Degree of crypt atypia correlates with progression to high-grade dysplasia/adenocarcinoma in non-dysplastic Barrett's oesophagus
- PMID: 37199687
- PMCID: PMC10562012
- DOI: 10.1111/his.14959
Degree of crypt atypia correlates with progression to high-grade dysplasia/adenocarcinoma in non-dysplastic Barrett's oesophagus
Abstract
Aims: Patients with non-dysplastic Barrett's oesophagus (BE) often show a wide range of 'atypical' histological features in the bases of the crypts. However, the significance of crypt atypia has never been evaluated, despite prior studies showing the presence of DNA content and other molecular abnormalities in this epithelium. The aim of this study was to evaluate whether the degree of crypt atypia in BE patients without dysplasia correlates with progression to high-grade dysplasia/adenocarcinoma (HGD/EAC).
Methods and results: Baseline biopsies from 114 BE patients without dysplasia, 57 who progressed to HGD/EAC (progressors) and 57 who did not progress (non-progressors), were included in the study. Biopsies were evaluated for the degree of basal crypt atypia on a three-point scale according to discrete histological criteria. In non-progressors, 64.9, 31.6 and 3.5% of biopsies had a crypt atypia score of 1, 2 and 3, respectively, with a mean score of 1.39 ± 0.56. The percentage of biopsies with an atypia score of 2 or 3 increased in progressors [42.1, 42.1 and 15.8% of biopsies scored 1, 2 or 3, respectively, with a mean score of 1.74 ± 0.72 (P = 0.004)]. The odds ratio of grade 3 crypt atypia for progression to HGD/EAC was 5.2 (95% confidence interval = 1.1-25.0, P = 0.04) and the findings did not change significantly when the data were analysed according to progression to either HGD or EAC.
Conclusions: This study shows that non-dysplastic crypts in BE are biologically abnormal, suggesting that neoplastic progression begins prior to the onset of dysplasia. The degree of crypt atypia in BE patients without dysplasia correlates with progression.
Keywords: Barrett's oesophagus; crypt atypia; dysplasia.
© 2023 John Wiley & Sons Ltd.
Conflict of interest statement
Disclosure statement: The authors have no conflicts of interest to disclose.
Figures


References
-
- BARRETT NR. Chronic peptic ulcer of the oesophagus and “oesophagitis”. Br J Surg. 1950. Oct;38(150):175–82. - PubMed
-
- Ormsby AH, Kilgore SP, Goldblum JR, Richter JE, Rice TW, Gramlich TL. The Location and Frequency of Intestinal Metaplasia at the Esophagogastric Junction in 223 Consecutive Autopsies : Implications for Patient Treatment and Preventive Strategies in Barrett ‘s Esophagus. Mod Pathol. 2000;6(13):614–20. - PubMed
-
- Ronkainen J, Aro P, Storskrubb T, Johansson SE, Lind T, Bolling-Sternevald E, et al. Prevalence of Barrett’s esophagus in the general population: an endoscopic study. Gastroenterology. 2005. Dec;129(6):1825–31. - PubMed
-
- Desai TK, Krishnan K, Samala N, Singh J, Cluley J, Perla S, et al. The incidence of oesophageal adenocarcinoma in non-dysplastic Barrett’s oesophagus: a meta-analysis. Gut. 2012. Jul;61(7):970–6. - PubMed