in the drawing and red in the diagram) that has replaced the normal squamous epithelium. The part of the LES that has been damaged is dilated, appearing anatomically like the stomach. The tubal part of the abdominal esophagus that is lined by squamous epithelium has shortened by 10 mm.
To learn more about this new method of diagnosing and treating GERD from the viewpoint of LES, look at this complimentary free chapter, Progression of GERD from the Perspective of LES Damage. In this chapter, I have created a theoretical construct of what happens when the abdominal LES undergoes damage in increments of 5 mm. This shows that there is a phase of compensated LES damage where the abdominal LES is damaged but retains functional competence. There is no LES failure or reflux.
About the Book:
GERD: A New Understanding of Pathology, Pathophysiology, and Treatment transforms the assessment of gastroesophageal reflux disease (GERD) from its present state, which is largely dependent on clinical definition and management, to a more objective scientific basis that depends on pathologic assessment.
- Provides a new method of assessment of GERD that has never previously been presented, creating a pathway to control.
- Describes a new pathologic test based on standard histology that can define lower esophageal sphincter damage.
- Sequential chapters outline the way GERD progresses from the perspective of the amount of damage to the lower esophageal sphincter.
- Provides new avenues of clinical research and technologic innovations in pathology and treatment aimed at preventing esophageal adenocarcinoma.
About the Author:
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.
If you found this article stimulating, you may be interested in accessing the entire book content on ScienceDirect. We are pleased to offer you a free chapter called “Progression of GERD From the Perspective of LES Damage.”
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