Barrett's esophagus (BE) is the only known precursor of esophageal adenocarcinoma, one of the few cancers with increasing incidence in developed countries. The pathogenesis of BE is unclear with regard to either the cellular origin of this metaplastic epithelium or the manner in which malignant transformation occurs, although recent data indicate a possible junctional origin of stem cells for BE. Treatment of BE may be achieved using endoscopic eradication therapy; however, there is a lack of discriminatory tools to identify individuals at sufficient risk for cancer development in whom intervention is warranted. Reduction in gastroesophageal reflux of gastric contents including acid is mandatory to achieve remission from BE after endoscopic ablation, and can be achieved using medical or nonmedical interventions. Research topics of greatest interest include the mechanism of BE development and transformation to cancer, risk stratification methods to identify individuals who may benefit from ablation of BE, optimization of eradication therapy, and surveillance methods to ensure that remission is maintained after eradication is achieved.
OBJECTIVES: Low-grade dysplasia (LGD) in Barrett's esophagus (BE) is generally inconspicuous on conventional and magnified endoscopy. Probe-based confocal laser endomicroscopy (pCLE) provides insight into gastro-intestinal mucosa at cellular resolution. We aimed to identify endomicroscopic features and develop pCLE diagnostic criteria for BE-related LGD. METHODS: This was a retrospective study on pCLE videos generated in 2 prospective studies. In phase I, 2 investigators assessed 30 videos to identify LGD endomicroscopic features, which were then validated in an independent video set (n = 25). Criteria with average accuracy >80% and interobserver agreement κ > 0.4 were taken forward. In phase II, 6 endoscopists evaluated the criteria in an independent video set (n = 57). The area under receiver operating characteristic curve was constructed to find the best cutoff. Sensitivity, specificity, interobserver, and intraobserver agreements were calculated. RESULTS: In phase I, 6 out of 8 criteria achieved the agreement and accuracy thresholds (i) dark nonround glands, (ii) irregular gland shape, (iii) lack of goblet cells, (iv) sharp cutoff of darkness, (v) variable cell size, and (vi) cellular stratification. The best cutoff for LGD diagnosis was 3 out of 6 positive criteria. In phase II, the diagnostic criteria had a sensitivity and specificity for LGD of 81.9% and 74.6%, respectively, with an area under receiver operating characteristic of 0.888. The interobserver agreement was substantial (κ = 0.654), and the mean intraobserver agreement was moderate (κ = 0.590). CONCLUSIONS: We have generated and validated pCLE criteria for LGD in BE. Using these criteria, pCLE diagnosis of LGD is reproducible and has a substantial interobserver agreement.
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