2014-04-24 18:25:37 UTC

Barrett’s Esophagus: Is It Time to Stop Lifelong Surveillance?

May 1, 2014


Srinivas Gaddam, MD, MPH

Division of Gastroenterology and Hepatology, Washington University School of Medicine, St. Louis, MO


Prateek Sharma, MD

Division of Gastroenterology and Hepatology, Veterans Affairs Medical Center, Kansas City, MO; Division of Gastroenterology and Hepatology, University of Kansas School of Medicine, Kansas City, KS

Barrett’s esophagus (BE) is a well-established risk factor for esophageal adenocarcinoma.1 Based on SEER database studies, the incidence of esophageal adenocarcinoma has been dramatically rising in the last three decades.2 Due to lack of alternative interventions to stem the rise of esophageal cancer, the focus has remained on diagnosis and surveillance of patients with BE. Therefore, current guidelines by all GI societies recommend enrollment of patients with BE in surveillance programs.

For many years now, endoscopic surveillance of all patients with BE seemed to make sense. Previous studies showed high risk of esophageal cancer in non-dysplastic BE (approximately 1 to 2 percent/year) and, based on small retrospective surgical case series, there appeared to be some merit to endless continued surveillance. However, over the last few years, several important papers were published that have changed our understanding of the natural history of non-dysplastic BE. In 2011, Hvid-Jensen et al. reported a low annual incidence of esophageal cancer of 0.12 percent in a large population-based cohort study on 11,028 Danish patients with BE.3 This was lower than the previously reported rate of 0.5 percent per year. Furthermore, a cohort study published by our group last year showed that this low risk of cancer was non-linear; the risk of cancer appeared to decrease over time4 — especially after five negative surveillance endoscopies. A case-control study based on the U.K.’s Clinical Practice Research Datalink, showed that only 2 percent of BE patients died of esophageal cancer over a 10-year period — they were more likely to die from other unrelated causes. Finally, in 2013, Corley et al., in a case-control, community-based study showed that surveillance offered no mortality benefit from esophageal adenocarcinoma.5

60 years after the first reported case, there is not even a definition for Barrett’s esophagus that is accepted worldwide.

So is there any alternate to surveillance; can we ablate the BE and forget surveillance or should we do nothing? There has been great interest in the long-term durability of a wide variety of endoscopic eradication therapies that are available today. A landmark paper by a multi-center randomized controlled trial, published in 2009, showed promising short-term results with successful eradication of dysplasia and intestinal metaplasia by radiofrequency ablation.6 In the BE research community, there was a sense of excitement about the availability of safe and effective treatments for non-dysplastic BE with the hope of achieving a “cure.” However, the recent data on low progression rates and recurrence rates up to 25 to 30 percent during long-term follow up have curbed our enthusiasm in this regard; complete eradication of intestinal metaplasia has been shown to be anything but perfect, leading to surveillance (again) post ablation — not a cost effective approach as shown by Hur C. et al.7

The other alternative is not doing anything i.e., are we ready to abandon ship on surveillance and ablation? For sure in those individuals with irregular z lines or intestinal metaplasia at the gastroesophageal junction, doing nothing appears to be appropriate. How about the other BE patients? Risk stratification is the key! While we are waiting for the right panel of biomarkers, there has been progress in assessing clinical and endoscopic features for predicting high-risk BE patients. A risk stratification tool based on a multicenter cohort of 3,600 patients using endoscopic and clinical/demographic factors to predict patients that are likely to have or progress to high-grade dysplasia or cancer was recently reported.8 This is currently in the process of external validation and if successfully validated, it will help risk stratify patients based on clinical and endoscopic features alone. We hope that a panel of biomarkers, combined with clinical and demographic factors will eventually be identified that are capable of predicting high-risk patients who are likely to progress to cancer. These patients may require intensive surveillance or primary prevention with safe and effective endoscopic eradication.

Barrett’s esophagus continues to be an area of controversy; this is evident in the fact that even 60 years after the first reported case, there is not even a definition for BE that is accepted worldwide. Similarly, in the field of surveillance of BE, the data are continuously evolving. Despite the vast improvement in our understanding of the disease over the last two decades, BE continues to be “unfinished business” that challenges researchers. The question “is it time to stop surveillance on my Barrett’s patients?” is a difficult one to conclusively answer at this time, but the newer data certainly point us away from lifelong surveillance.

Drs. Gaddam and Sharma have no conflicts to disclose.


1. Sharma P. Clinical practice. Barrett’s esophagus. N Engl J Med 2009;361:2548-56.

2. Pohl H, Welch HG. The role of overdiagnosis and reclassification in the marked increase of esophageal adenocarcinoma incidence. J Natl Cancer Inst 2005;97:142-6.

3. Hvid-Jensen F, Pedersen L, Drewes AM, Sorensen HT, Funch-Jensen P. Incidence of adenocarcinoma among patients with Barrett’s esophagus. N Engl J Med 2011;365:1375-83.

4. Gaddam S, Singh M, Balasubramanian G, Thota P, Gupta N, Wani S, Higbee AD, Mathur SC, Horwhat JD, Rastogi A, Young PE, Cash BD, Bansal A, Vargo JJ, Falk GW, Lieberman DA, Sampliner RE, Sharma P. Persistence of nondysplastic Barrett’s esophagus identifies patients at lower risk for esophageal adenocarcinoma: results from a large multicenter cohort. Gastroenterology 2013;145:548-53 e1.

5. Corley DA, Mehtani K, Quesenberry C, Zhao W, de Boer J, Weiss NS. Impact of endoscopic surveillance on mortality from Barrett’s esophagus-associated esophageal adenocarcinomas. Gastroenterology 2013;145:312-9 e1.

6. Shaheen NJ, Sharma P, Overholt BF, Wolfsen HC, Sampliner RE, Wang KK, Galanko JA, Bronner MP, Goldblum JR, Bennett AE, Jobe BA, Eisen GM, Fennerty MB, Hunter JG, Fleischer DE, Sharma VK, Hawes RH, Hoffman BJ, Rothstein RI, Gordon SR, Mashimo H, Chang KJ, Muthusamy VR, Edmundowicz SA, Spechler SJ, Siddiqui AA, Souza RF, Infantolino A, Falk GW, Kimmey MB, Madanick RD, Chak A, Lightdale CJ. Radiofrequency ablation in Barrett’s esophagus with dysplasia. N Engl J Med 2009;360:2277-88.

7. Hur C, Choi SE, Rubenstein JH, Kong CY, Nishioka NS, Provenzale DT, Inadomi JM. The cost effectiveness of radiofrequency ablation for Barrett’s esophagus. Gastroenterology 2012;143:567-75.

8. Gaddam S, Vargo JJ, Kanakadandi V, Lieberman DA, Gupta N, Wani S, Higbee AD, Mathur SC, Thota PN, Sampliner RE, Falk GW, Cash BD, Horwhat JD, Bansal A, Rastogi A, Young PE, Sharma P. 342 A Clinical Prediction Model to Risk-Stratify Patients with Barrett’s Esophagus (BE): Results from a Large, Multicenter Cohort. Gastroenterology 2013;144:S-71-S-72.

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