ObjectiveSurveillance interval protocols after complete remission of intestinal metaplasia (CRIM) post radiofrequency ablation (RFA) in Barrett’s oesophagus (BE) are currently empiric and not based on substantial evidence. We aimed to assess the timeline, location and patterns of recurrence following CRIM to inform these guidelines.DesignData on patients undergoing RFA for BE were obtained from prospectively maintained databases of five (three USA and two UK) tertiary referral centres. RFA was performed until CRIM was confirmed on two consecutive endoscopies.Results594 patients achieved CRIM as of 1 May 2017. 151 subjects developed recurrent BE over a median (IQR) follow-up of 2.8 (1.4–4.4) years. There was 19% cumulative recurrence risk of any BE within 2 years and an additional 49% risk over the next 8.6 years. There was no evidence of a clinically meaningful change in the recurrence hazard rate of any BE, dysplastic BE or high-grade dysplasia/cancer over the duration of follow-up, with an estimated 2% (95% CI −7% to 12%) change in recurrence rate of any BE in a doubling of follow-up time. 74% of BE recurrences developed at the gastro-oesophageal junction (GOJ) (24.1% were dysplastic) and 26% in the tubular oesophagus. The yield of random biopsies from the tubular oesophagus, in the absence of visible lesions, was 1% (BE) and 0.2% (dysplasia).ConclusionsBE recurrence risk following CRIM remained constant over time, suggesting that lengthening of follow-up intervals, at least in the first 5 years after CRIM, may not be advisable. Sampling the GOJ is critical to detecting recurrence. The requirement for random biopsies of the neosquamous epithelium in the absence of visible lesions may need to be re-evaluated.
Background: Discovery of methylated-DNA-markers (MDMs) of esophageal-squamous-cell-carcinoma (ESCC) has sparked interest in assessing these markers in tissue. We evaluated MDMs in ESCC from three geographically and ethnically distinct populations, and explored the feasibility of assaying MDMs from DNA obtained by swallowed-balloon-devices. Methods: MDMs were assayed in ESCC and normal tissues from the US, Iran, and China, and from exfoliative cytology specimens obtained by balloons in a Chinese population. Areas under the receiver-operatingcurve (AUCs) of MDMs discriminating ESCC from normal were calculated. Random forest prediction models were built, trained on US cases and controls and calibrated to US-only controls (Model 1), and three-country controls (Model 2). Statistical tests were used to assess the relationship between dysplasia and MDM levels in balloons. Results: Extracted DNA from 333 ESCC, and 322 normal tissues were analyzed, in addition to archival DNA from 98 balloons. For ESCC, Model 1 validated in Iranian and Chinese tissues with AUCs of 0.90 and 0.87, and Model 2 yielded AUCs of 0.99, 0.96, and 0.94 in tissues from the US, Iran, and China, respectively. In Chinese balloons, MDMs showed a statistically significant trend of increasing levels with increasing grades of dysplasia (p<0.004). Conclusions: MDMs accurately discriminate ESCC from normal esophagus in tissues from high and low incidence countries. Preliminary data suggest that levels of MDMs assayed in DNA from swallowed-balloondevices increase with dysplasia grade. Larger studies are needed to validate these results.
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