Diabetes mellitus and risk of prostate cancer: an updated meta-analysis based on 12 case–control and 25 cohort studies
Diabetes mellitus and risk of prostate cancer: an updated meta-analysis based on 12 case–control and 25 cohort studies
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DOI：
10.1007/s00592-012-0439-5
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发表时间：
2012-11
影响因子：
3.8
通讯作者：
Fan Zhang;Yuan Yang;L. Skrip;D. Hu;Yang Wang;Chunguang Wong;JingFu Qiu;H. Lei
中科院分区：
文献类型：
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作者：
Fan Zhang;Yuan Yang;L. Skrip;D. Hu;Yang Wang;Chunguang Wong;JingFu Qiu;H. Lei
糖尿病与前列腺癌风险之间的关联已得到广泛研究。然而，研究结果仍然不一致和矛盾。本研究采用荟萃分析方法，探讨了纳入更多近期研究的关系，并提供了更有力的证据，不受任何个别研究的限制。通过检索截至 2012 年 5 月 18 日的 Pubmed 和 Cochrane 对照试验中央注册库确定了相关研究。使用相对风险 (RR) 评估了糖尿病与前列腺癌风险之间的关系强度。使用固定效应或随机效应模型来计算汇总 RR。进行分层分析和敏感性分析，并通过 Egger 检验和 Begg 检验评估发表偏倚。纳入了 12 项病例对照研究，涉及 9,767 例病例和 19,790 例对照，以及 25 项队列研究，涉及 118,825 例病例。纳入的队列研究中，随访人数为 29,963 人至 6,264,890 人。仅在我们的病例对照研究分析（RR = 0.846，95% CI [0.710，1.009]）或仅队列研究分析（RR = 0.925，95% CI [0.811，1.054]）中，糖尿病与前列腺癌的发病率没有显着相关性。然而，通过亚组分析，仅考虑基于人群的研究（RR = 0.719，95% CI [0.637，0.812]）、在美国进行的队列研究（RR = 0.789，95% CI [0.727，0.857]）以及随访时间超过 5 年的研究时，发现糖尿病和前列腺癌之间存在统计学显着关联。与非糖尿病患者患前列腺癌的风险相比，在病例对照和队列研究中，使用胰岛素治疗的糖尿病患者的前列腺癌发病率均降低。结果表明，糖尿病与前列腺癌发病率降低有关，特别是在美国人群中。此外，糖尿病发病后的时间与前列腺癌发病率的降低呈正相关。然而，目前的结论应该仔细考虑，并通过进一步的研究来证实。
The association between diabetes and risk of prostate cancer has been investigated widely. However, study results remain inconsistent and contradictory. Using a meta-analytic approach, the present study explore the relationship incorporating more recent studies and provide more powerful evidence without the limitations of any individual study. Relevant studies were identified by searching Pubmed and the Cochrane Central Register of Controlled Trials through May 18, 2012. The strength of the relationship between diabetes mellitus and risk of prostate cancer was assessed using relative risk (RR). Either a fixed effects or random effects model was used to calculate the pooled RRs. Stratification analyses and sensitivity analyses were conducted, and publication bias was assessed by Egger’s test and Begg’s test. Twelve case–control studies involving 9,767 cases and 19,790 controls, and 25 cohort studies involving 118,825 cases were included. The person-years of follow-up ranged from 29,963 to 6,264,890 among included cohort studies. Diabetes was not significantly associated with incidence of prostate cancer in our analysis of case–control studies only (RR = 0.846, 95 % CI [0.710, 1.009]) or that of cohort studies only (RR = 0.925, 95 % CI [0.811, 1.054]). However, through subgroup analyses, statistically significant associations between diabetes and prostate cancer were found when considering population-based studies only (RR = 0.719, 95 % CI [0.637, 0.812]), cohort studies conducted in the United States (RR = 0.789, 95 % CI [0.727, 0.857]), and studies with follow-up of more than 5 years. Compared to risk of prostate cancer among people without diabetes, diabetic patients using insulin treatment experienced reduced incidence of prostate cancer in both case–control and cohort studies. The results suggest that diabetes mellitus is associated with decreased incidence of prostate cancer, specifically in the population of the United States. In addition, the time since onset of diabetes was positively associated with decreasing incidence of prostate cancer. The present conclusions should be considered carefully, however, and confirmed with further studies.