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• W1996356095 abstract "See “Durability of radiofrequency ablation in Barrett's esophagus with dysplasia,” by Shaheen NJ, Overholt BF, Sampliner RE, et al, on page 460. See “Durability of radiofrequency ablation in Barrett's esophagus with dysplasia,” by Shaheen NJ, Overholt BF, Sampliner RE, et al, on page 460. The AIM Dysplasia Trial was a multicenter, randomized, sham-controlled trial comparing radiofrequency ablation (RFA) and endoscopic surveillance to endoscopic surveillance alone for the management of patients with Barrett's esophagus (BE) and low-grade dysplasia (LGD) or high-grade dysplasia (HGD).1Shaheen N.J. Sharma P. Overholt B.F. et al.Radiofrequency ablation in Barrett's esophagus with dysplasia.N Engl J Med. 2009; 360: 2277-2288Crossref PubMed Scopus (1092) Google Scholar Participants undergoing active therapy could have received up to 4 RFA treatments in the first year. Outcomes were assessed by endoscopy with biopsies of any visible abnormality and 4-quadrant random biopsies every 1cm throughout the BE segment. If dysplasia was diagnosed a second pathologist at a central laboratory confirmed dysplasia, with discordant diagnoses resolved by a third pathologist at the central laboratory. The trial reported that after 1-year of follow-up, 85.7% of patients treated with RFA had eradication of dysplasia and 77.4% of treated patients had eradication of all intestinal metaplasia. Although encouraging, these results focused on surrogate endpoints and longer follow-up was necessary to observe the durability of remission of dysplasia and metaplasia, and whether these surrogates correlated with clinical end points of reduction in cancer incidence and mortality. The sham arm was dissolved after 1 year of follow-up; participants in the sham arm were offered RFA, and all RFA-treated patients (initial active therapy and sham cross-over therapy) were followed for 2 years. This provides a longer timeframe to evaluate the efficacy of RFA to induce remission from dysplasia and metaplasia. Subsequently, participants in whom intestinal metaplasia was not present at the 2-year follow-up examination were asked to be observed for an additional 3 years, for a total of 5 years of follow-up in these individuals. Of note, patients could receive additional RFA treatment during the second and third years owing to persistent/recurrent intestinal metaplasia that was either confirmed by histology or suspected at the time of endoscopy. This analysis provides information about the safety and efficacy of RFA to be used as a form of suppressive therapy to treat recurrent dysplasia and metaplasia to reduce cancer incidence. The report in this issue of Gastroenterology is an interim analysis of the 2- and 3-year outcomes of the planned 5-year follow-up of study participants who received RFA therapy.2Shaheen N.J. Overholt B.F. Sampliner R.E. et al.Durability of radiofrequency ablation in Barrett's esophagus with dysplasia.Gastroenterology. 2011; 141: 460-468Abstract Full Text Full Text PDF PubMed Scopus (352) Google Scholar Of the 106 participants who underwent RFA, 101 (95%) had no dysplasia and 99 of these (93% of total) had no intestinal metaplasia after 2 years of follow-up. However, by intention to treat (considering the 13 participants who left the study for any reason as treatment failures), the proportion of participants who received RFA and did not have dysplasia at the 2-year time point was 85% and the proportion without intestinal metaplasia was 83%. It is important to note that 55% of participants had RFA repeated after the first year of follow-up. Therefore, RFA was an effective means to keep disease in remission, but was not used as a “cure” for BE in the majority of participants. The durability of response after achieving remission was explored further in the second analysis of this paper. Of the participants in whom dysplasia was eradicated at any point in the trial, 85% of those initially diagnosed with HGD and 90% of those with LGD remained free of dysplasia 3 years after eradication without additional RFA therapy. Concerning intestinal metaplasia, 75% of participants remained free of disease without repeated RFA once eradication of metaplasia was achieved. At the opposite end of the spectrum, 5 patients had progressive disease despite receiving RFA. Two developed cancer (one from LGD, one from HGD), and 3 progressed from LGD to HGD and these had initially received RFA (non-sham arm). The overall rate of progression is low—the annual risk of cancer is 0.55%— but this also illustrates the point that patients both with LGD as well as HGD are at risk of cancer development, even after RFA therapy. Finally, with respect to safety only 4 serious adverse events were reported (3.4%) consisting of gastrointestinal hemorrhage, chest pain and nausea. No perforations or deaths were noted, and the rate of stricture formation was 7.6%. Subsquamous metaplasia was diagnosed postablation in 4 patients (3.8%). This study adds to the growing body of evidence supporting RFA as an effective means to treat dysplasia associated with BE.3Fleischer D.E. Overholt B.F. Sharma V.K. et al.Endoscopic radiofrequency ablation for Barrett's esophagus: 5-year outcomes from a prospective multicenter trial.Endoscopy. 2010; 42: 781-789Crossref PubMed Scopus (189) Google Scholar, 4Sharma V.K. Jae Kim H. Das A. et al.Circumferential and focal ablation of Barrett's esophagus containing dysplasia.Am J Gastroenterol. 2009; 104: 310-317Crossref PubMed Scopus (97) Google Scholar It does not seem, however, that this can be achieved with a single series of RFA sessions. Instead, more than half of patients can expect to undergo repeated treatments in the second or third year after initial therapy. For this reason, the term “remission” is appropriate and intensive surveillance is necessary to detect and retreat areas of persistent or recurrent metaplasia and dysplasia. Although the use of RFA cannot at this time be considered a cure for BE, this study does provide reassurance that RFA can be repeated safely, and remission can be reestablished when metaplasia or dysplasia recurs. There are several issues that must be addressed for the efficacy reported in these clinical trials to be translated into effectiveness of RFA for the BE population outside of the research setting. The procedure is fairly straightforward, but no device is completely “idiot proof” and there will no doubt be complications based on greater volumes of patients being treated and a wider variety of patients treated owing to less stringent selection, and less effective treatment by less experienced endoscopists than those involved in the AIM Dysplasia trial. Continued monitoring via endoscopic registries will be essential to determine the degree to which the results reported in study conditions can be reproduced in community practice. More important, quality metrics for RFA should be established to ensure that endoscopists performing RFA are properly trained and are achieving the expected goals of therapy. The surrogate outcomes of metaplasia and dysplasia remission need to be correlated with the clinical outcome of cancer prevention. The use of dysplasia as the marker for disease progression is fraught with problems, including sampling error and differentiation from inflammation resulting in substantial intra- and interobserver variation. It is imperative that better means of risk stratification be developed and employed before further expansion of indications for treatment. Molecular markers, regardless of whether they represent mechanisms of disease or whether they are the result of disease progression can be useful for risk stratification.5Reid B.J. Blount P.L. Rabinovitch P.S. Biomarkers in Barrett's esophagus.Gastrointest Endosc Clin North Am. 2003; 13: 369-397Abstract Full Text Full Text PDF PubMed Scopus (121) Google Scholar, 6Merlo L.M. Shah N.A. Li X. et al.A comprehensive survey of clonal diversity measures in Barrett's esophagus as biomarkers of progression to esophageal adenocarcinoma.Cancer Prev Res (Phila). 2010; 3: 1388-1397Crossref PubMed Scopus (121) Google Scholar The cost-effectiveness of interventions to reduce mortality from cancer will be improved greatly by the discovery and implementation of markers that improve our ability to identify patients with BE who are at risk for cancer development beyond what is currently possible using dysplasia.7Rubenstein J.H. Vakil N. Inadomi J.M. The cost-effectiveness of biomarkers for predicting the development of oesophageal adenocarcinoma.Aliment Pharmacol Ther. 2005; 22: 135-146Crossref PubMed Scopus (21) Google Scholar The presence of intestinal metaplasia that lies below the newly generated squamous epithelium (subsquamous intestinal metaplasia [SSIM]) remains problematic. Although the proportion of patients with SSIM after RFA in this study was 3.8%, it is known that this also occurs with relatively high frequency in patients with BE even before endoscopic therapy. In this trial, the proportion harboring SSIM at study entry was 25%. Surveillance to detect metaplasia and dysplasia hidden by squamous epithelium is a major issue, and it may be that any type of ablation that is associated with persistent or recurrent BE could inhibit accurate assessment of the risk for disease progression. To detect and manage SSIM, newer techniques of risk stratification must be developed to provide effective surveillance. Again, the key may lie in abandoning the use of dysplasia in favor of or supplementing with more sensitive and specific molecular markers of disease that may be detected below the superficial epithelium. RFA is an attractive alternative to other management strategies. For HGD, this is especially true; esophagectomy is associated with substantial morbidity and mortality. Endoscopic mucosal resection is a viable alternative, but in many cases is a complementary therapy to RFA and not a competitor.8Namasivayam V. Wang K.K. Prasad G.A. Endoscopic mucosal resection in the management of esophageal neoplasia: current status and future directions.Clin Gastroenterol Hepatol. 2010; 8: 743-754Abstract Full Text Full Text PDF PubMed Scopus (30) Google Scholar Additionally, surveillance is a poor use of resources and has never been tested in prospective studies to reduce cancer mortality. Although several retrospective analyses have demonstrated an association between prior endoscopy and reduced mortality9Corley D.A. Levin T.R. Habel L.A. et al.Surveillance and survival in Barrett's adenocarcinomas: a population-based study.Gastroenterology. 2002; 122: 633-640Abstract Full Text Full Text PDF PubMed Scopus (432) Google Scholar, 10Kearney D.J. Crump C. Maynard C. et al.A case-control study of endoscopy and mortality from adenocarcinoma of the esophagus or gastric cardia in persons with GERD.Gastrointest Endosc. 2003; 57: 823-829Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar other studies highlight the possibility of lead or length time bias leading to these observations.11Rubenstein J.H. Sonnenberg A. Davis J. et al.Effect of a prior endoscopy on outcomes of esophageal adenocarcinoma among United States veterans.Gastrointest Endosc. 2008; 68: 849-855Abstract Full Text Full Text PDF PubMed Scopus (78) Google Scholar Moreover, cost-effectiveness analysis reveals a fairly low “bar” for RFA to be the optimal strategy for patients with BE and HGD or LGD.12Inadomi J.M. Somsouk M. Madanick R.D. et al.A cost-utility analysis of ablative therapy for Barrett's esophagus.Gastroenterology. 2009; 136: 2101-2114Abstract Full Text Full Text PDF PubMed Scopus (150) Google Scholar This is in part because of the potential effectiveness of RFA to prevent cancer but equally the lack of effectiveness of surveillance to treat cancer. It is acknowledged that there is debate whether LGD represents an elevated risk of cancer.13Sharma P. Low-grade dysplasia in Barrett's esophagus.Gastroenterology. 2004; 127: 1233-1238Abstract Full Text Full Text PDF PubMed Scopus (35) Google Scholar It should be recognized, however, that LGD is often misdiagnosed owing to the presence of inflammation, which represents the underlying process of acid injury. For this reason, inflammation should be suppressed with proton pump inhibitor treatment to optimize evaluation for dysplasia. In addition, a second review by an experienced pathologist should be performed before intervention in any patient diagnosed with dysplasia. There is most certainly an entity that has elevated cancer risk above baseline yet less than HGD that would still benefit from ablation; however, the problem lies in its definition and clinical recognition. The management of patients with BE without dysplasia is not addressed by this study and it would be premature to extrapolate these findings to all BE patients. Even more controversial would be treatment if the definition of BE is expanded to include columnar epithelium without goblet cells, which has been advocated.14Riddell R.H. Odze R.D. Definition of Barrett's esophagus: time for a rethink—is intestinal metaplasia dead?.Am J Gastroenterol. 2009; 104: 2588-2594Crossref PubMed Scopus (127) Google Scholar The main issue surrounding nondysplastic BE remains the natural history, because the vast majority of patients never develop cancer. Any intervention, no matter how safe and effective, cannot improve survival if the patient would have never developed cancer! Again, the root of the problem lies in our definition of disease. We do not know who has BE—we currently use age, presence of symptoms of gastroesophageal reflux disease, and perhaps race to dictate who gets screened. Women still get screened despite evidence that their risk of esophageal adenocarcinoma is similar to the risk of breast cancer among men.15Rubenstein J.H. Scheiman J.M. Sadeghi S. et al.Esophageal adenocarcinoma incidence in individuals with gastroesophageal reflux: synthesis and estimates from population studies.Am J Gastroenterol. 2011; 106: 254-260Crossref PubMed Scopus (68) Google Scholar Moreover, a substantial proportion of patients who develop esophageal adenocarcinoma do not have prior gastroesophageal reflux disease symptoms.16Lagergren J. Bergstrom R. Lindgren A. et al.Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma.N Engl J Med. 1999; 340: 825-831Crossref PubMed Scopus (2566) Google Scholar We need better stratification tools to identify patients most likely to harbor BE. Moreover, the diagnosis of BE is insufficient to embark on surveillance or therapy, because only a small number of the entire BE population will develop esophageal adenocarcinoma. We need improved methods to determine which patients with BE are at risk of progressing to cancer, and it is clear that dysplasia is insufficient to provide the necessary risk stratification. Once we identify patients with BE, and those with BE who are most likely to develop cancer, we now have therapy that can effectively ablate most metaplasia and dysplasia. Despite the fact that single-point cure is not achieved, chronic management with repeated RFA seems to provide remission from dysplasia. RFA is appealing because it may be able to treat a premalignant lesion, and it is still better to prevent cancer than to treat cancer. Although this is not “polypectomy,” it is much more enticing than surveillance with esophagectomy for cancer. The unanswered questions remain whether remission can be maintained over the lifetime of the patient, how often undetected SSIM progresses to cancer, and whether the results from trials conducted by expert endoscopists can be translated to clinical practice. Download .mpg (38.64 MB) Help with mpg files Video Durability of Radiofrequency Ablation in Barrett's Esophagus With DysplasiaGastroenterologyVol. 141Issue 2PreviewRadiofrequency ablation (RFA) can eradicate dysplasia and intestinal metaplasia in patients with dysplastic Barrett's esophagus (BE), and reduce rates of esophageal adenocarcinoma. We assessed long-term rates of eradication, durability of neosquamous epithelium, disease progression, and safety of RFA in patients with dysplastic BE. Full-Text PDF" @default.
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• W1996356095 title "Time to Burn? Endoscopic Ablation for Barrett's Esophagus" @default.
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