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Barrett esophagus 2
Lecture 4
Norman Barrett
• Norman Rupert Barrett (1903-1979) was
an Australian-born British thoracic
surgeon who is primarily remembered
for describing Barrett’s oesophagus in
1950.
Barret esophagus
• Barrett's oesophagus, sometimes called
Barrett syndrome or
• Columnar epithelium lined lower oesophagus (CELLO).
Barrett Esophagus
Barrett esophagus is a complication of
chronic GERD ( 5-15%) that is characterized by
intestinal metaplasia within
the esophageal squamous mucosa.
• Barrett esophagus is defined as the replacement
of the normal distal stratified squamous mucosa
by metaplastic columnar epithelium containing
goblet cells.
Epidemiology
• The incidence of Barrett esophagus is rising,
and it is estimated to occur in as many as 10%
of individuals with symptomatic GERD.
• Barrett esophagus is most common in white
(Caucasian) males and it typically presents between
40 and 60 years of age.
• The greatest concern in Barrett esophagus is
that it confers an increased risk of
esophageal adenocarcinoma.
A pre-malignant condition
Molecular studies suggest that
Barrett epithelium may be more
similar to adenocarcinoma than
to normal esophageal epithelium,
consistent with the view that
Barrett esophagus is a pre-
malignant condition.
Epithelial dysplasia
Epithelial dysplasia, considered to be
a pre-invasive lesion, is detected in
0.2% to 2.0% of persons with
Barrett esophagus each year and is
associated with prolonged
symptoms and increased patient
age
90%Although the vast majority of esophageal
adenocarcinomas are associated with Barrett
esophagus,
it is important to remember that most
(90%) individuals with Barrett
esophagus do not develop esophageal
tumors.
Red Patches
Barrett esophagus can be recognized as one or
several tongues or patches of red, velvety
mucosa extending upward from the
gastroesophageal junction.
Alternates
Metaplastic mucosa
alternates with residual
smooth, pale squamous
(esophageal) mucosa and
interfaces with light-brown columnar
(gastric) mucosa distally.
Long segment & Short segment
High-resolution endoscopes have increased the
sensitivity of Barrett esophagus detection. This
has led to subclassification of Barrett esophagus
as long segment, in which 3 cm or more of
esophagus is involved, or short segment, in
which less than 3 cm is involved. It is not yet
clear if the risk of dysplasia in short segment
disease is less than in long segment Barrett
esophagus.
Long-segment Barrett’s esophagus
NEJM 2002; 346: 836
Short Segment Barrett’s
Irregular z-line above hiatal hernia
Courtesy of Dr. C. Mel WilcoxCourtesy of Dr. C. Mel Wilcox
What we want to prevent --
Cancer Arising in Barrett’s
Courtesy of Dr. C. Mel WilcoxCourtesy of Dr. C. Mel Wilcox
Diagnosis• Diagnosis of Barrett esophagus requires both
endoscopic evidence of abnormal mucosa above
the gastroesophageal junction and histologically
documented intestinal metaplasia.
Goblet cells
• Goblet cells, which have distinct mucous vacuoles
that stain pale blue by H&E and impart the shape
of a wine goblet to the remaining
cytoplasm, define intestinal metaplasia and are
necessary for diagnosis of
Barrett esophagus
Goblet Cells
Intestinal metaplasia
• The requirement for intestinal metaplasia
reflects the fact that this feature correlates
with neoplastic risk.
• Foveolar mucus cells, which do not have
distinct mucous vacuoles are insufficient for
diagnosis.
Role of Endoscopy
The requirement for an endoscopic abnormality
helps to prevent misdiagnosis
if metaplastic goblet cells within the cardia are
included in the biopsy.
Dysplasia
• When dysplasia is present, it is classified as low
grade or high grade. Increased epithelial
proliferation, often with atypical mitoses,
nuclear hyperchromasia and stratification,
irregularly clumped chromatin, increased
nuclear-to-cytoplasmic ratio, and a failure of
epithelial cells to mature as they migrate to the
esophageal surface are present in both grades
of dysplasia.
Dysplasia cont.
• Gland architecture is frequently abnormal
and is characterized by budding, irregular
shapes, and cellular crowding.
• High-grade dysplasia exhibits more severe
cytologic and architectural changes.
Intramucosal carcinoma is
characterized by invasion of
neoplastic epithelial cells into the
lamina propria.
Barrett esophagus. A, Normal gastroesophageal junction. B, Barrett
esophagus. Note the small islands of paler squamous mucosa within the Barrett mucosa. C,
Histologic appearance of the gastroesophageal junction in Barrett esophagus. Note the
transition between esophageal squamous mucosa (left) and Barrett metaplasia, with
abundant metaplastic goblet cells (right).
Clinical Features.
• Barrett esophagus can only be identified thorough
endoscopy and biopsy,
which are usually prompted by GERD symptoms
(dysphagia, heartburn,
regurgitation of sour-tasting
gastric contents & attacks of
severe chest pain).
Treatment
Surgical resection, or esophagectomy,
Photodynamic therapy,
Laser ablation, and
Endoscopic mucosectomy.
Future Hope
Management of esophageal dysplasia is evolving,
and it is hoped that improved molecular
understanding of neoplastic progression
may allow development of chemopreventive
approaches that reduce incidence of
esophageal adenocarcinoma.
Points to Remember
1. In Barrett's esophagus, the tissue lining the esophagus is
replaced by tissue that is similar to the lining of the intestine.
2. Barrett's esophagus is associated with gastroesophageal reflux
disease (GERD).
3. Improvement in GERD symptoms with acid-reducing drugs may
decrease the risk of developing Barrett's esophagus.
4. Barrett's esophagus is diagnosed through an upper
gastrointestinal endoscopy and biopsies.
5. People who have Barrett's esophagus should have periodic
surveillance endoscopies and biopsies.
6. Endoscopic treatments are used to destroy Barrett's tissue,
which will hopefully be replaced with normal esophageal tissue.
7. Removal of most of the esophagus is recommended if a person
with Barrett's esophagus is found to have severe dysplasia or
cancer and can tolerate a surgical procedure.
L4 barrett esophagus 2

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L4 barrett esophagus 2

  • 2. Norman Barrett • Norman Rupert Barrett (1903-1979) was an Australian-born British thoracic surgeon who is primarily remembered for describing Barrett’s oesophagus in 1950.
  • 3. Barret esophagus • Barrett's oesophagus, sometimes called Barrett syndrome or • Columnar epithelium lined lower oesophagus (CELLO).
  • 4. Barrett Esophagus Barrett esophagus is a complication of chronic GERD ( 5-15%) that is characterized by intestinal metaplasia within the esophageal squamous mucosa. • Barrett esophagus is defined as the replacement of the normal distal stratified squamous mucosa by metaplastic columnar epithelium containing goblet cells.
  • 5.
  • 6. Epidemiology • The incidence of Barrett esophagus is rising, and it is estimated to occur in as many as 10% of individuals with symptomatic GERD. • Barrett esophagus is most common in white (Caucasian) males and it typically presents between 40 and 60 years of age. • The greatest concern in Barrett esophagus is that it confers an increased risk of esophageal adenocarcinoma.
  • 7. A pre-malignant condition Molecular studies suggest that Barrett epithelium may be more similar to adenocarcinoma than to normal esophageal epithelium, consistent with the view that Barrett esophagus is a pre- malignant condition.
  • 8. Epithelial dysplasia Epithelial dysplasia, considered to be a pre-invasive lesion, is detected in 0.2% to 2.0% of persons with Barrett esophagus each year and is associated with prolonged symptoms and increased patient age
  • 9. 90%Although the vast majority of esophageal adenocarcinomas are associated with Barrett esophagus, it is important to remember that most (90%) individuals with Barrett esophagus do not develop esophageal tumors.
  • 10. Red Patches Barrett esophagus can be recognized as one or several tongues or patches of red, velvety mucosa extending upward from the gastroesophageal junction.
  • 11. Alternates Metaplastic mucosa alternates with residual smooth, pale squamous (esophageal) mucosa and interfaces with light-brown columnar (gastric) mucosa distally.
  • 12. Long segment & Short segment High-resolution endoscopes have increased the sensitivity of Barrett esophagus detection. This has led to subclassification of Barrett esophagus as long segment, in which 3 cm or more of esophagus is involved, or short segment, in which less than 3 cm is involved. It is not yet clear if the risk of dysplasia in short segment disease is less than in long segment Barrett esophagus.
  • 14. Short Segment Barrett’s Irregular z-line above hiatal hernia Courtesy of Dr. C. Mel WilcoxCourtesy of Dr. C. Mel Wilcox
  • 15. What we want to prevent -- Cancer Arising in Barrett’s Courtesy of Dr. C. Mel WilcoxCourtesy of Dr. C. Mel Wilcox
  • 16. Diagnosis• Diagnosis of Barrett esophagus requires both endoscopic evidence of abnormal mucosa above the gastroesophageal junction and histologically documented intestinal metaplasia.
  • 17. Goblet cells • Goblet cells, which have distinct mucous vacuoles that stain pale blue by H&E and impart the shape of a wine goblet to the remaining cytoplasm, define intestinal metaplasia and are necessary for diagnosis of Barrett esophagus
  • 19. Intestinal metaplasia • The requirement for intestinal metaplasia reflects the fact that this feature correlates with neoplastic risk. • Foveolar mucus cells, which do not have distinct mucous vacuoles are insufficient for diagnosis.
  • 20. Role of Endoscopy The requirement for an endoscopic abnormality helps to prevent misdiagnosis if metaplastic goblet cells within the cardia are included in the biopsy.
  • 21.
  • 22. Dysplasia • When dysplasia is present, it is classified as low grade or high grade. Increased epithelial proliferation, often with atypical mitoses, nuclear hyperchromasia and stratification, irregularly clumped chromatin, increased nuclear-to-cytoplasmic ratio, and a failure of epithelial cells to mature as they migrate to the esophageal surface are present in both grades of dysplasia.
  • 23. Dysplasia cont. • Gland architecture is frequently abnormal and is characterized by budding, irregular shapes, and cellular crowding. • High-grade dysplasia exhibits more severe cytologic and architectural changes. Intramucosal carcinoma is characterized by invasion of neoplastic epithelial cells into the lamina propria.
  • 24. Barrett esophagus. A, Normal gastroesophageal junction. B, Barrett esophagus. Note the small islands of paler squamous mucosa within the Barrett mucosa. C, Histologic appearance of the gastroesophageal junction in Barrett esophagus. Note the transition between esophageal squamous mucosa (left) and Barrett metaplasia, with abundant metaplastic goblet cells (right).
  • 25. Clinical Features. • Barrett esophagus can only be identified thorough endoscopy and biopsy, which are usually prompted by GERD symptoms (dysphagia, heartburn, regurgitation of sour-tasting gastric contents & attacks of severe chest pain).
  • 26. Treatment Surgical resection, or esophagectomy, Photodynamic therapy, Laser ablation, and Endoscopic mucosectomy.
  • 27. Future Hope Management of esophageal dysplasia is evolving, and it is hoped that improved molecular understanding of neoplastic progression may allow development of chemopreventive approaches that reduce incidence of esophageal adenocarcinoma.
  • 28. Points to Remember 1. In Barrett's esophagus, the tissue lining the esophagus is replaced by tissue that is similar to the lining of the intestine. 2. Barrett's esophagus is associated with gastroesophageal reflux disease (GERD). 3. Improvement in GERD symptoms with acid-reducing drugs may decrease the risk of developing Barrett's esophagus. 4. Barrett's esophagus is diagnosed through an upper gastrointestinal endoscopy and biopsies. 5. People who have Barrett's esophagus should have periodic surveillance endoscopies and biopsies. 6. Endoscopic treatments are used to destroy Barrett's tissue, which will hopefully be replaced with normal esophageal tissue. 7. Removal of most of the esophagus is recommended if a person with Barrett's esophagus is found to have severe dysplasia or cancer and can tolerate a surgical procedure.