Barrett’s Registry Collaboration of academic centers in Ireland reveals high progression rate of low-grade dysplasia and low risk from nondysplastic Barrett’s esophagus: report of the RIBBON network

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.

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.


2015 ◽  
Vol 61 (1) ◽  
pp. 158-167 ◽  
Author(s):  
Kavel Visrodia ◽  
Prasad G. Iyer ◽  
Cathy D. Schleck ◽  
Alan R. Zinsmeister ◽  
David A. Katzka

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.


2014 ◽  
Vol 79 (5) ◽  
pp. AB114-AB115
Author(s):  
Kavel Visrodia ◽  
Prasad G. Iyer ◽  
Cathy D. Schleck ◽  
Alan R. Zinsmeister ◽  
David a. Katzka

2006 ◽  
Vol 63 (5) ◽  
pp. AB127 ◽  
Author(s):  
Virender Sharma ◽  
H. Jae Kim ◽  
Roxane Mclaughlin ◽  
Michelle Moirano ◽  
Michael Crowell ◽  
...  

2018 ◽  
Vol 16 (9) ◽  
pp. 1529-1530 ◽  
Author(s):  
Joel H. Rubenstein ◽  
Akbar K. Waljee ◽  
Ben Dwamena ◽  
Jacques Bergman ◽  
Michael Vieth ◽  
...  

Author(s):  
Isabella Ekheden ◽  
Jonas F. Ludvigsson ◽  
Li Yin ◽  
Peter Elbe ◽  
Weimin Ye

Abstract Background The poor survival of patients with gastroesophageal cancers may improve if additional esophageal precursor lesions to Barrett’s esophagus and squamous dysplasia are identified. We estimated the risk for gastroesophageal cancers among patients with various histopathological abnormalities in the esophagus, including Barrett’s esophagus, subdivided by histopathological types. Methods Histopathology data from esophageal biopsies obtained 1979–2014 were linked with several national population-based registers in Sweden. Patients were followed from 2 years after the first biopsy date until cancer, death, emigration, esophagectomy/gastrectomy or end of follow-up, 31st of December 2016, whichever came first. We estimated standardized incidence ratios (SIRs) as measures of relative risk with the Swedish general population as reference. Results In total 367 esophageal adenocarcinoma (EAC) cases were ascertained during 831,394 person-years of follow-up. The incidence rate (IR) for EAC was 0.1 per 1000 person-years for normal morphology, 0.2–0.5 for inflammatory changes, and 0.8–2.9 for metaplasia. The IR was 1.0 per 1000 person-years (95% confidence interval 0.7–1.3) among patients with non-dysplastic intestinal metaplasia, 0.9 (0.8–1.1) in non-dysplastic gastric/glandular metaplasia and 2.9 (2.0–4.2) among columnar metaplasia patients with low-grade dysplasia. The SIRs were 11.7 (95% confidence interval 8.6–15.5), 12.0 (10.0–14.2) and 30.2 (20.5–42.8), respectively. The SIRs for gastric cardia adenocarcinoma (GCA) were moderately elevated. Conclusions For the first time, we demonstrate that patients with esophageal inflammatory and other metaplastic abnormalities than Barrett’s esophagus have an increased risk of EAC and GCA compared to the general population. Moreover, patients with different histopathologic subtypes of Barrett’s esophagus have a comparable risk for EAC.


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