Paneth cell metaplasia is seen in 31% of cases of Barrett's esophagus. It is more commonly seen in non-dysplastic Barrett's esophagus and Barrett's with indefinite or low-grade dysplasia. The presence of Paneth cell metaplasia is associated with less regression of Barrett's esophagus, though it does not increase risk of progression. Patients without Paneth cell metaplasia were three times more likely to experience regression of Barrett's esophagus.

1. Journal Club
Dr. Akshay Agarwal
Moderator: Dr. Shilpi Sahu

2. Significance of Paneth Cell
Metaplasia in Barrett
Esophagus
A Morphologic and Clinicopathologic study
Authors:
Wei Chen, MD, Wendy L. Frankel, MD, Xiaoping
Zhou, MD, Martha M. Yearsley, MD (Department
of Pathology)
Kevin M. Cronley, MD (Gastroenterology,
Hepatobiliary and Nutrition)
Lianbo Yu, PhD (Center for Biostatistics)
The Ohio State Univeristy Wexner Medical Center,
Columbus

4. Published in American Journal of Clinical
Pathology
May 2015
Volume 143
Issue 5
Page 665-671

8. Metaplasia
Adaptive Change of One Mature epithelium to a
different Mature epithelium in response to a
stimulus
Types of Metaplasia related to our context:
Intestinal Metaplasia (Barrett Esophagus)
Paneth Cell Metaplasia

9. Dr. Norman Barrett
1903–1979

10. Australian born Britisher
Thoracic Surgeon
Adelaide, Australia. Year 195

12. Barrett’s Esophagus
Barrett first described the columnar metaplasia in
1950.
An association with gastroesophageal reflux was
made in 1953.
An association with adenocarcinoma was made
in 1975.

18. Risk Factors
Barrett's esophagus occurs due to chronic
inflammation due to:
GERD
Swallowing a corrosive substance such as lye.
• Complications:
• Peptic Ulcer
• Stricture
• Dysplasia
• Adenocarcinoma

21. Categories for Dysplasia
Negative for dysplasia
Indefinite for dysplasia
Low grade
High grade
Intra-mucosal Adenocarcinoma

25. Introduction
Increase in 6-fold incidence of Esophageal
Adenocarcinoma in the past 30 years
Most develop from Barrett Esophagus
It carries 0.5% annual increased risk for
malignancy

26. Consequences of Barrett
Esophagus
Barrett
Esophagus
High Grade
Dysplasia
Adenocarcinoma
Regress
to normal
Stay or regress

27. In a Nut Shell

28. Material and Methods
Inclusion Criteria:
Esophageal Biopsy specimen with a diagnosis of
Intestinal Metaplasia (957 cases)
Cases available for review (757 cases)
Cases that had complete clinical follow up data
for atleast 1 year. (299 cases)
Length of Barrett esophagus segment
Duration of Disease
Proton Pump Inhibitor treatment history

29. Exclusion Criteria:
Cases treated with Endoscopic mucosal
resection, radiofrequency ablation,
esophagectomy
Cases with initial diagnosis of esophageal
Adenocarcinoma.

30. Results
Paneth cell Metaplasia
Age: 24-88 yr
M:F – 1.8:1
No Paneth cell
Metaplasia
22-92 yr
2.4:1

31. Paneth cells identified in 31% (234/757)
PCM was found more in IM with No dysplasia
(31%)
PCM was also present in Indefinite for dysplasia
and Low grade dysplasia category (37%)
PCM was lower in High grade dysplasia (13%)

32. Group
(cases
)
NFD
(626)
IFD
(48)
LGD
(38)
HGD
(24)
EAC
(21)
PCM 31% 38% 37% 21% 5%
NPCM 69% 62% 63% 79% 95%

33. PCM more in long segment (37%) than short
segment (24%) Barrett Esophagus.
NO significant difference in the prevalence of
PCM between patients who had PPI therapy and
who didn’t.

34. Follow up Results
Out of 299 cases, in the group of PCM with BE,
69% cases remained the same
11% progressed to higher grade of dysplasia or
Ca.
20% regressed to lesser grades of dysplasia, no
dysplasia or even no IM
In the group of No PCM with BE,
31% regressed

35. Conclusion
No PCM patients were 3 times more likely to
regress
Patients with short-segment BE were 4 times
more likely to regress
Patients with BE positive for dysplasia were 7.8
times likely to progress
Male BE were 10 times more likely to progress

36. Take Home Message
Paneth Cell Metaplasia is associated with less
disease regression and is not associated with
more disease progression.