Alcohol intake and pancreatic cancer risk: a pooled analysis of fourteen cohort studies.
Alcohol intake and pancreatic cancer risk: a pooled analysis of fourteen cohort studies.
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DOI：
10.1158/1055-9965.epi-08-0880
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发表时间：
2009-03
期刊：
影响因子：
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通讯作者：
Smith-Warner SA
中科院分区：
文献类型：
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作者：
Genkinger JM;Spiegelman D;Anderson KE;Bergkvist L;Bernstein L;van den Brandt PA;English DR;Freudenheim JL;Fuchs CS;Giles GG;Giovannucci E;Hankinson SE;Horn-Ross PL;Leitzmann M;Männistö S;Marshall JR;McCullough ML;Miller AB;Reding DJ;Robien K;Rohan TE;Schatzkin A;Stevens VL;Stolzenberg-Solomon RZ;Verhage BA;Wolk A;Ziegler RG;Smith-Warner SA
几乎没有危险因素与胰腺癌的病因有关。从理论上讲，酒精会促进癌症的发生。然而，流行病学研究报告了与饮酒与胰腺癌风险相关的不一致结果。我们对14项前瞻性队列研究的主要数据进行了汇集分析。研究样本包括862,664人，其中2187人被确认为胰腺癌病例。使用COX比例风险模型计算特定研究的相对风险(RR)和95%可信区间(CI)，然后使用随机效应模型进行合并。饮酒与胰腺癌风险呈轻微正相关(合并多变量RR=1.2 2，比较≥30克/天至0克/天的95%可信区间1.03-1.45；p值，研究间异质性检验=0.80)。在这一比较中，正相关性只在女性中具有统计学意义，尽管性别之间的结果差异在统计学上没有显著差异(p值，交互作用检验=0.19)。当我们将分析限制在胰腺腺癌的病例中时，酒精摄入量的结果略有增强。与每天摄入5克和0克≥相比，葡萄酒、啤酒和烈性酒中的酒精之间没有统计学上的显著相关性。与超重和肥胖个体相比，正常体重个体的饮酒与胰腺癌风险之间存在更强的正相关性(p值，交互作用检验=0.01)。我们的发现与每天饮酒30克或更多的人患胰腺癌的风险略有增加是一致的。
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 (RR) and 95% confidence intervals (CI) 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 RR =1.22, 95% CI 1.03–1.45 comparing ≥ 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 ≥ 5 to 0 grams/day. A stronger positive association between alcohol consumption and pancreatic cancer risk was observed among normal weight individuals compared to 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.