FA02.05: PROGRESSION RATE OF BARRETT’S ESOPHAGUS FROM NATIONAL REGISTRY OF EXPERT CENTERS IS MUCH GREATER THAN ANTICIPATED FROM POPULATION STUDIES

2018 ◽  
Vol 31 (Supplement_1) ◽  
pp. 4-4
Author(s):  
Lisa O'Byrne ◽  
Roy Verhage ◽  
Marie O'Brien ◽  
Dermot O'Toole ◽  
Cian Muldoon ◽  
...  

Abstract Background Barrett's Esophagus (BE) is well established as the main pathological precursor for esophageal adenocarcinoma (EAC). Progression to high grade dysplasia (HGD) or EAC varies widely between population based studies and specialized BE registries from high volume centers. No such data existed from the Republic of Ireland until 2011 when a multicenter registry was established involving three centers to more accurately determine the risk of progression to EAC in the Irish population. Methods A detailed clinical, endoscopic and pathological database includes 3397 patients from January 2008 to July 2017, with BE defined by the presence of specialized intestinal metaplasia (SIM). A prospective web based database was used to gather information from three designated esophageal centers with initial and follow up data abstracted by a data manager and overseen by a project manager. Results 325 were excluded following a diagnosis of HGD or EAC at index biopsy, or being a tertiary referral, leaving 3072 with a median age of 61 and a 2.1:1 male to female ratio and a median follow up of 3 years, and 5024 person years. 127 (4%) cases progressed to HGD/EAC, 65 after one year of follow up. 55 (2%) developed EAC were identified, 30 of those within one year. The overall incidence HGD/EAC was 2.53% per year, 1.3% if the first year is excluded. The risk of progression to EAC alone was 1.09% per year, 0.5% excluding the first year. Low grade dysplasia (LGD) on index biopsy was associated with a progression rate of 11.7% per year, 4.2% with the first year excluded. Conclusion With strict data entry and pathologic quality assurance, progression rates for non-dysplastic BE was several fold higher than population studies, highlighting caution in abstracting from population data. True LGD, as evidenced in a recent report by Kestens et al.1 represent high risk disease, with most of the risk evident within the first year. Reference: 1. Kestens C, Offerhaus G, van Baal J, Siersema PD. Patients wtih Barrett's esophagus and persistent low-grade dysplasia have an increased risk for high- grade dysplasia and cancer. Clin Gastroenterol Hepatol. 2016;14:956–962 Disclosure All authors have declared no conflicts of interest.

2020 ◽  
Vol 33 (10) ◽  
Author(s):  
Lisa M O’Byrne ◽  
Jolene Witherspoon ◽  
Roy J J Verhage ◽  
Marie O’Brien ◽  
Cian Muldoon ◽  
...  

Summary Barrett’s esophagus (BE) is the main pathological precursor of esophageal adenocarcinoma (EAC). Progression to high-grade dysplasia (HGD) or EAC from nondysplastic BE (NDBE), low-grade dysplasia (LGD) and indefinite for dysplasia (IND) varies widely between population-based studies and specialized centers for many reasons, principally the rigor of the biopsy protocol and the accuracy of pathologic definition. In the Republic of Ireland, a multicenter prospective registry and bioresource (RIBBON) was established in 2011 involving six academic medical centers, and this paper represents the first report from this network. A detailed clinical, endoscopic and pathologic database registered 3,557 patients. BE was defined strictly by both endoscopic evidence of Barrett’s epithelium and the presence of specialized intestinal metaplasia (SIM). A prospective web-based database was used to gather information with initial and follow-up data abstracted by a data manager at each site. A total of 2,244 patients, 1,925 with no dysplasia, were included with complete follow-up. The median age at diagnosis was 60.5 with a 2.1:1 male to female ratio and a median follow-up time of 2.7 years (IQR 1.19–4.04), and 6609.25 person years. In this time period, 125 (5.57%) progressed to HGD/EAC, with 74 (3.3%) after 1 year of follow-up and 38 (1.69%) developed EAC, with 20 (0.89%) beyond 1 year. The overall incidence of HGD/EAC was 1.89% per year; 1.16% if the first year is excluded. The risk of progression to EAC alone overall was 0.57% per year, 0.31% excluding the first year, and 0.21% in the 1,925 patients who had SIM alone at diagnosis. Low-grade dysplasia (LGD) progressed to HGD/EAC in 31% of patients, a progression rate of 12.96% per year, 6.71% with the first year excluded. In a national collaboration of academic centers in Ireland, the progression rate for NDBE was similar to recent population studies. Almost one in two who progressed was evident within 1 year. Crucially, LGD diagnosed and confirmed by specialist gastrointestinal pathologists represents truly high-risk disease, highlighting the importance of expertise in diagnosis and management, and providing indirect support for ablative therapies in this context.


Endoscopy ◽  
2007 ◽  
Vol 39 (07) ◽  
pp. 581-587 ◽  
Author(s):  
C. Lim ◽  
D. Treanor ◽  
M. Dixon ◽  
A. Axon

2016 ◽  
Vol 2016 ◽  
pp. 1-4
Author(s):  
Megan Murphy ◽  
Christina Tofani ◽  
Kunjal Gandhi ◽  
Anthony Infantolino

Background. Barrett’s esophagus is associated with an increased risk of adenocarcinoma. Dysplasia in Barrett’s esophagus is a precursor to adenocarcinoma. Rarely, dysplastic polypoid lesions are superimposed on Barrett’s esophagus. Most reported cases of polypoid dysplasia in Barrett’s esophagus have been advanced on presentation and treated with esophagectomy. We describe two cases of polypoid changes in Barrett’s esophagus and treatment with polypectomy followed by radiofrequency ablation.Cases. A 75 yo male presented with esophageal polyps, which on biopsy showed gastric cardia/foveolar mucosa with focal intestinal metaplasia without dysplasia. Biopsy of intervening flat mucosa was consistent with nondysplastic Barrett’s esophagus. Extensive hot snare polypectomies were performed followed by RFA. One year later, repeat EGD revealed no evidence of Barrett’s esophagus. A 61 yo male presented with esophageal polyps, which on biopsy showed gastric cardia/foveolar mucosa with intestinal metaplasia and foci of low-grade dysplasia. Extensive hot snare polypectomies were performed followed by RFA. At repeat EGD, four months later, an esophageal mass was found. Biopsy of the mass showed invasive adenocarcinoma. The patient was referred for esophagectomy.Conclusion. This case series shows two outcomes, one with successful eradication of dysplasia and the other with disease progression to invasive adenocarcinoma requiring esophagectomy.


2013 ◽  
Vol 144 (5) ◽  
pp. S-73-S-74 ◽  
Author(s):  
Lucas C. Duits ◽  
Kai Yi N. Phoa ◽  
Wouter L. Curvers ◽  
Fiebo J. ten Kate ◽  
Gerrit A. Meijer ◽  
...  

2020 ◽  
Vol 33 (9) ◽  
Author(s):  
Andrew J Henn ◽  
Kevin Y Song ◽  
Amy A Gravely ◽  
Hector Mesa ◽  
Shahnaz Sultan ◽  
...  

Summary Patients with Barrett’s esophagus (BE) are at increased risk of esophageal adenocarcinoma (EAC). The risk is largely based on the degree of dysplasia. Dysplasia cannot always be differentiated from inflammatory changes, and therefore may be classified as indefinite for dysplasia (IND). The risk of progressive dysplasia in patients with IND is unclear. Our aim is to characterize the risk of progression in US veterans with BE-IND. We performed a single-center retrospective cohort study of patients with BE-IND between 2006 and 2016. All IND was diagnosed by consensus conference with an expert gastrointestinal (GI) pathologist or review by an expert GI pathologist and persistence was defined as IND present on subsequent endoscopic biopsy. The primary outcome was the incidence rate of high-grade dysplasia (HGD)/EAC. Secondary outcomes included any progression including incident low-grade dysplasia (LGD), any prevalent dysplasia and risk factors for dysplastic progression, namely persistent IND. Risk factors for progression were assessed using univariate and multivariate analysis with logistic regression. Among 107 patients with BE-IND, there were no incident cases of HGD/EAC. Twenty patients (18.7%) developed incident LGD during a median follow-up of 2.39 years (interquartile range, 1.13–5.17). The annual rate of progression to LGD was 5.95 per 100 patient-years (95% CI, 3.73–9.02). Prevalent dysplasia was common (9.3%). Eight patients had prevalent LGD, one patient had prevalent HGD and one patient had prevalent EAC. Twenty-eight patients (30.1%) were found to have persistent IND. Among those with persistent IND, 10 (36%) patients progressed to LGD (none to HGD/EAC). The progression rate to LGD for patients with persistent IND was 7.86 (95% CI, 3.99–14.02) cases per 100 patient-years versus 4.78 (95% CI, 2.48–8.52) for nonpersistent IND (P = 0.036). The odds ratio for progression to LGD in persistent IND was 3.06 (95% CI, 1.08–8.64). In multivariate analysis adjusting for age, smoking history, presence of hiatal hernia and BMI > 30, persistent IND remained significant (OR 3.23; 95% CI, 1.04–9.98). Regression to nondysplastic BE was very common. Seventy-one (61%) patients developed complete and sustained regression of all dysplastic changes at last follow-up. Persistent IND, present in one-third of patients with IND, is an independent risk factor for progression to LGD. Although no patients in this cohort developed HGD/EAC, prevalent dysplasia was common (9.3%). Taken together, patients with IND should receive close surveillance for both prevalent and incident dysplasia especially if IND is persistent.


Sign in / Sign up

Export Citation Format

Share Document