David Lieberman, Marco J. Bruno, Sreekar Vennalaganti, Kevin F. Kennedy, Patrick E. Young, Brooks D. Cash, Fouad J. Moawad, Richard E. Sampliner, Manon C.W. Spaander, Prashanth Vennalaganti, Prateek Sharma, Ajay Bansal, Sharad C. Mathur, Neil Gupta, John J. Vargo, Srinivas Gaddam, Gary W. Falk, Prashanthi N. Thota, Sravanthi Parasa, and Gastroenterology & Hepatology
Background & Aims A system is needed to determine the risk of patients with Barrett's esophagus for progression to high-grade dysplasia (HGD) and esophageal adenocarcinoma (EAC). We developed and validated a model to determine of progression to HGD or EAC in patients with BE, based on demographic data and endoscopic and histologic findings at the time of index endoscopy. Methods We performed a longitudinal study of patients with BE at 5 centers in United States and 1 center in Netherlands enrolled in the Barrett's Esophagus Study database from 1985 through 2014. Patients were excluded from the analysis if they had less than 1 year of follow up, were diagnosed with HGD or EAC within the past year, were missing baseline histologic data, or had no intestinal metaplasia. Seventy percent of the patients were used to derive the model and 30% were used for the validation study. The primary outcome was development of HGD or EAC during the follow-up period (median 5.9 years). Survival analysis was performed using the Kaplan-Meier method. We assigned a specific number of points to each BE risk factor, and point totals (scores) were used to create categories of low, intermediate, and high risk. We used Cox regression to compute hazard ratios (HR) and 95% CIs to determine associations between risk of progression and scores. Results Of 4584 patients in the database, 2697 were included in our analysis (84.1% men; 87.6% Caucasian; mean age, 55.4±20.1 years; mean body mass index, 27.9±5.5; mean length of BE, 3.7 cm±3.2). During the follow-up period, 154 patients (5.7%) developed HGD or EAC, with an annual rate of progression of 0.95%. Male sex, smoking, length of BE, and baseline-confirmed low-grade dysplasia were significantly associated with progression. Scores assigned identified patients with BE that progressed to HGD or EAC with a c-statistic of 0.76 (95% CI, 0.72–0.80) ( P P =.99), determined from the validation cohort. Conclusions We developed a scoring system (called progression of BE (PIB) score) based on male sex, smoking, length of BE, and baseline low-grade dysplasia) that identified patients with BE at low, intermediate, and high risk groups for HGD or EAC. This scoring system might be used in management of patients.