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It was a pleasure to receive a letter from Dr. Michael Zinner inviting us to write a prospective on the chapters from Drs. Daniel Tong and Simon Law from Hong Kong on cancer of the esophagus and Drs. Jon Wee, Shelby Steward, and Raphael Bueno from The Brigham and Women’s Hospital, Harvard Medical School, on surgical procedures to resect and replace the esophagus. We begin by stating both chapters are exceedingly well written, informative, and enlightening. Our reading identified areas where we were moved to comment based on our personal experience. The comments usually take the form of additional thoughts or alternatives. Occasionally, we raise a note of caution or take a controversial point of view.


The specific reason for the dramatic increase in adenocarcinoma of the esophagus continues to remain a mystery, even though it represents the largest epidemiologic change ever recorded for a solid cancer.1 Reasons proposed for the significant and continuous increase in incidence of esophageal adenocarcinoma are the epidemics of obesity and gastroesophageal reflux disease (GERD).2 The latter can result in the complication of Barrett esophagus and its subsequent development into high-grade dysplasia. As Tong and Law point out, high-grade dysplasia is the last preinvasive stage in the metaplasia–dysplasia–cancer sequence and has become the focus of efforts to combat the problem. Intensive surveillance of patients with Barrett esophagus is proposed as a strategy to identify high-grade dysplasia prior to the evolvement of cancer and treat it with endoscopic mucosal resection or ablation. To date, the results of intensive surveillance have been disappointing, and the work involved in ablation and its required unlimited follow-up is extremely expensive. Further, Tong and Law indicate a 20% recurrence rate after an average follow-up of 2.4 years, and the median length of Barrett mucosa in which the recurrent lesion occurred was only 0.6 cm, which is significantly shorter and more difficult to identify than the pretreatment length.

Disappointment with intensive surveillance as a solution to the Barrett esophagus problem has stimulated an interest in the possibility of surgically preventing the development of Barrett esophagus. The progression of GERD to Barrett esophagus in patients who are receiving treatment with proton pump inhibitors (PPIs) has been reported by several investigators.3-5 This has led to concerns that PPI therapy does not address all aspects of the disease and patients who are at risk of progression need to be identified early in the course of their disease in order to prevent the development of visible Barrett esophagus. Recently, it has been reported that biopsies of the squamocolumnar junction that show microscopic intestinalized metaplastic cardiac mucosa in endoscopically normal patients with GERD are predictive of the evolvement of visible Barrett esophagus.6

A further indicator of progression toward visible Barrett esophagus is a permanent structural alteration of the lower esophageal sphincter (LES) on manometry, resulting ...

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