Risk of Conventional Dysplasia and Adenocarcinoma in Patients with Barrett's Esophagus and Crypt Dysplasia: A Prospective Follow-Up Study of 214 Patients
A Srivastava, DP Coco, CA Sanchez, DS Cowan, RD Odze. Dartmouth Hitchcock Medical Center, Lebanon; Brigham & Women's Hospital, Boston; Fred Hutchinson Cancer Center & University of Washington, Seattle
Background: We have previously reported clinical and molecular data to support the theory that dysplasia in Barrett's esophagus (BE) begins in the crypt bases and progresses to evolve the surface epithelium with time. The aim of this study was to evaluate the association of crypt dysplasia (CD) with conventional full-crypt dysplasia, and with esophageal adenocarcinoma (EA), in a large prospective follow up study of high risk BE patients with long term follow up.
Design: 3999 routinely processed esophageal biopsies from 214 patients (M/F ratio: 170/44, mean age: 63 years, mean BE segment length: 5.7 cm) followed for a mean of 90.4 months (range: 2.3-176 months), all of whom had a baseline endoscopy between 1995-1999 and at least one follow up endoscopy, were included in the study. None of the patients had adenocarcinoma at, or prior to, baseline endoscopy. All biopsies were evaluated in a blinded fashion for the presence and grade of conventional low (LGD) and high grade dysplasia, (HGD), and for CD, defined as per previously published criteria as dysplasia-like changes limited to the crypt bases but without evidence of surface involvement.
Results: Of the 214 pts, 20 patients had CD (9.3%), 22 (10.3%) patients had LGD, and 16 (7.5%) patients had HGD at baseline endoscopy. Overall, 13/20 (65%) CD patients had synchronous or metachronous conventional dysplasia or cancer upon follow up. Of the 20 pts with CD at baseline endoscopy, 5 (25%) CD patients had synchronous LGD, 3 (15%) had HGD, and 12 (60%) did not have conventional LGD or HGD. Upon follow-up, 2/12 CD patients without conventional dysplasia developed LGD (16.7%), 2 (16.7%) developed HGD, and 1 (8.3%) developed adenocarcinoma at the time of most recent endoscopy. In addition, 2 of the CD cases with synchronous conventional dysplasia at baseline also developed EA upon follow up.
Conclusions: Our data provides evidence that CD represents an early precursor of conventional dysplasia in BE. The finding of CD in a biopsy specimen from patients with BE should alert the pathologist to the possibility of synchronous or metachronous dysplasia or cancer. Larger studies with adenocarcinoma as the principle outcome are needed to validate these findings.
Wednesday, March 24, 2010 9:30 AM
Poster Session V # 67, Wednesday Morning