Clin Gastroenterol H：巴雷特食管与2型糖尿病相关

　　向心性肥胖通过力学机制和（或）代谢机制会增加巴雷特食管（BE）和食管腺癌（EAC）的风险，如高胰岛素血症。近日，美国罗契斯特梅奥医院的Prasad G. Iyer进行了一项流行病学研究，以确定2型糖尿病（DM2）前期是否与巴雷特食管相关。在一项基于大量人群的病例对照研究中，DM2是BE的一项危险因素，独立于肥胖（根据BMI测量）和其他危险因素（吸烟和GERD）。这些数据表明，应在BE发病机制及食管致癌作用方面探索与DM2相关的代谢途径。该文在线发表于4月15日《临床胃肠病学与肝脏病学》（Clinical Gastroenterology and Hepatology）杂志上。

　　研究者通过英国综合医疗研究数据库（GPRD）进行了一项以人群为基础的病例对照研究，该数据库是英国初级保健数据库，包含了超过800万个学科的信息。研究确定BE病例（根据预先验证代码；n＝14245）和非BE对照组病例（根据发病率密度取样；n＝70361）。两组在年龄、性别、登记日期、随访持续时间和区域方面相匹配。我们通过条件单变量和多变量回归分析评估了DM2诊断前与BE的相关性。混杂因素评估包括吸烟、体质指数（BMI）肥胖测量和胃食管反流病（GERD）。

　　与对照组相比，BE组病例吸烟者可能更多（52.4%对49.9%），平均BMI更高（27.2对26.9），DM2患病率更高（5.8%对5.3%）。在多变量分析中，DM2与BE 49%的危险增加相关，独立于其他已知危险因素（比值比，1.49；95%可信区间，1.16-1.91）。此相关性女性比男性更显著。敏感性分析结果恒定。

与糖尿病相关的拓展阅读：

• Diabetes Care：良好的血糖和血压控制有益于延长糖尿病患者生存期
• Diabetic Med：高血压患者治疗时HDL低预示新发糖尿病风险更高
• AACE2013：糖尿病治疗方案
• NEJM：美国糖尿病防治十年进展回顾
• NEJM：糖尿病治疗有进展但仍存不足 更多信息请点击：有关糖尿病更多资讯

Association of Barrett’s Esophagus with Type II Diabetes Mellitus: Results from a Large Population-Based Case Control Study
BACKGROUND & AIMS
entral obesity could increase risk for Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC) by mechanical and/or metabolic mechanisms, such as hyperinsulinemia. We performed an epidemiologic study to determine if there whether prior type 2 diabetes mellitus (DM2) is associated with BE.
METHODS
We performed a population-based case-control study using the General Practice Research Database (GPRD), a United Kingdom primary care database that contains information from more than 8 million subjects, to identify cases of BE (using previously validated codes; n=14,245) and matched controls without BE (by age, sex, enrollment date, duration of follow up, and practice region, by incidence density sampling; n=70,361). We assessed the association of a prior diagnosis of DM2 with BE, using conditional univariate and multivariable regression analysis. Confounders assessed included smoking, obesity measured by BMI, and gastroesophageal reflux disease (GERD).
RESULTS
BE cases were more likely than controls to have smoked (52.4% vs 49.9%), have a higher mean BMI (27.2 vs 26.9), and a higher prevalence of DM2 than controls (5.8% vs 5.3%). On multivariable analysis, DM2 was associated with a 49% increase in the risk of BE, independent of other known risk factors (odds ratio, 1.49; 95% confidence interval, 1.16-1.91). This association was stronger in women than men. Results remained stable with sensitivity analyses.
CONCLUSIONS
In a large population based case-control study, DM2 was a risk factor for BE, independent of obesity (as measured by BMI) and other risk factors (smoking and GERD). These data suggest that metabolic pathways related to DM2 should be explored in BE pathogenesis and esophageal carcinogenesis.