• Barrett's oesophagus
• dysplasia
• therapeutic endoscopy

低度发育不良(乐金显示器)巴雷特食管(BE),1due 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.2However, 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 ( ).3Similarly, several other studies have shown IOAs ranging from 0.17 to 0.32.4 5Similarly, 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.7Thus, the current expert best practice recommendation is to have an expert gastrointestinal pathologist confirm the diagnosis of LGD,8–10repeat 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 cancer8and consideration for either …