Esophagus

3 - Progression of Barrett’s Esophagus (BE) and Dysplasia Detected by Wide Area Transepithelial Sampling With Computer-Assisted 3D Analysis (WATS3D) Confirms the Clinical Significance of Crypt Dysplasia

Monday, October 8
8:24 AM - 8:36 AM
Location: Terrace Ballroom (level 400)

Category: Esophagus
Nicholas J. Shaheen, MD, MPH, FACG1, Michael S. Smith, MD, MBA2, John R. Goldblum, MD3, Robert D. Odze, MD4
1University of North Carolina, Chapel Hill, NC; 2Mount Sinai West & Mount Sinai St. Luke's Hospitals, New York, NY; 3Cleveland Clinic, cleveland, OH; 4Harvard Medical School, Boston, MA

Award: ACG Governors Award for Excellence in Clinical Research

Introduction: Endoscopic surveillance of BE is performed to identify progression to neoplasia. WATS3D sampling (CDx Diagnostics, Suffern, NY), an adjunct to forceps biopsy, uses brush cytology to evaluate routine histologic and cytologic features.  While the diagnosis of non-dysplastic BE (NDBE), low-grade dysplasia (LGD) and high-grade dysplasia (HGD) on WATS is made using standard biopsy tissue morphologic criteria, BE with crypt dysplasia (CD) is diagnosed in instances where dysplasia-like atypia involves the crypts, but not the surface epithelium (figure). The importance of CD is unclear. Our aim was to assess the risk of progression of WATS-reported CD to HGD/EAC, and to compare this to the progression rate of both WATS-detected NDBE and WATS-detected LGD.

Methods: We analyzed patients (pts) who underwent WATS as part of routine care from 2013-2018.  Eligible pts had two WATS ≥6 months apart. Pts were categorized by initial WATS findings (NDBE, CD and LGD).  Pt-years (pt-yrs) of observation were calculated by multiplying the mean period of follow-up by the number of pts with each histology.  Progression, defined as a subsequent WATS finding of either HGD or EAC, was assessed for each group.  The crude progression rate, expressed as percent progressing per pt-yr, was calculated.

Results: A total of 151,224 WATS cases (76% male, mean age 68) were catalogued, with 43,145 (29%) having goblet cell metaplasia. Of these, 4,512 pts had two samples separated by ≥6 months.  A total of 4,049 pts who had NDBE on baseline WATS were followed for an average of 1.4 yrs between assays (5,736 pt-yrs total) and experienced 19 progressions to HGD/EAC, for a rate of 0.33%/pt-yr.  An additional 380 pts had CD on baseline WATS and were followed for a mean of 1.25 yrs between assays (475 pt-yrs total).  These pts experienced 10 progressions to HGD/EAC, for a rate of 2.1%/pt-yr. The overall rate of progression of CD to any neoplasia (LGD/HGD/EAC) was 9.9%/pt-yr. Finally, 83 pts had WATS-detected LGD at baseline and were followed for a mean of 1.25 years between assays (103.7 pt-yrs total).  These LGD pts experienced 8 progressions to HGD/EAC, for a rate of 7.7%/pt-yr (Table).

Discussion: A finding of NDBE or LGD on WATS predicts progression to HGD/EAC at rates that are comparable to, or higher than, the reported risk of progression in forceps biopsy-confirmed NDBE and LGD.  Crypt dysplasia reported on WATS has a risk of progression comparable to that of forceps biopsy-confirmed LGD.

WATS Computer Synthesized En Face View of Crypt Dysplasia. Computer synthesized 3-dimensional en face image of the crypt reveals dysplastic effacement of the honeycomb pattern (top tissue fragment) when compared to NDBE (lower tissue fragment).
Table. Progression rates of NDBE (BE), CD, and LGD to more severe dysplasia.

Disclosures:
Nicholas Shaheen: CDx Medical – Grant/Research Support.
Michael Smith: CDx Diagnostics – Consultant, Grant/Research Support.
John Goldblum: CDx Medical – Grant/Research Support.
Robert Odze: CDx Medical – Grant/Research Support.

Nicholas J. Shaheen

Professor of Medicine and Epidemiology; Chief, Division of Gastroenterology and Hepatology
University of North Carolina
Chapel Hill, NC, US

Nicholas Shaheen, MD, MPH, FACG, is the Bozymski-Heizer Distinguished Professor of Medicine at the University of North Carolina School of Medicine, and the Chief of the Division of Gastroenterology and Hepatology at UNC. Dr. Shaheen completed his undergraduate degree at Harvard University and earned his medical degree at the University of Chicago, Pritzker School of Medicine, where he also completed his internship and residency. He completed his clinical fellowship training at the University of North Carolina (UNC), where he also earned his masters degree at the School of Public Health. Concurrently, he completed a National Institutes of Health-sponsored fellowship in Epidemiology. He joined the faculty at UNC in 1998. His research interest is in the epidemiology and management of esophageal diseases. He is the author of over 300 journal articles related to reflux disease, eosinophilic esophagitis, Barrett's esophagus, and esophageal cancer. Dr. Shaheen receives research funding from the National Institutes of Health and multiple private foundations and corporations to pursue clinical and translational research in esophageal diseases. Dr. Shaheen is a past president of the North Carolina Society of Gastroenterology, past Chairman of the Clinical Practice section of the AGA, and currently is the Director of the ACG Institute. He is a Fellow of the ACG, AGA, and ACP.

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3 - Progression of Barrett’s Esophagus (BE) and Dysplasia Detected by Wide Area Transepithelial Sampling With Computer-Assisted 3D Analysis (WATS3D) Confirms the Clinical Significance of Crypt Dysplasia



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