While the presence of GERD symptoms was one of the first recognized and strongest risk factors identified for BE, the presence of GERD alone is not sufficient to

recommend screening. Up to 40% of US adults experience GERD on a monthly basis (28), yet despite the increasing incidence of EAC there are still fewer than 10,000 new Inhibitors,research,lifescience,medical cases of EAC diagnosed per year (29). Up to 40% of patients who have adenocarcinoma of the esophagus report no history of chronic GERD (30). Eliminating patients from screening based on a lack of symptoms could exclude a large portion of those who might have their cancers detected at an early, presymptomatic stage. Additionally, difficulties recognizing mucosal lesions (31),sampling error (32), and disagreement over pathologic interpretation (33) can decrease the effectiveness of endoscopic screening.

For these reasons, the decision of who and when to screen should be individualized (1,4). Endoscopic diagnosis Barrett’s esophagus (BE) presents on endoscopy as characteristic Inhibitors,research,lifescience,medical salmon-pink colored extensions (or “tongues”) of mucosa that grow into the esophagus above the esophageal gastric junction (EGJ). For screening and surveillance, four quadrant biopsies are taken along every 2 cm of the BE type mucosa and submitted to pathology in separate containers. While Inhibitors,research,lifescience,medical this approach samples only a small Inhibitors,research,lifescience,medical fraction of the affected lining, it allows the opportunity to recognize dysplasia and focus subsequent biopsies on the appropriate area if dysplasia is identified (4). Traditionally, BE is termed long segment if the tongues are 3 cm or more in length, short segment BE when less than 3 cm, and ultra-short segment BE when less than 1 cm (34). The exact location of the biopsy relative to the Z-line and EGJ is important Inhibitors,research,lifescience,medical to know, as ultra-short

BE can be difficult to differentiate from an irregular EGJ and is thought to carry significantly less risk of cancer development than traditional BE (34-38). Additionally, intestinal metaplasia below the EGJ should not be diagnosed as BE. The changes are thought to have a different etiology, often arising secondary to Helicobacter pylori infection, and the significance as a precursor to EAC is uncertain (35,39-41). For these reasons, changes in this Carnitine dehydrogenase region should be given a descriptive diagnosis of intestinal metaplasia. Accurate assessment of the extent of BE on endoscopy is clinically important because more extensive BE carries a higher risk of cancer development (42,43), however there is a high degree of inter- and intraobserver variation (44-46). The Prague C&M Criteria (47) is a consensus-driven, validated system which utilizes standardized ABT-378 in vivo landmarks – thesquamocolumnar junction, the EGJ, the extent of circumferential columnar lining, and the proximal extension of the columnar mucosa – to determine the length of BE.