A systematic review and meta-analysis of tobacco use and prostate cancer mortality and incidence in prospective cohort studies.

A systematic review and meta-analysis of tobacco use and prostate cancer mortality and incidence in prospective cohort studies.
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DOI:
10.1016/j.eururo.2014.08.059
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发表时间:
2014-12
期刊:
影响因子:
23.4
通讯作者:
Freedland SJ
Freedland SJ
中科院分区:
医学1区
文献类型:
--
作者:
Islami F;Moreira DM;Boffetta P;Freedland SJ

文献摘要

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早期对24项前瞻性研究进行的荟萃分析表明吸烟与前列腺癌(PCa)发病率和死亡率之间存在关联,其中未检查每单位烟草使用的剂量-反应关联和风险。我们研究了烟草使用的几个指标与PCa死亡率(主要结果)和发病率(次要结果)之间的关系,包括剂量反应关系。通过检索PubMed和Web of Science数据库(截至2014年1月21日)和相关文章的参考文献列表,确定前瞻性研究的相关文章。使用随机效应方法计算组合相对风险(RR)和95%置信区间(CI)。我们还计算了吸烟和PCa死亡的人群归因风险(PAR)。我们在该荟萃分析中纳入了51篇文章(11823例PCa死亡,50349例事件病例和4082606例队列参与者)。目前吸烟与PCa死亡风险增加相关(RR:1.24; 95%CI,1.18-1.31),几乎没有异质性和发表偏倚的证据。每天吸烟的数量与PCa死亡率有剂量反应关系(p = 0.02;每天吸烟20支的RR:1.20)。在美国和欧洲,吸烟和PCa死亡的PAR分别为6.7%和9.5%,相当于这两个地区每年死亡人数>10 000人。目前吸烟与PCa事件呈负相关(RR:0.90; 95%CI,0.85-0.96),结果具有高度异质性。然而,在1995年或更早完成的研究中(认为在前列腺特异性抗原筛查时代之前完成),曾经吸烟与PCa事件呈正相关(RR:1.06; 95%CI,1.00-1.12),异质性很小。来自观察性研究的综合证据显示,吸烟与致死性PCa之间存在适度但具有统计学显著性的相关性。吸烟似乎是PCa死亡的一个可改变的危险因素。吸烟会增加前列腺癌死亡的几率。不吸烟可以防止这种伤害和许多其他与烟草有关的疾病。
An association between tobacco smoking and prostate cancer (PCa) incidence and mortality was suggested in an earlier meta-analysis of 24 prospective studies in which dose–response associations and risks per unit of tobacco use were not examined. We investigated the association between several measures of tobacco use and PCa mortality (primary outcome) and incidence (secondary outcome) including dose–response association. Relevant articles from prospective studies were identified by searching the PubMed and Web of Science databases (through January 21, 2014) and reference lists of relevant articles. Combined relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random effects methods. We also calculated population attributable risk (PAR) for smoking and PCa mortality. We included 51 articles in this meta-analysis (11 823 PCa deaths, 50 349 incident cases, and 4 082 606 cohort participants). Current cigarette smoking was associated with an increased risk of PCa death (RR: 1.24; 95% CI, 1.18–1.31), with little evidence for heterogeneity and publication bias. The number of cigarettes smoked per day had a dose–response association with PCa mortality ( p = 0.02; RR for 20 cigarettes per day: 1.20). The PAR for cigarette smoking and PCa deaths in the United States and Europe were 6.7% and 9.5%, respectively, corresponding to >10 000 deaths/ year in these two regions. Current cigarette smoking was inversely associated with incident PCa (RR: 0.90; 95% CI, 0.85–0.96), with high heterogeneity in the results. However, in studies completed in 1995 or earlier (considered as completed before the prostate-specific antigen screening era), ever smoking showed a positive association with incident PCa (RR: 1.06; 95% CI, 1.00–1.12) with little heterogeneity. Combined evidence from observational studies shows a modest but statistically significant association between cigarette smoking and fatal PCa. Smoking appears to be a modifiable risk factor for PCa death. Smoking increases the chance of prostate cancer death. Not smoking prevents this harm and many other tobacco-related diseases.