Rahman Farah, Cotterchio Michelle, Cleary Sean P, Gallinger Steven
Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada.
Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada; Prevention and Cancer Control, Cancer Care Ontario, Toronto, Ontario, Canada.
PLoS One. 2015 Apr 9;10(4):e0124489. doi: 10.1371/journal.pone.0124489. eCollection 2015.
Evidence is inconsistent regarding alcohol and pancreatic cancer risk, although heavy drinking may increase risk.
A population-based case-control study was conducted using 345 pancreas cancer cases diagnosed 2011-2012 and 1,285 frequency-matched controls from Ontario, Canada. Logistic regression was used to evaluate alcohol consumption and pancreatic cancer risk; data was also stratified by sex and smoking status to assess interaction.
Alcohol consumption was not associated with pancreatic cancer risk (age-adjusted odds ratio=0.78, 95% CI: 0.58, 1.05 for 1 - 3 drinks/week; age-adjusted odds ratio=0.86, 95% CI: 0.63, 1.17 for 4 - 20 drinks/week), however there was a non-significant increased risk for heavy drinkers consuming ≥ 21 drinks/week (age-adjusted odds ratio=1.35, 95% CI: 0.81, 2.27). Cigarette smoking modified the alcohol-cancer relationship; among current smokers, heavy alcohol consumption was associated with a significantly increased pancreatic cancer risk (age-adjusted odds ratio=4.04, 95% CI: 1.58, 10.37), whereas this significant association with heavy drinking was not observed among non-smokers (age-adjusted odds ratio=2.01, 95% CI: 0.50, 8.18). Furthermore, light - moderate alcohol intake was associated with increased pancreas cancer risk among current smokers.
While alcohol was not significantly associated with pancreatic cancer risk, smoking status modified this relationship such that among current smokers, alcohol intake was associated with a greater than two-fold increased risk of pancreatic cancer. The results should be interpreted with caution due to small sample sizes within subgroups and correction for multiple comparisons should be considered. These findings should be replicated in larger studies where more precise estimates of risk can be obtained.
关于酒精与胰腺癌风险的证据并不一致，尽管大量饮酒可能会增加风险。
开展了一项基于人群的病例对照研究，使用了2011年至2012年确诊的345例胰腺癌病例以及来自加拿大安大略省的1285名频率匹配的对照。采用逻辑回归评估饮酒情况与胰腺癌风险；数据还按性别和吸烟状况进行分层以评估相互作用。
饮酒与胰腺癌风险无关（每周饮用1 - 3杯酒，年龄调整后的优势比 = 0.78，95%置信区间：0.58，1.05；每周饮用4 - 20杯酒，年龄调整后的优势比 = 0.86，95%置信区间：0.63，1.17），然而，每周饮用≥21杯酒的重度饮酒者风险有非显著性增加（年龄调整后的优势比 = 1.35，95%置信区间：0.81，2.27）。吸烟改变了酒精与癌症的关系；在当前吸烟者中，大量饮酒与胰腺癌风险显著增加相关（年龄调整后的优势比 = 4.04，95%置信区间：1.58，10.37），而在非吸烟者中未观察到大量饮酒与胰腺癌风险的显著关联（年龄调整后的优势比 = 2.01，95%置信区间：0.50，8.18）。此外，当前吸烟者中轻度至中度饮酒与胰腺癌风险增加相关。
虽然酒精与胰腺癌风险无显著关联，但吸烟状况改变了这种关系，使得在当前吸烟者中，酒精摄入与胰腺癌风险增加两倍以上相关。由于亚组内样本量较小，结果应谨慎解释，并且应考虑对多重比较进行校正。这些发现应在更大规模的研究中重复验证，以获得更精确的风险估计。
