Barrett Esophagus: When to Endoscope

Abstract

Increasing interest in identifying an effective strategy for decreasing the burden of esophageal adenocarcinoma (EAC) has been fuelled by the rising EAC rates worldwide, the morbidity associated with esophagectomy, and the development of endoscopic methods for curing early-stage EAC. In the face of this enthusiasm, however, we should be cautious about continuing our current evidence-free approach to screening and one with unclear benefits and unclear costs to the community. The literature is increasingly recognizing that the value of traditional endoscopy for screening and surveillance of Barrett esophagus may be more limited than initially believed. A better understanding of the risk factors for Barrett esophagus and progression to dysplasia and a more individualized risk calculation will be useful in defining populations to consider for Barrett screening. The development of novel, nonendoscopic screening techniques and of less expensive endoscopic techniques holds promise for a cost-effective screening and surveillance method to curtail the increasing rates of EAC.

The importance of a second opinion in the diagnosis of Barrett’s esophagus: a “real life” study

“…In fact, since it is well known that Barrett's epithelium may progress to adenocarcinoma over a period of time (34,35), it is of paramount importance to detect the early phases of neoplastic transformation, that is, LGD. Since patients with BE usually enter a surveillance program (36), and the finding of dysplasia prompts repeated endoscopic and pathologic controls (37), thus raising the health costs (38), efforts should be made not to overemphasize the diagnosis of dysplasia in this setting. On the other hand, further efforts should be made to obtain diag- LGD in BE LGD in BE 2 C3M4…”

Aneusomy detected by fluorescence in‐situ hybridization has high positive predictive value for Barrett's dysplasia

“…The probes used were the Vysis Esophageal FISH probe kit, Vysis 04N19-020, consisting of the probes: CDKN2A (9p12) in spectrum red, HER-2 (17q11. [2][3][4][5][6][7][8][9][10][11][12] in spectrum green, CMYC (8q24.12-13) in spectrum aqua and ZNF217(20q13) in spectrum gold. Three microlitre were dispensed manually onto a coverslip, onto which the targeted tissue slide was placed.…”

“…[5][6][7] Despite its known imperfections, dysplasia, identified visually by histopathologists, remains the most reliable marker for cancer risk. 8,9 DNA fluorescence in-situ hybridization (FISH) for specific sequences 10 is well established in diagnostic histopathology. Previous studies have identified genetic alterations associated with dysplasia and adenocarcinoma in Barrett's oesophagus.…”

“…The loci most often altered in dysplasia and adenocarcinoma included CDKN2A, which encodes p16 (9p12), HER2 (17q11. [2][3][4][5][6][7][8][9][10][11][12], CMYC (8q24. [12][13] and ZNF217 (20q13.2).…”

Endoscopic surveillance of gastrointestinal premalignant lesions

“…This decrease in progression risk has important implications in the surveillance of Barrett’s esophagus since the effectiveness and cost effectiveness of surveillance are dependent on progression rate from Barrett’s to esophageal adenocarcinoma. (8) …”