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What we talk about when we talk about low-grade dysplasia
  1. Patrick Yachimski
  1. Correspondence to Dr Patrick Yachimski, Division of Gastroenterology, Hepatology & Nutrition, Vanderbilt University Medical Center, 1660 The Vanderbilt Clinic, Nashville, TN 37232-5280, USA; patrick.yachimski{at}vanderbilt.edu

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Nearly a decade has elapsed since initial publication of a multicentre randomised trial of porfimer sodium photodynamic therapy (psPDT) for the treatment of Barrett's oesophagus (BO) containing high-grade dysplasia (HGD).1 With the addition of endoscopic mucosal resection (EMR) and radiofrequency ablation (RFA) to the therapeutic armamentarium, a seismic shift has now ensued in the treatment landscape of BO-associated mucosal neoplasia. An ever-increasing proportion of patients with BO HGD or T1 oesophageal adenocarcinoma (OAC), opt for endoscopic therapy rather than surgery.2 Durable disease remission is achievable for the majority of patients, with most instances of recurrence being amenable to further endoscopic management and with low rates of salvage oesophagectomy or oesophageal cancer-related mortality.3

Compared with a significant post-treatment stricture rate (>30% for PDT1) and prolonged duration of photosensitivity following psPDT, the relatively lower toxicity profile of newer-generation endoscopic therapies (<10% stricture rate for RFA4) has enabled consideration of whether prophylactic endoscopic therapy may be offered, in lieu of surveillance, to an expanded treatment pool of patients with pathology less advanced than HGD. Indeed, an endoscopic ablation strategy for BO has been envisioned as analogous to the widespread practice of screening colonoscopy and resection of adenomatous polyps for prevention of colorectal cancer.5

Yet at the same time, epidemiological investigation has prompted a recalibration of the risk of BO neoplastic progression. An annual progression rate from non-dysplastic BO to OAC of 0.12% was reported from a …

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