Gastroenterology

Gastroenterology

Volume 149, Issue 3, September 2015, Pages 567-576.e3
Gastroenterology

Original Research
Full Report: Clinical—Alimentary Tract
Radiofrequency Ablation Is Associated With Decreased Neoplastic Progression in Patients With Barrett's Esophagus and Confirmed Low-Grade Dysplasia

https://doi.org/10.1053/j.gastro.2015.04.013Get rights and content

Background & Aims

Barrett's esophagus (BE) with low-grade dysplasia (LGD) can progress to high-grade dysplasia (HGD) and esophageal adenocarcinoma (EAC). Radiofrequency ablation (RFA) has been shown to be an effective treatment for LGD in clinical trials, but its effectiveness in clinical practice is unclear. We compared the rate of progression of LGD after RFA with endoscopic surveillance alone in routine clinical practice.

Methods

We performed a retrospective study of patients who either underwent RFA (n = 45) or surveillance endoscopy (n = 125) for LGD, confirmed by at least 1 expert pathologist, from October 1992 through December 2013 at 3 medical centers in the United States. Cox regression analysis was used to assess the association between progression and RFA.

Results

Data were collected over median follow-up periods of 889 days (interquartile range, 264−1623 days) after RFA and 848 days (interquartile range, 322−2355 days) after surveillance endoscopy (P = .32). The annual rates of progression to HGD or EAC were 6.6% in the surveillance group and 0.77% in the RFA group. The risk of progression to HGD or EAC was significantly lower among patients who underwent RFA than those who underwent surveillance (adjusted hazard ratio = 0.06; 95% confidence interval: 0.008−0.48).

Conclusions

Among patients with BE and confirmed LGD, rates of progression to a combined end point of HGD and EAC were lower among those treated with RFA than among untreated patients. Although selection bias cannot be excluded, these findings provide additional evidence for the use of endoscopic ablation therapy for LGD.

Section snippets

Patients and Settings

The source cohort came from 3 referral centers within the Barrett's Esophagus Translational Research Network (BETRNet) consortium funded by the National Cancer Institute: the University of Pennsylvania, Columbia University, and the Mayo Clinic. Within this cohort, BE patients who had a diagnosis of LGD as verified by histopathology from October 1992 (the date of earliest registration of LGD patients available) to December 2013 were identified for study inclusion. The inclusion criteria for this

Patients and Barrett's Characteristics

A total of 170 patients met inclusion criteria: 125 underwent surveillance only and 45 underwent RFA (Figure 1; Supplementary Figure 1). The 2 groups were similar in baseline characteristics, except for higher proton pump inhibitor use in the RFA patients and center differences in the proportion of patients undergoing ablation (Table 1). There were numerically, but not statistically, more visible macroscopic lesions detected in the surveillance group compared with the ablated group (10.4% vs

Discussion

In this multicenter study of patients with confirmed LGD, we observed a high progression rate to HGD or adenocarcinoma in the surveillance group; however, progression rates were much lower with RFA. We estimate that for every 3 patients treated with RFA, 1 additional patient with LGD will avoid progression to HGD or EAC within 3 years. We were not able to demonstrate a significant reduction in EAC, although this was a rare event and, as such, our power to determine a difference was much less

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  • Cited by (0)

    This article has an accompanying continuing medical education activity on page e13. Learning Objective: Upon completion of this exercise, successful learners will be able to (a) discuss management of low-grade dysplasia in Barrett's esophagus, (b) identify strategies to reduce the risk of low-grade dysplasia advancing to high-grade dysplasia, and (c) discuss the role of specialized GI pathologists in pathologic review of biopsies diagnosed as low-grade dysplasia by general pathologists.

    Conflicts of interest These authors disclose the following: Julian A. Abrams has served as a consultant to C2 Therapeutics. He has received research support from C2 Therapeutics and Covidien. Charles J. Lightdale has served as a consultant to Boston Scientific, C2 Therapeutics, CSA Medical, Mauna Kea Technologies, and NinePoint Medical. He has received royalties from Cook Medical. Prasad G. Iyer has received research support from Takeda Pharmaceuticals. Kenneth K. Wang has received research support from BaRRx, Pinnacle Pharma, and CSA. James D. Lewis has served as a consultant to Takeda, Amgen, Millennium Pharmaceuticals, Pfizer, Abbott, Prometheus, Nestle, Lilly, and Shire. He has received research funding from Shire, Takeda, and Centocor. Gray W. Falk serves as a consultant to CDX and receives research support from CDX. Meenakshi Bewtra has received research support from Janssen and Imedex. The remaining authors disclose no conflicts.

    Funding This work was supported by the National Institutes of Health (NIH)/National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) T32 DK007740 (Clinical Epidemiology Training in Gastroenterology), the NIDDK 1 K08 DK084347-01, the NIH K24-DK078228, the NIH/NCI U54-CA163004, the NIH/NIDDK P30DK050306 Center for Molecular Studies in Digestive and Liver Diseases, and the NIH/NCI P01-CA098101 and institutional funds.

    Author names in bold designate shared co-first authors.

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