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Confocal laser endomicroscopy: A new gold standard for the assessment of mucosal healing in ulcerative colitis
Author(s) -
Macé Vincent,
Ahluwalia Amrita,
Coron Emmanuel,
Le Rhun Marc,
Boureille Arnaud,
Bossard Céline,
Mosnier JeanFrançois,
MatysiakBudnik Tamara,
Tarnawski Andrzej S
Publication year - 2015
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.12748
Subject(s) - medicine , ulcerative colitis , pathology , colonoscopy , crypt , endomicroscopy , intestinal mucosa , gold standard (test) , endoscopy , colitis , inflammatory bowel disease , gastroenterology , colorectal cancer , confocal , cancer , disease , geometry , mathematics
Background and Aim Endoscopic assessment of mucosal healing in ulcerative colitis ( UC ) is increasingly accepted as a measure of disease activity, therapeutic goal, and the key prognostic indicator. While regular endoscopy evaluates appearance of the mucosal surface, confocal laser endomicroscopy ( CLE ) enables in vivo visualization of subepithelial mucosa at 1000× magnification during ongoing endoscopy. Our aims were to determine using CLE whether endoscopically normal appearing colonic mucosa in patients with UC in remission ( UC ‐ IR ) has fully regenerated mucosal structures, resolved inflammation, and to identify the mechanisms. Methods Twelve patients (six controls and six with UC ‐ IR ) underwent colonoscopy using CLE and intravenous fluorescein infusion. During colonoscopy, CLE images of colonic mucosa and conventional mucosal biopsies were obtained and evaluated using image‐analysis systems. We quantified; (i) regeneration of colonic crypts and blood microvessels; (ii) cyclooxygenase 2 (COX2) expression; (iii) mitochondrial DNA (mt DNA ) mutations; (iv) inflammatory infiltration; and (v) vascular permeability ( VP ). Results In control subjects, CLE demonstrated normal colonic crypts and microvasculature. COX 2 expression was minimal, and < 7% crypts showed mt DNA mutations. Colonic mucosa of UC ‐ IR patients had impaired and distorted crypt regeneration, increased COX 2, 69% crypts with mt DNA mutations, persistent inflammation, and abnormal vascular architecture with increased VP (all P < 0.001 vs normal mucosa). Conclusions (i) Endoscopically normal appearing colonic mucosa of patients with UC ‐ IR remains abnormal: CLE demonstrates impaired crypt regeneration, persistent inflammation, distinct abnormalities in angioarchitecture and increased vascular permeability; molecular imaging showed increased COX 2 and mt DNA mutations; (ii) CLE may serve as a new gold standard for the assessment of mucosal healing in UC .