The natural history of low‐grade dysplasia in Barrett's esophagus and risk factors for progression

Abstract

Background and Aim Barrett's esophagus is associated with increased risk of esophageal adenocarcinoma. The optimal management of low‐grade dysplasia arising in Barrett's esophagus remains controversial. We performed a retrospective study from a tertiary referral center for Barrett's esophagus neoplasia, to estimate time to progression to high‐grade dysplasia/esophageal adenocarcinoma in patients with confirmed low‐grade dysplasia compared with those with downstaged low‐grade dysplasia from index presentation and referral. We analyzed risk factors for progression. Methods We analyzed consecutive patients with low‐grade dysplasia in Barrett's esophagus referred to a single tertiary center (July 2006–October 2018). Biopsies were reviewed by at least two expert pathologists. Results One hundred and forty‐seven patients referred with suspected low‐grade dysplasia were included. Forty‐two of 133 (32%) of all external referrals had confirmed low‐grade dysplasia after expert histopathology review. Multivariable analysis showed nodularity at index endoscopy (P < 0.05), location of dysplasia (P = 0.05), and endoscopic therapy after referral (P = 0.09) were associated with progression risk. At 5 years, 59% of patients with confirmed low‐grade dysplasia had not progressed versus 74% of patients in the cohort downstaged to non‐dysplastic Barrett's esophagus. Conclusion Our data show variability in the diagnosis of low‐grade dysplasia. The cumulative incidence of progression and time to progression varied across subgroups. Confirmed low‐grade dysplasia had a shorter progression time compared with the downstaged group. Nodularity at index endoscopy and multifocal low‐grade dysplasia were significant risk factors for progression. It is important to differentiate these high‐risk subgroups so that decisions on surveillance/endotherapy can be personalized.

Endoscopic features of low-grade dysplastic Barrett’s

“…Perhaps visible lesions are in fact more advanced LGD compared with non-visible lesions. This is in keeping with the recent report from Hussein et al that nodular BE-LGD was an independent risk factor for progression to HGD/cancer [9]. This is also consistent with the previous report from Pech et al that nodular BE lesions often harbor more advanced dysplasia [24].…”

“…HGD/cancer [9]. This is also consistent with Pech et al's previous report that nodular BO lesions often harbor more advanced dysplasia [24].…”

“…This was considerably lower than the 50.4% of visible LGD lesions identified at BRU assessment (in the same cohort). Our high proportion of visible lesions was also significantly more than the current reported rates from other expert Barrett's centres (6.4 -18.7%) [7,8,9,10,19,20].…”

“…These findings are important in provoking discussion on whether LGD is more detectable endoscopically than originally appreciated and whether this should be a marker of quality endoscopy in future guidelines. This is relevant given that LGD, confirmed by an expert gastrointestinal pathologist, carries a 0.4% to 13.4% per patient per year risk for progression to HGD or cancer 99 1111 1212 1919 2020 . In our cohort, 11.1% of patients had a visible LGD lesion detected in the community.…”

“…Whilst Tsoi et al, in a cohort of 75 patients with BO-LGD, identified 18.7% of patients had visible BO-LGD lesions [8]. Furthermore, Hussein et al recently identified that nodular BO-LGD at index endoscopy was associated with progression to neoplasia [9]. Separately, Tsoi et al described a subset of BO-LGD patients with a diffusely nodular, multifocal LGD phenotype (DEVLB) that also appeared to be associated with an increased risk of progression to HGD or cancer [10].…”