Antireflux surgery for dysplastic Barrett's esophagus.

Abstract

Nearly a decade ago I came home from DDW with scars on my ego, having been scolded by gastroenterologists for touting the ability of laparoscopic fundoplication to protect patients with Barrett’s esophagus from the ravages of esophageal cancer. As high volume laparoscopic antireflux surgeons with many Barrett’s patients treated, quite a number of us (Hunter, Pellegrini, Peters, Oberg, and others) had observed and reported extremely low rates of cancer development in our Barrett’s patients under annual surveillance after fundoplication, rates much lower than medical surveillance studies of patients on PPIs. As a result of this intellectual dissonance, I challenged Eugene Chang, an extremely bright surgical resident at our institution to answer the question: Does laparoscopic fundoplication protect against cancer in patients with Barrett’s esophagus? The result was a very well performed systematic review of the literature, with a mixed message [1]. All in, Barrett’s patients were less likely to develop cancer after fundoplication, BUT the literature was dominated by case series—such as ours—where selection bias may have favored younger, healthier patients with short segment Barrett’s, excellent compliance with care recommendations, and less endstage physiology (strictures, motor disorders, giant hernias, etc.). When we looked at RCT’s (1) and case-controlled series (4) we could not demonstrate a difference. It was no longer clear that fundoplication prevented the progression of Barrett’s esophagus to cancer. So with my tail between my legs, I changed my tune… but only a little. This review by Allaix and Patti has covered all the bases, found all the relevant studies, and summarized them well. While we may not be able to PROVE that fundoplication prevents cancer, we can show that the factors that cause cancer (unrelenting reflux by acid and bile) are better treated with a functional valve (fundoplication) than with PPIs. PPIs rarely normalize esophageal acid exposure in Barrett’s patients. Because GERD patients often have symptom reduction when Barrett’s metaplasia develops, the only way to insure that Barrett’s patients on PPI have adequate acid exposure reduction is to perform esophageal pH studies while the patient is on a PPI. Even if PPI dosage is elevated to ‘‘nuclear’’ levels and esophageal acid is eliminated, there is still bile… and other refluxate… In addition, surrogate markers for cancer progression in Barrett’s esophagus are down regulated after fundoplication, suggesting that pathways favoring proliferation and cell dysregulation respond to the elimination of bile and acid. Lastly, the data seem pretty reproducible that a failed fundoplication puts a Barrett’s patient at higher risk for esophageal cancer. So maybe fundoplication really does make a difference? With all this background, the question addressed in this paper is ‘‘what about dysplastic Barrett’s?’’ Here the data gets a little slim. Low grade dysplasia (LGD) is the ‘slipperiest’ diagnosis in esophageal disease. When looking at the same slide, pathologists will frequently disagree over the diagnosis of LGD. Subsequent endoscopies in the same patient, with or without treatment, will frequently demonstrate different findings (no dysplasia, high grade dysplasia (HGD), or intramucosal cancer). So it’s hard to know what to do with LGD. At one time, we thought it should be treated with radiofrequency ablation (RFA) and pH control (fundoplication or PPI), but now the evanescent nature of LGD drives us more toward continued surveillance and pH control only.