• Barrett's oesophagus
• dysplasia
• therapeutic endoscopy

Low-grade dysplasia (LGD) in Barrett’s oesophagus (BE),1 due to the inconsistency in its diagnosis, identification and cancer progression, has been a management challenge for gastroenterologists. LGD, as classified by the Vienna classification, includes a histological subtype of BE where nuclei are hyperchromatic, enlarged and stratified, with this change extending to the surface epithelial cells and loss of surface maturation.2 However, there is a coexistent inflammation-mediated epithelial injury that can make the histopathological diagnosis difficult.

There is significant variability in the histopathological diagnosis and progression rates of LGD. A recent, large, multicentre study involving pathologists from the USA and Europe demonstrated that the interobserver agreement (IOA) for the diagnosis of LGD is very poor ( ).3 Similarly, several other studies have shown IOAs ranging from 0.17 to 0.32.4 5 Similarly, there is also a wide range in progression rates (0.02%6– 11.4%4) from LGD to neoplasia, and other studies also report either regression or persistence of LGD without neoplastic progression. A recent study also demonstrated that BE referral centres identified high grade dysplasia/esophageal adenocarcinoma (HGD/EAC) in 27% of the patients referred with a recent diagnosis of LGD, suggesting overestimation of neoplastic progression.7 Thus, the current expert best practice recommendation is to have an expert gastrointestinal pathologist confirm the diagnosis of LGD,8–10 repeat examination with white-light endoscopy (consideration for virtual chromoendoscopy) within 3–6 months of confirmed LGD to rule out higher grade lesions, that is, coexisting high-grade dysplasia or cancer8 and consideration for either …