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PTU-144 Can we Predict Patients with Barrett’S Dysplasia who will Progress to Malignancy Despite Endotherapy; Results of a Prospective, Single Centre Experience
  1. H C Mcewan1,
  2. J Going2,
  3. G Fullarton3,
  4. A J Morris4
  1. 1Walton Building, University Department of Surgery, Glasgow Royal Infirmary
  2. 2Pathology, Southern General Hospital
  3. 3Surgery
  4. 4Gastroenterology, Glasgow Royal Infirmary, Glasgow, UK

Abstract

Introduction In the treatment of Barrett’s patients with intramucosal cancer (IMC) and high grade dysplasia (HGD), there is mounting evidence to support a combined endoscopic approach of endoscopic mucosal resection (EMR) and radiofrequency ablation (RFA). Despite the efficacy and safety of endotherapy in the treatment of IMC and HGD, some patients fail to respond to treatment or progress to oesophageal adenocarcinoma (EAC). We sought to examine the factors associated with the failure to respond or the progression to EAC from a tertiary referral practise.

Methods 105 patients with a mean age of 70 (range 43 – 90) years with HGD or IMC were treated between July 2008 and December 2012. The treatment protocol involved EMR of all nodular areas with subsequent RFA of all remaining Barretts epithelium. The RFA technique involved a combination of circumferential (HALO 360) followed by subsequent focal ablation (HALO 90) of residual areas of Barrett’s tongues or islands. Patients were deemed to have completed endotherapy on eradication of dysplasia. A maximum of 2 HALO 360’s and 3 HALO 90’s were allowed. Patients who failed to respond to endotherapy or developed EAC were withdrawn from endotherapy. Median follow up was 9 (3 – 41) months.

Results 105 patients were treated (29 IMC and 76 HGD). Eighty patients have completed the treatment protocol to date (median of 1 HALO 360 and 1 HALO 90) and 42 (52%) of these had initial EMR. Eleven patients died during follow up, 2 from oesophageal cancer and the remaining 9 from non-oesophageal related causes. Eradication of Barrett’s dysplasia was achieved in 80/91 (87%) and eradication of metaplasia in 61/91 (67%). Five (4.7%) patients progressed to EAC and 3 (2.8%) patients failed treatment as their IMC or HGD was refractory to RFA and required surgery. The demographics for those that progressed to EAC compared to those that did not (Non-EAC) are as follows. EAC; males 5 (100%), mean initial Barrett’s length 7cm, those having pre-halo EMR 4 (80%) and initial pathology of 2 IMC (40%) and 3 HGD (60%). Non-EAC group; males 71 (73%), females 26 (27%), mean initial Barrett’s length 7 cm, those having pre-halo EMR 42 (43%) and initial pathology of 28 IMC (28%) and 69 HGD (71%). Finally the time from first RFA to developing malignancy was a mean of 182 (42 – 733) days.

Conclusion In this cohort, there is a 4.7% chance of developing EAC, 2.8% of patients could not complete planned endotherapy and an 8.5% chance of death from non-oesophageal diseases. These outcomes are independent of the demographic, pathologic and endoscopic variables studied.

Disclosure of Interest None Declared

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