Meta-analysis:: the use of non-steroidal anti-inflammatory drugs and pancreatic cancer risk for different exposure categories

Meta-analysis:: the use of non-steroidal anti-inflammatory drugs and pancreatic cancer risk for different exposure categories
复制标题

DOI:
10.1111/j.1365-2036.2007.03495.x
复制
发表时间:
2007-10-15
影响因子:
7.6
通讯作者:
Delle Fave, G.
Delle Fave, G.
中科院分区:
医学1区
文献类型:
--
作者:
Capurso, G.;Schuenemann, H. J.;Delle Fave, G.

文献摘要

被引文献

相似文献

背景更好地了解胰腺导管腺癌(PDAC)的风险预测因素可以为针对这种致命癌症的预防工作提供信息。阿司匹林(阿萨)和非甾体抗炎药(NSAIDS)可能对几种胃肠道肿瘤有保护作用,但它们在PDAC发生中的作用尚不清楚。目的对阿萨/NSAIDS暴露与PDAC风险之间的关系进行系统评价和荟萃分析。科克伦系统综述数据库和已识别论文的参考文献列表以及纳入的观察性文献(队列或病例对照)研究和随机对照试验,检查阿萨和/或NSAID暴露量和PDAC的发生率或死亡率。我们定义了三个类别(低,中,高),暴露时间和dose.Results的基础上,我们的入选标准(四个队列,三个病例对照,和一个随机对照试验研究)招募6301例患者在1971年至2004年,所有,但一项研究发生在美国。低、中和高暴露组的合并OR分别为0.99(0.83-1.19)、1.11(0.84-1.47)和1.09(0.67-1.75),具有相当大的异质性(I-2范围为60-86%)。仅阿萨使用,研究设计或性别的敏感性分析没有发现额外的重要信息。结论本研究没有显示阿萨/NSAID和PDAC之间的关联。北美对照组的基线暴露量较大可能掩盖了其中的关联。需要进行更多的研究,特别是在欧洲,以澄清这一问题。
Background A better understanding of predictors of risk for pancreatic ductal adenocarcinoma (PDAC) could inform preventive efforts against this lethal cancer. While aspirin (ASA) and non-steroidal anti-inflammatory drugs (NSAIDS) might protect against several gastrointestinal cancers, their role in the development of PDAC remains unclear.Aim To conduct a systematic review and meta-analysis on the relation between ASA/NSAIDs exposure and the risk of PDAC.Methods We searched Pubmed, Embase, Scopus, Cochrane database of systematic reviews and reference lists of identified papers and included observational (cohort or case-control) studies and randomized controlled trials examining exposure to ASA and/or NSAIDs and the incidence or mortality of PDAC. We defined three categories (low, intermediate, high), based on exposure duration and dose.Results Eight studies fulfilled our inclusion criteria (four cohort, three case controls, and one randomized controlled trial studies) enrolling 6301 patients between 1971-2004; all but one study took place in the US. The pooled OR were 0.99 (0.83-1.19), 1.11 (0.84-1.47) and 1.09 (0.67-1.75) in the low, intermediate and high exposure groups respectively, with considerable heterogeneity (I-2 ranging 60-86%). Sensitivity analysis by ASA use only, study design or sex did not reveal additional important information.Conclusions This study did not show an association between ASA/NSAIDs and PDAC. The large baseline exposure in controls in North-America may have obscured an association. There is need for additional studies, especially in Europe, to clarify this issue.