Summary
Background
Present diagnosis and management of gastroesophageal reflux disease (GERD)
has resulted in a dramatic increase in the incidence of esophageal adenocarcinoma. This
is due to failure to identify pathologic changes of early GERD; at present, pathology is
limited to management of Barrett esophagus (BE).
Methods
Convincing evidence have confirmed that cardiac mucosa distal to the
squamocolumnar junction in the endoscopically normal person is a metaplastic GERD-induced esophageal epithelium, and not a normal proximal gastric epithelium.
Results
When cardiac mucosa is recognized as a metaplastic esophageal epithelium, it
becomes self-evident that the present endoscopic definition of the gastro-esophageal
junction is incorrect, and there exists a dilated distal esophagus (DDE) in what is
incorrectly termed the “gastric cardia” presently mistaken for proximal stomach. It also
becomes clear that the length of the DDE correlates with the presence and severity of
GERD and represents the pathology of the entire spectrum of GERD. Further, it allows
recognition that the DDE, measured as the gap between esophageal squamous epithelium
and gastric oxyntic mucosa that is composed of cardiac mucosa, represents the pathologic
anatomy of damage to the abdominal segment of the lower esophageal sphincter (LES).
Conclusion
The new understanding of the significance of cardiac mucosa provides a new and highly accurate histologic method of assessment of LES damage, the primary cause of
GERD. This opens a new door to complete histologic assessment of GERD from its etiologic standpoint and to new research that permit early diagnosis of GERD at its outset.
Ultimately, such early diagnosis has the potential to reverse the increasing trend of
esophageal adenocarcinoma.
New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage