Introduction: The incidence of adenocarcinoma (AC) in columnar-lined esophagus (CLE) with low-grade dysplasia (LGD) has been variously reported as around between 0% and 12% per annum (p.a.) in small series. The fate of non-progressive LGD is also controversial. The aim of this study was to examine the population with LGD in CLE, the rate of development of high-grade dysplasia (HGD) and AC and also examine those patients who remained with LGD or reverted to non-dysplastic CLE in a large cohort from UK National Barrett's Esophagus Registry (UKBOR). Methods: Medical records of 283 patients with LGD in CLE from 7 UK centers registering with UKBOR were examined and data extracted on histological follow-up. Incidence data were modelled using an exact Poisson distribution. Results: 144 patients had 290 biopsies prior to LGD diagnosis (median time from CLE diagnosis to LGD 2.77 years, maximum 17.36 years). Of these, 141 patients (97.9%) had non-dysplastic CLE at diagnosis (including 18 [12.5%] with changes indefinite for dysplasia), 2 had HGD and 1 had AC (with LGD being biopsied at an urgent follow-up OGD); 3 patients had findings of HGD between initial diagnosis of ndCLO and LGD and 38 (26.4%) had findings of indefinite for dysplasia.217 had 535 biopsies after initial LGD diagnosis. 17 (11.8%) patients had biopsies of AC following LGD (including the patient with AC prior to LGD) and 12 developed HGD. 75 (34.6%) had persistent LGD for at least one further set of biopsies and 45 (20.7%) had LGD at their most recent set of biopsies, with the remaining patients having reverted to indefinite for dysplasia (37 patients, 17.1%) or non-dysplastic CLE (111 patients, 51.2%) at their most recent set of biopsies. The annual incidence of AC in LGD was 17/633.7 patient-years of follow-up (2.7% p.a. 95% confidence interval 1.6-4.3% p.a.). A further 12 patients developed HGD during follow-up, yielding a combined annual incidence of HGD and AC of 29/633.7 (4.6% p.a. 95% confidence 3.1-6.6% p.a.). Conclusion: In a large cohort of 243 patient s with LGD, 148 (68.2%) had reverted to non-dysplastic CLE or indefinite changes for dysplasia at final follow-up. Patients found to have LGD are at a significant risk of developing HGD and AC compared to those without dysplasia and should be followed-up closely to enable early detection of HGD/AC.