Image-Enhanced Endoscopy and Molecular Biomarkers Vs Seattle Protocol to Diagnose Dysplasia in Barrett's Esophagus.


Journal

Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
ISSN: 1542-7714
Titre abrégé: Clin Gastroenterol Hepatol
Pays: United States
ID NLM: 101160775

Informations de publication

Date de publication:
11 2022
Historique:
received: 15 11 2021
revised: 21 01 2022
accepted: 28 01 2022
pubmed: 21 2 2022
medline: 2 11 2022
entrez: 20 2 2022
Statut: ppublish

Résumé

Dysplasia in Barrett's esophagus often is invisible on high-resolution white-light endoscopy (HRWLE). We compared the diagnostic accuracy for inconspicuous dysplasia of the combination of autofluorescence imaging (AFI)-guided probe-based confocal laser endomicroscopy (pCLE) and molecular biomarkers vs HRWLE with Seattle protocol biopsies. Barrett's esophagus patients with no dysplastic lesions were block-randomized to standard endoscopy (HRWLE with the Seattle protocol) or AFI-guided pCLE with targeted biopsies for molecular biomarkers (p53 and cyclin A by immunohistochemistry; aneuploidy by image cytometry), with crossover to the other arm after 6 to 12 weeks. The primary end point was the histologic diagnosis from all study biopsies (trial histology). A sensitivity analysis was performed for overall histology, which included diagnoses within 12 months from the first study endoscopy. Endoscopists were blinded to the referral endoscopy and histology results. The primary outcome was diagnostic accuracy for dysplasia by real-time pCLE vs HRWLE biopsies. Of 154 patients recruited, 134 completed both arms. In the primary outcome analysis (trial histology analysis), AFI-guided pCLE had similar sensitivity for dysplasia compared with standard endoscopy (74.3%; 95% CI, 56.7-87.5 vs 80.0%; 95% CI, 63.1-91.6; P = .48). Multivariate logistic regression showed pCLE optical dysplasia, aberrant p53, and aneuploidy had the strongest correlation with dysplasia (secondary outcome). This 3-biomarker panel had higher sensitivity for any grade of dysplasia than the Seattle protocol (81.5% vs 51.9%; P < .001) in the overall histology analysis, but not in the trial histology analysis (91.4% vs 80.0%; P = .16), with an area under the receiver operating curve of 0.83. Seattle protocol biopsies miss dysplasia in approximately half of patients with inconspicuous neoplasia. AFI-guided pCLE has similar accuracy to the current gold standard. The addition of molecular biomarkers could improve diagnostic accuracy.

Sections du résumé

BACKGROUND & AIMS
Dysplasia in Barrett's esophagus often is invisible on high-resolution white-light endoscopy (HRWLE). We compared the diagnostic accuracy for inconspicuous dysplasia of the combination of autofluorescence imaging (AFI)-guided probe-based confocal laser endomicroscopy (pCLE) and molecular biomarkers vs HRWLE with Seattle protocol biopsies.
METHODS
Barrett's esophagus patients with no dysplastic lesions were block-randomized to standard endoscopy (HRWLE with the Seattle protocol) or AFI-guided pCLE with targeted biopsies for molecular biomarkers (p53 and cyclin A by immunohistochemistry; aneuploidy by image cytometry), with crossover to the other arm after 6 to 12 weeks. The primary end point was the histologic diagnosis from all study biopsies (trial histology). A sensitivity analysis was performed for overall histology, which included diagnoses within 12 months from the first study endoscopy. Endoscopists were blinded to the referral endoscopy and histology results. The primary outcome was diagnostic accuracy for dysplasia by real-time pCLE vs HRWLE biopsies.
RESULTS
Of 154 patients recruited, 134 completed both arms. In the primary outcome analysis (trial histology analysis), AFI-guided pCLE had similar sensitivity for dysplasia compared with standard endoscopy (74.3%; 95% CI, 56.7-87.5 vs 80.0%; 95% CI, 63.1-91.6; P = .48). Multivariate logistic regression showed pCLE optical dysplasia, aberrant p53, and aneuploidy had the strongest correlation with dysplasia (secondary outcome). This 3-biomarker panel had higher sensitivity for any grade of dysplasia than the Seattle protocol (81.5% vs 51.9%; P < .001) in the overall histology analysis, but not in the trial histology analysis (91.4% vs 80.0%; P = .16), with an area under the receiver operating curve of 0.83.
CONCLUSIONS
Seattle protocol biopsies miss dysplasia in approximately half of patients with inconspicuous neoplasia. AFI-guided pCLE has similar accuracy to the current gold standard. The addition of molecular biomarkers could improve diagnostic accuracy.

Identifiants

pubmed: 35183768
pii: S1542-3565(22)00189-6
doi: 10.1016/j.cgh.2022.01.060
pii:
doi:

Substances chimiques

Tumor Suppressor Protein p53 0
Biomarkers 0

Types de publication

Clinical Trial Protocol Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2514-2523.e3

Subventions

Organisme : Cancer Research UK
Pays : United Kingdom
Organisme : Department of Health
Pays : United Kingdom
Organisme : Medical Research Council
ID : RG84369
Pays : United Kingdom

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Mathew Vithayathil (M)

Medical Research Council Cancer Unit, University of Cambridge, United Kingdom.

Ines Modolell (I)

Department of Gastroenterology, University Hospital National Health Service Foundation Trust, United Kingdom.

Jacobo Ortiz-Fernandez-Sordo (J)

Nottingham Digestive Diseases Centre, National Institute of Health Research Nottingham Biomedical Research Centre, United Kingdom.

Dahmane Oukrif (D)

Department of Histopathology, University College London Hospital, Longdon, United Kingdom.

Apostolos Pappas (A)

Medical Research Council Cancer Unit, University of Cambridge, United Kingdom.

Wladyslaw Januszewicz (W)

Medical Research Council Cancer Unit, University of Cambridge, United Kingdom; Department of Gastroenterology, Hepatology and Clinical Oncology, Medical Centre for Postgraduate Education, Warsaw, Poland.

Maria O'Donovan (M)

Department of Histopathology, Cambridge University Hospital National Health Service Foundation Trust, United Kingdom.

Andreas Hadjinicolaou (A)

Medical Research Council Cancer Unit, University of Cambridge, United Kingdom; Department of Gastroenterology, University Hospital National Health Service Foundation Trust, United Kingdom.

Michele Bianchi (M)

Medical Research Council Cancer Unit, University of Cambridge, United Kingdom.

Adrienn Blasko (A)

Medical Research Council Cancer Unit, University of Cambridge, United Kingdom.

Jonathan White (J)

Nottingham Digestive Diseases Centre, National Institute of Health Research Nottingham Biomedical Research Centre, United Kingdom.

Philip Kaye (P)

Department of Histopathology, Nottingham University Hospitals National Health Service Trust, University of Nottingham, United Kingdom.

Marco Novelli (M)

Department of Histopathology, University College London Hospital, Longdon, United Kingdom.

Lorenz Wernisch (L)

BIOS Health, Ltd, Cambridge, United Kingdom; Medical Research Council Biostatistics Unit, University of Cambridge, United Kingdom.

Krish Ragunath (K)

Nottingham Digestive Diseases Centre, National Institute of Health Research Nottingham Biomedical Research Centre, United Kingdom.

Massimiliano di Pietro (M)

Medical Research Council Cancer Unit, University of Cambridge, United Kingdom; Department of Gastroenterology, University Hospital National Health Service Foundation Trust, United Kingdom. Electronic address: md460@cam.ac.uk.

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