Genkinger Jeanine M, Spiegelman Donna, Anderson Kristin E, Bergkvist Leif, Bernstein Leslie, van den Brandt Piet A, English Dallas R, Freudenheim Jo L, Fuchs Charles S, Giles Graham G, Giovannucci Edward, Hankinson Susan E, Horn-Ross Pamela L, Leitzmann Michael, Männistö Satu, Marshall James R, McCullough Marjorie L, Miller Anthony B, Reding Douglas J, Robien Kim, Rohan Thomas E, Schatzkin Arthur, Stevens Victoria L, Stolzenberg-Solomon Rachael Z, Verhage Bas A J, Wolk Alicja, Ziegler Regina G, Smith-Warner Stephanie A
Department of Oncology, Lombardi Cancer Center, Georgetown University Medical Center, Washington, DC, USA.
Cancer Epidemiol Biomarkers Prev. 2009 Mar;18(3):765-76. doi: 10.1158/1055-9965.EPI-08-0880. Epub 2009 Mar 3.
Few risk factors have been implicated in pancreatic cancer etiology. Alcohol has been theorized to promote carcinogenesis. However, epidemiologic studies have reported inconsistent results relating alcohol intake to pancreatic cancer risk.
We conducted a pooled analysis of the primary data from 14 prospective cohort studies. The study sample consisted of 862,664 individuals among whom 2,187 incident pancreatic cancer cases were identified. Study-specific relative risks and 95% confidence intervals were calculated using Cox proportional hazards models and then pooled using a random effects model.
A slight positive association with pancreatic cancer risk was observed for alcohol intake (pooled multivariate relative risk, 1.22; 95% confidence interval, 1.03-1.45 comparing >or=30 to 0 grams/day of alcohol; P value, test for between-studies heterogeneity=0.80). For this comparison, the positive association was only statistically significant among women although the difference in the results by gender was not statistically significant (P value, test for interaction=0.19). Slightly stronger results for alcohol intake were observed when we limited the analysis to cases with adenocarcinomas of the pancreas. No statistically significant associations were observed for alcohol from wine, beer, and spirits comparing intakes of >or=5 to 0 grams/day. A stronger positive association between alcohol consumption and pancreatic cancer risk was observed among normal weight individuals compared with overweight and obese individuals (P value, test for interaction=0.01).
Our findings are consistent with a modest increase in risk of pancreatic cancer with consumption of 30 or more grams of alcohol per day.
胰腺癌病因中涉及的风险因素较少。酒精被认为可促进致癌作用。然而，流行病学研究报告了酒精摄入量与胰腺癌风险之间的不一致结果。
我们对14项前瞻性队列研究的原始数据进行了汇总分析。研究样本包括862,664人，其中确诊了2187例胰腺癌新发病例。使用Cox比例风险模型计算各研究的相对风险和95%置信区间，然后使用随机效应模型进行汇总。
酒精摄入量与胰腺癌风险之间观察到轻微正相关（汇总多变量相对风险为1.22；95%置信区间，比较每日饮酒≥30克与0克的情况为1.03 - 1.45；P值，研究间异质性检验 = 0.80）。对于此比较，尽管按性别划分的结果差异无统计学意义（P值，交互作用检验 = 0.19），但这种正相关仅在女性中具有统计学意义。当我们将分析限于胰腺腺癌病例时，观察到酒精摄入量的结果略强。比较每日摄入量≥5克与0克时，葡萄酒、啤酒和烈酒中的酒精均未观察到统计学显著关联。与超重和肥胖个体相比，正常体重个体中观察到酒精消费与胰腺癌风险之间存在更强的正相关（P值，交互作用检验 = 0.01）。
我们的研究结果与每日摄入30克或更多酒精会适度增加胰腺癌风险一致。
