Prevalent low-grade dysplasia: the strongest predictor of malignant progression in Barrett's columnar-lined oesophagus.

Dear Professor Emad El-Omar, We read with interest the work by Duits et al who find that validated low-grade dysplasia (LGD) is highly predictive of malignant progression in Barrett’s oesophagus (BO). Yachimski stresses the need for this important finding to be validated in other centres. Our experience of prevalent LGD as a predictor of malignant progression in BO in the West of Scotland strongly reinforces the conclusions of our colleagues in the Netherlands. Patients with BO diagnosed between 1994 and 2009 at one centre (Glasgow Royal Infirmary (GRI)) all had BO visible endoscopically, with biopsy-proven metaplastic glandular mucosa in the tubular oesophagus. Exclusions for residence outside GRI catchment area, severe comorbidities, refusal of surveillance, loss to follow-up, high-grade dysplasia (HGD) or oesophageal adenocarcinoma (OA) at diagnosis (or ascertained within 1 year of index endoscopy), or being indefinite for dysplasia (n=15) left 145 short (≤3 cm) and 577 long (>3 cm) patients with BO in surveillance. Biopsy protocol was by endoscopist’s choice. Endoscopy was biennial without LGD, and 3–6 monthly after LGD ascertainment. Patients with new HGD or OA were offered endoscopic treatment or surgery. Proton pump inhibitors (PPIs) were prescribed throughout. Death and its causes were ascertained from the regional registrar. Follow-up was from entry to progression, death or 31 December 2012. Age and BO length thresholds were taken as <65, 65–74, >75 years; ≤3 cm, >3 cm. Progression-free survival was examined with the Kaplan–Meier estimator and Cox’s proportional hazards regression of progression to HGD or OAwith the following factors: prevalent dysplasia as originally reported, age, gender, segment length and social deprivation, using R V.3.0.2, with libraries survival andmuhaz. Our 722-person cohort of 437 men (1st quartile:median:3rd quartile 53:63:72 years) and 285 women (61:69:78 years) underwent 74 989 months’ follow-up (75:109:137 months). N=58 patients with prevalent dysplasia were slightly older (median 67 vs 64 years, p<0.05) and more likely to be male (40 men, 18 women, p<0.02). Of these 58, 21 (36%) progressed to HGD (9) or OA (12) at overall rates of 2.0% and 2.7% per annum, respectively (p<0.001). Of the 664 patients without identified prevalent dysplasia, 85 progressed: 54 (8%) to LGD at 0.93% per annum. Only 10 (1.5%) developed HGD at 0.17% per annum and 21 (3.2%) OA, at 0.36% per annum. LGD was powerfully predictive of progression, with HR 10.8 (95% CI 5.9 to 18.1) for progression to