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Abstract

Increasingly practicing gastroenterologists are faced with the dilemma of how to manage patients with Barrett’s esophagus who develop high-grade epithelial dysplasia. This issue has been compounded by recent studies suggesting that patients with both long- and short-segment Barrett’s esophagus progress from dysplasia to invasive carcinoma (Am J Gastroenterol 2000;95:1888–1893). With a heightened awareness of dysplasia and carcinoma associated with short-segment Barrett’s esophagus combined with improved patient selection and screening criteria, gastroenterologists are identifying patients with short-segment Barrett’s esophagus with unprecedented frequency. Consequently, the chance of encountering either prevalent or incident epithelial dysplasia at endoscopic biopsy of such patients in community clinical practice is more likely than ever before. Can the practicing gastroenterologist be confident that they are dealing with a dysplastic lesion with no propensity for metastases? In our study, we attempted to objectively assess the ability of gastrointestinal (GI) pathologists to determine accurately the presence of invasive carcinoma. Clearly, even experienced GI pathologists under ideal circumstances (using surgical resection specimens, not biopsy specimens) have difficulty making such a diagnosis. So where does this leave the clinician? Despite the use of molecular markers of risk for the development of dysplasia/carcinoma, such as mutated p53 expression and DNA ploidy assessment, the dilemma of how to manage this disease is still a challenge. Currently, interpretation of biopsy material by a “good” GI pathologist remains the gold standard upon which treatment decisions, including surgical management, is based. Despite the weaknesses of histologic interpretation highlighted in our study, to date there has been no tumor marker or molecular test that can match the ability of the GI pathologist to identify the presence of early invasive carcinoma. Given the complex interplay of molecular events involved in tumor progression and invasion, it may be some time before the “magic” molecule is found. Until that time, the clinician’s relationship with the designated GI pathologist is a critical component of patient care. Good correlation between what is found on preoperative endoscopic biopsy and the subsequent surgical resection specimen may be a more important determinant of a “good” GI pathologist than academic reputation, alignment with a prestigious institution, or experience alone. Increased attention, therefore, by the practicing clinician to the track record of one’s GI pathologist may be the very factor that will lessen the struggle to separate bad from worse in Barrett’s-related epithelial dysplasia.