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HOME > Clin Endosc > Volume 57(6); 2024 > Article
Editorial Risk of Barrett’s esophagus progression to esophageal adenocarcinoma
Lahari Kota1orcid, Amy Tyberg2orcid
Clinical Endoscopy 2024;57(6):763-764.
DOI: https://doi.org/10.5946/ce.2024.273
Published online: November 25, 2024

1Department of Internal Medicine, Hackensack University Medical Center, Hackensack, NJ, USA

2Division of Advanced and Therapeutic Endoscopy, Department of Medicine, Hackensack University Medical Center, Hackensack, NJ, USA

Correspondence: Amy Tyberg Hackensack University Medical Center, 186 Rochelle Ave, Rochelle Park, NJ 07662, USA E-mail: Amy.Tyberg@gmail.com
• Received: October 11, 2024   • Revised: October 12, 2024   • Accepted: October 14, 2024

© 2024 Korean Society of Gastrointestinal Endoscopy

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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See the article "Progression to cancer in patients with confirmed dysplasia compared to dysplasia downgraded to non-dysplastic metaplasia in Barrett’s esophagus: a retrospective cohort study in Sweden" on page 768.
Esophageal adenocarcinoma (EAC) is increasing in prevalence in the United States due to higher rates of gastroesophageal reflux disease (GERD) and obesity.1 Barrett’s esophagus (BE) is intestinal metaplasia caused by chronic damage to the esophageal lining and is a known precursor for EAC. Given that the five-year survival rate for EAC is approximately 50% with localized diseases, 30% with regional diseases, and 6% with distant diseases, surveillance and risk stratification of those with BE is imperative for early detection of pre-cancerous dysplastic transformation and early initiation of preventative treatment.2
The histologic findings of dysplasia in BE can be defined using the Vienna classification which is as follows: (1) no dysplasia or non-dysplastic BE (NDBE), (2) indeterminate dysplasia (IND) when unable to determine if true dysplasia is present versus inflammatory changes, (3) low-grade adenoma or dysplasia (LGD), (4) high-grade adenoma or dysplasia (HGD), carcinoma in situ, suspicion of invasion, or intramucosal carcinoma, and (5) carcinoma. Risk of progression to EAC varies depending on the classification. A cohort based study of 11,028 patients in Denmark with BE found that progression to EAC was greater in those with LGD compared to those with NDBE with 5.1 cases per 1,000 person-years in LGD as opposed to 1.0 case per 1,000 person-years.3 Other large cohort studies have indicated that the annual cancer risk in those without dysplasia is 0.12% to 0.40% as opposed to 1% in those with LGD and greater than 5% for patients with HGD.4 Regrettably, studies have demonstrated significant inter-observer variability in classifying dysplastic BE, especially LGD and IND. Therefore, all guidelines recommend verification of BE dysplasia classification by a second pathologist with expertise in BE prior to management decisions.
There is clear evidence that endoscopic eradication therapies (EET) in the setting of BE with dysplasia can prevent progression to EAC. These techniques include endoscopic mucosal resection (EMR), endoscopic submucosal dissection, radiofrequency ablation (RFA), and cryoablation.5 Accordingly, 2022 practice guidelines from the American College of Gastroenterology (ACG) and 2024 Clinical Practice Guidelines from the American Gastroenterological Association give a strong recommendation for EET with subsequent surveillance in cases of HGD. EET is recommended conditionally in LGD (with endoscopic surveillance an acceptable alternative in the ACG guidelines) and not at all in NDBE.5,6 However, management of IND remains variable and with a lack of consensus, with some guidelines suggesting management similar to NDBE and others recommending surveillance endoscopy every 6 months until findings conform to NDBE or LGD.1,6-8
The study by Elbe et al.9 in this issue of Clinical Endoscopy provides important data on the management of dysplastic BE. This study both validates the importance of secondary pathology review for patients with dysplastic BE, and provides convincing evidence that patients classified as confirmed IND on double-pathologist review should be managed similarly to those with LGD. In this study, 423 patients initially diagnosed with BE with dysplasia from Ersta Hospital in Sweden between 1998 to 2012 were followed for up to 26 years to monitor the progression of their BE to cancer. All patients had their dysplastic specimens re-evaluated by expert pathologists and their diagnoses were updated per the Vienna classification to indeterminate IND, LGD, HGD, and NDBE. The authors noted that 60% of those with an initial diagnosis of BE dysplasia were downgraded to NDBE upon reclassification, 20% to LGD, and 20% as IND. The overall risk of progression from BE to EAC was 8.1% with an annual incidence of 0.87% total, 0.41% in NDBE, 1.43% in IND, and 1.84% in LGD. The risk of progression to cancer in LGD was four times more than those with NDBE. Notably, there was no significant difference in the risk of progression between LGD and IND. This study is strong in terms of sample size as well as follow-up duration, but limited by the lack of data about extraneous variables such as lifestyle factors, obesity, duration of GERD, medication use or other interventions, and BE segment circumference and length.9
This study adds support to data from a recent meta-analysis that the risk of progression to EAC in IND is similar to LGD, and should be managed as such–which per some guidelines would mean consideration of EET.10 However, a decision of whether to proceed with EET for IND must incorporate consideration of the risks of potential overtreatment versus the risks of potential missed opportunity in prevention of EAC. Adverse events from RFA with or without EMR can be as high as 8.8% including strictures, bleeding, and in rare cases, perforation; yet 5-year survival in EAC with localized disease is only 50%.2,6 Further investigation into the long-term benefits and risks of endoscopic interventions for cases of IND is warranted.
  • 1. Whiteman DC, Appleyard M, Bahin FF, et al. Australian clinical practice guidelines for the diagnosis and management of Barrett's esophagus and early esophageal adenocarcinoma. J Gastroenterol Hepatol 2015;30:804–820.ArticlePubMed
  • 2. American Cancer Society (ACS). Cancer facts & figures 2024. ACS; 2024.
  • 3. Hvid-Jensen F, Pedersen L, Drewes AM, et al. Incidence of adenocarcinoma among patients with Barrett's esophagus. N Engl J Med 2011;365:1375–1383.ArticlePubMed
  • 4. Dulai GS, Guha S, Kahn KL, et al. Preoperative prevalence of Barrett's esophagus in esophageal adenocarcinoma: a systematic review. Gastroenterology 2002;122:26–33.ArticlePubMed
  • 5. Shaheen NJ, Falk GW, Iyer PG, et al. Diagnosis and Management of Barrett's Esophagus: An Updated ACG Guideline. Am J Gastroenterol 2022;117:559–587.ArticlePubMedPMC
  • 6. Rubenstein JH, Sawas T, Wani S, et al. AGA clinical practice guideline on endoscopic eradication therapy of Barrett's esophagus and related neoplasia. Gastroenterology 2024;166:1020–1055.ArticlePubMedPMC
  • 7. Fitzgerald RC, di Pietro M, Ragunath K, et al. British Society of Gastroenterology guidelines on the diagnosis and management of Barrett's oesophagus. Gut 2014;63:7–42.ArticlePubMed
  • 8. Weusten B, Bisschops R, Coron E, et al. Endoscopic management of Barrett's esophagus: European Society of Gastrointestinal Endoscopy (ESGE) Position Statement. Endoscopy 2017;49:191–198.ArticlePubMed
  • 9. Elbe P, Öst Å, Mellbom L, et al. Progression to cancer in patients with confirmed dysplasia compared to dysplasia downgraded to non-dysplastic metaplasia in Barrett’s esophagus: a retrospective cohort study in Sweden. Clin Endosc 2024;57:768–774.Article
  • 10. Krishnamoorthi R, Mohan BP, Jayaraj M, et al. Risk of progression in Barrett's esophagus indefinite for dysplasia: a systematic review and meta-analysis. Gastrointest Endosc 2020;91:3–10.ArticlePubMed

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    • A bidirectional Mendelian randomization study integrating genome-wide association studies, expression quantitative trait locus, and methylation quantitative trait locus data revealed causal relationship between heavy cigarette dependence and Barrett’s eso
      Zhou An, Meichun Zeng, Xianhua Wang
      SAGE Open Medicine.2025;[Epub]     CrossRef

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      Risk of Barrett’s esophagus progression to esophageal adenocarcinoma
      Clin Endosc. 2024;57(6):763-764.   Published online November 25, 2024
      DOI: https://doi.org/10.5946/ce.2024.273
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