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Barrett’s esophagus (BE) is the partial replacement, from the gastro-esophageal junction (GEJ) proximally, of esophageal squamous epithelium with metaplastic columnar epithelium. It develops in patients with gastroesophageal reflux disease (GERD) because of chronic injury and inflammation of the esophageal epithelium. Many other factors have also significance. BE is the only known precursor to esophageal adenocarcinoma (EAC), the incidence of which has been increased faster in Western world in the past four decades [1, 2]. In the United States, the incidence of EAC increased from 3.6 cases per 1,000,000 in 1973 to 25.6 per 1,000,000 in 2006 [1]. Since EAC is frequently detected at an advanced stage, the prognosis remains poor. The 5-year survival rate of patients with locally advanced EAC undergoing curative resection is around 15–20% [3]. So detection at an early stage of neoplastic progression may be important in improving survival. The risk of developing EAC is 30–40-fold higher in patients with BE compared with the general population [4, 5]. The development of EAC in BE has been shown to occur through a multistep process of increasing grades of epithelial dysplasia, from no dysplasia to low-grade dysplasia (LGD), high-grade dysplasia (HGD) and finally EAC [6]. In two studies of 136 and 170 patients with nondysplastic Barrett's esophagus (NDBE), followed for approximately 4 years, the rate of progression to EAC was 0.5% per patient-year [7, 8]. The risk additionally increases if Barrett’s dysplasia is present. The annual incidence of EAC in patients with LGD and HGD is about 1.7% and 6.6% respectively [9]. In another study of 75 BE patients with HGD, 16% developed EAC over a mean follow-up period of 7.3 years [10]. In last years, there are many new data for the pathogenesis and the natural history of BE, which raise many points regarding surveillance of BE and risk stratification for EAC, and current role

Diagnosis and Management of Barrett’s Esophagus with and Without Dysplasia