Development and Validation of a Model to Determine Risk of Progression of Barrett's Esophagus to Neoplasia
Development and Validation of a Model to Determine Risk of Progression of Barrett's Esophagus to Neoplasia
复制标题
DOI：
10.1053/j.gastro.2017.12.009
复制
发表时间：
2018-04-01
期刊：
影响因子：
29.4
通讯作者：
Sharma, Prateek
中科院分区：
文献类型：
--
作者：
Parasa, Sravanthi;Vennalaganti, Sreekar;Sharma, Prateek
背景与目的：需要一个系统来确定Barrett食管患者进展为高度异型增生（HGD）和食管腺癌（EAC）的风险。我们开发并验证了一种模型，以确定BE患者进展为HGD或EAC，基于人口统计学数据以及索引内镜检查时的内镜和组织学结果。方法：我们对1985年至2014年入组Barrett食管研究数据库的美国5家中心和荷兰1家中心的BE患者进行了一项纵向研究。如果患者的随访时间少于1年，在过去一年内被诊断为HGD或EAC，基线组织学数据缺失或没有肠上皮化生，则将其从分析中排除。70%的患者用于推导模型，30%用于验证研究。主要结局是随访期间（中位数，5.9年）发生HGD或EAC。采用Kaplan-Meier法进行生存分析。我们为每个BE风险因素分配了特定数量的分数，并使用总分数（分数）创建低，中等和高风险类别。我们使用考克斯回归计算风险比和95%置信区间，以确定进展风险与评分之间的关联。研究结果：在数据库中的4584例患者中，2697例被纳入我们的分析（84.1%男性; 87.6%白人;平均年龄55.4 ± 20.1岁;平均体重指数27.9 ± 5.5 kg/m2;平均BE长度3.7 ± 3.2 cm）。在随访期间，154例患者（5.7%）发生HGD或EAC，年进展率为0.95%。男性、吸烟、BE长度和基线证实的低度异型增生与进展显著相关。分配的评分确定了进展为HGD或EAC的BE患者，c-统计量为0.76（95%置信区间，0.72-0.80; P <0.001）。校准斜率为0.9966（P = .99），由验证队列确定。结论：我们基于男性性别、吸烟、BE长度和基线低度异型增生开发了一种评分系统（Barrett食管进展评分），该系统可识别HGD或EAC低、中、高风险BE患者。该评分系统可用于患者的管理。
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 and 95% confidence intervals 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 kg/m(2); mean length of BE, 3.7 +/- 3.2 cm). 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% confidence interval, 0.72-0.80; P < .001). The calibration slope was 0.9966 (P = .99), determined from the validation cohort. CONCLUSIONS: We developed a scoring system (Progression in Barrett's Esophagus 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 for HGD or EAC. This scoring system might be used in management of patients.