The Differential Effects of Statins on the Risk of Developing Pancreatic Cancer: A Case-Control Study in Two Centres in the United Kingdom

The Differential Effects of Statins on the Risk of Developing Pancreatic Cancer: A Case-Control Study in Two Centres in the United Kingdom
复制标题

DOI:
10.1007/s10620-013-2778-7
复制
发表时间:
2013-11-01
影响因子:
3.1
通讯作者:
Hart, A. R.
Hart, A. R.
中科院分区:
医学3区
文献类型:
--
作者:
Carey, F. J.;Little, M. W.;Hart, A. R.

文献摘要

被引文献

相似文献

他汀类药物如何预防胰腺癌有合理的生物学机制,尽管来自普通人群的流行病学研究的证据是相互矛盾的。本研究采用配对病例对照研究方法,对胰腺癌患者和一组年龄、性别相似的皮肤科基底细胞癌患者进行了研究。参与者的医疗记录进行了审查,以了解诊断前他汀类药物的使用信息。使用条件Logistic回归估计胰腺癌发生的比值比和95%CI。在男性、女性、吸烟者和2型糖尿病患者中进行亚组分析,确定了252例病例(中位年龄71岁,范围48-73岁,51%为女性)和504例对照,其中23%的病例为常规他汀类药物使用者,对照组为21%。在一般研究人群中,胰腺癌与定期使用他汀类药物之间没有关联(OR 0.82,95% CI 0.53-1.23,p = 0.33)。然而,在男性吸烟者中,与未开具他汀类药物处方的男性吸烟者相比,定期使用他汀类药物与胰腺癌几率显著降低相关(OR 0.11,95% CI 0.01-0.96,p = 0.05)。在2型糖尿病患者中,他汀类药物的使用与降低几率无关(OR 0.92,95%CI 0.35-2.45,p = 0.80),没有性别效应。他汀类药物的使用应在胰腺癌的病因学研究中进行测量,但应在特定的亚组中进行分析。未来的工作应调查他汀类药物作为化学预防剂在这个高风险的亚组。
There are plausible biological mechanisms for how statins may prevent pancreatic cancer, although the evidence from epidemiological studies in the general population is conflicting. This study aims to clarify whether statins exert their effects in specific sub-groups, namely, gender, smoking status and diabetes.A matched case-control study was conducted in patients diagnosed with pancreatic cancer, and a group of dermatology patients of similar ages and gender, diagnosed with basal cell carcinoma. Participants' medical records were reviewed for information on statin use prior to diagnosis. Odds ratios and 95 % CIs for the development of pancreatic cancer were estimated using conditional logistic regression. Subgroup analysis was performed in men, women, smokers and those with type 2 diabetes.Two hundred fifty-two cases (median age 71 years, range 48-73 years, 51 % women) and 504 controls were identified, of which 23 % of cases were regular statin users versus 21 % of controls. In the general study population there was no association between pancreatic cancer and regular statin use (OR 0.82, 95 % CI 0.53-1.23, p = 0.33). However, in male smokers, regular statin use was associated with significantly reduced odds of pancreatic cancer compared to male smokers not prescribed a statin (OR 0.11, 95 % CI 0.01-0.96, p = 0.05). In patients with type 2 diabetes statins use was not associated with reduced odds (OR 0.92, 95 % CI 0.35-2.45, p = 0.80), with no gender effects.In male smokers, statins may reduce the odds of pancreatic cancer. Statin use should be measured in aetiological studies of pancreatic cancer but analysed in specific sub-groups. Future work should investigate statins as chemopreventative agents in this high risk sub-group.