使用Statin与巴金森氏症风险增加有关


  【24drs.com】来自大型国家理赔资料库的新研究发现显示,使用statin类降胆固醇药物与巴金森氏症(PD)风险增加有关,与以前的研究(认为该类药物对于PD有保护效果)相反。
  
  资深作者、宾州宾州医学院研究副主席Xuemei Huang医师表示,我们检视了20,000名巴金森氏症患者,探讨使用statin类药物是否与风险增加或降低有关,我们发现,使用statin类药物者的PD风险比较高,所以,这和之前的假设相反。
  
  虽然高胆固醇曾显示对于PD风险有保护效果,使用statin类药物的角色一直是争论所在。
  
  2012年在线发表于神经学志、支持具有效益的研究显示,使用statin类药物适度减少巴金森氏症。
  
  Huang医师等人探讨他们自己之前的一篇研究时发现,事实上,使用statin类药物与风险增加有关,他们想在新研究中对更大型的研究对象进一步探讨这项关联。
  
  为了发表于美国神经科协会(ANA)2016年会的这篇新研究,研究者转为使用MarketScan商业理赔与遭遇资料库的数据,介于2008年1月1日至2012年12月31日间的30,343,035名40-65岁者的资料。
  
  这些研究对象中,根据原发性或次发性诊断、使用巴金森氏症治疗药物,进行了深部脑刺激手术,共有21,559人被认为患有PD。
  
  在横断面分析中,校正年龄、性别、其它共病症,如高血脂症、糖尿病、高血压与冠状动脉疾病之后,使用降胆固醇药物—包括statin类或非statin类,都与巴金森氏症风险盛行率显著较高有关(胜算比[OR], 1.61 - 1.67; P < .0001)。
  
  至于对比的神经退化组,研究者也探讨了使用statin与阿兹海默氏症的关联,但是仅发现极小的关联(OR, 1.01 - 1.12;P = .055)。
  
  高血脂患者的降胆固醇药物与PD之关联最强,对PD风险的影响上,亲脂性或亲水性statin类药物之间并无显著差异,其它非statin类降胆固醇药物也是(没有差异)。
  
  Huang医师解释,我们知道,文献的整体价值有利于高胆固醇与巴金森氏症的有益结果相关,所以,statin类药物可能是因为治疗了高胆固醇而减少了保护效果。
  
  另一个可能是,statin类药物不只可以阻断胆固醇合成,也阻断了细胞功能所必须之辅酶Q10的合成。
  
  研究者也根据治疗期间将研究对象分类,将2,458组PD案例与对照组进行滞后配对案例控制分析。
  
  横断面分析中,statin类和非statin类降胆固醇药物都与PD有关,但是在治疗期间的滞后案例控制分析中,只有statin类药物与PD风险有显著关联。
  
  开始使用statin类药物后最初几年的风险最高(使用小于1年:OR, 1.93;使用1-2.5年:OR ,1.83 ;2.5年以上:OR, 1.37;趋势P < .0001)。
  
  Huang医师表示,当开始使用statin类药物时,巴金森氏症的风险增加,所以,我们认为可能是statin类药物未遮蔽巴金森氏症,也就是说,人们可能已处于发生巴金森氏症的状态,当他们使用statin类药物控制高胆固醇时,推了巴金森氏症一把、使它发生临床症状。
  
  根据这个资料,我们认为,在倡导statin类药物对巴金森氏症有保护力之前,应小心谨慎。因为,这些资料还不完全清楚。
  
  今年初发表于药物流行病学与药物安全期刊的一篇统合分析认为,statin类药物角色不一致之原因的证据之一是,许多研究无法校正胆固醇值。
  
  在这篇报告中,没有校正的这些研究显示statin的保护效果(相对风险:0.75),但是,有校正胆固醇或高脂血症的研究则显示没有保护效果:校正高脂血症之研究的相对风险为0.91,校正胆固醇之研究的相对风险是1.04。
  
  作者们表示,statin类药物对于巴金森氏症风险的明显保护效果,至少有一部份可由statin适应症的混杂性来解释。
  
  此外,2013年发表于神经学期刊的另一篇统合分析认为,最近的文献关于statin类药物对PD的保护效果有明显的发表偏见。
  
  Huang医师指出,目前这篇研究是少数报导statin类药物对帕金森氏症之可能负面影响的研究之一。
  
  资料来源:http://www.24drs.com/
  
  Native link:Statin Use Linked to Increased Parkinson's Risk
  

Statin Use Linked to Increased Parkinson's Risk

By Nancy A. Melville
Medscape Medical News

BALTIMORE — New findings from a large national claims database show the use of cholesterol-lowering statin drugs to be associated with an increased risk for Parkinson's disease (PD), contrary to previous research suggesting the drugs have a protective effect for PD.

"We identified 20,000 Parkinson's disease patients and looked at whether using statins was associated with a higher or lower risk, and we found people using statins have a higher risk of the disease, so this is the opposite of what has been hypothesized," senior author Xuemei Huang, MD, PhD, vice chair for research at Penn State College of Medicine, Hershey, Pennsylvania, told Medscape Medical News.

While high cholesterol has been shown to have a protective effect on the risk for PD, the role of statin use has been the subject of debate.

Among studies supporting a benefits was research published in 2012 in the Archives of Neurology showing a "modest Parkinson's disease reduction" with the use of statins.

In looking at the issue in a previous study of their own, Dr Huang and colleagues in fact found an increased risk associated with statin use, and they sought in the new study to further explore the association in a much larger cohort.

For the new study, presented here at the American Neurological Association (ANA) 2016 Annual Meeting, the researchers turned to data from the MarketScan Commercial Claims and Encounters database, including information on 30,343,035 persons aged 40 to 65 years between January 1, 2008, and December 31, 2012.

Of the subjects, 21,559 were identified as having PD on the basis of criteria of having a primary or secondary diagnosis, using anti-Parkinson's medication, or having deep-brain stimulation surgery.

In the cross-sectional analysis, the use of cholesterol-lowering drugs, including statins or nonstatins, was associated with a significantly higher prevalence of Parkinson's disease (odds ratio [OR], 1.61 - 1.67; P < .0001) after adjustment for age, sex, and other comorbidities, such as hyperlipidemia, diabetes, hypertension, and coronary artery disease.

For a comparative neurodegenerative group, the researchers also looked at the association of statin with diagnosis of Alzheimer's disease but found only a minimal association (OR, 1.01 - 1.12; P = .055).

The associations of cholesterol-lowering medications with PD were strongest among patients with hyperlipidemia, and there were no significant differences between lipophilic or hydrophilic statins, as well as the other nonstatin cholesterol-lowering drugs, in their effect on PD risk.

"We know that overall weight of the literature favors that higher cholesterol is associated with beneficial outcomes in Parkinson's disease, so it's possible that statins take away that protection by treating the high cholesterol," Dr Huang explained.

"Another possibility is that statins can block not only the cholesterol synthesis but also synthesis of coenzyme Q10 that is essential for cell function."

The researchers also stratified persons according to how long they had been receiving treatment by using a lagged matched case-control analysis of 2458 pairs of PD cases and controls.

In the cross-sectional analysis, both statins and nonstatin cholesterol-lowering drugs were associated with PD, but in the lagged case-control analysis of treatment duration, only statins remained significantly associated with PD risk.

The highest risk was linked to the earlier period after starting statins (OR, 1.93 for less than 1 year of use; 1.83 for 1 to 2.5 years; and 1.37 for 2.5 years or more; P trend < .0001).

"The increased risk of Parkinson's is more likely when statins are first used, so we think it could be that the statins 'unmasked' Parkinson's," Dr. Huang said. "Namely, people may be already on the way to Parkinson's and when they use statins to control the high cholesterol, it gives Parkinson's a push to reveal its clinical symptoms.

"Based on this data, we think caution should be taken before advancing statins to be protective of Parkinson's disease," she added. "The data are not clear yet."

A meta-analysis published earlier this year in the journal Pharmacoepidemiology and Drug Safety suggests that one reason for the inconsistencies in evidence of the role of statins is that many studies fail to adjust for cholesterol levels.

In that report, studies that did not make the adjustment showed a protective effect of statins (relative risk, 0.75), but those that did adjust for cholesterol or hyperlipidemia showed no protective effect: Those adjusting for hyperlipidemia had a relative risk of 0.91, and for cholesterol, the relative risk was 1.04.

"The apparent protective effect of statins on risk of Parkinson's disease is at least partially explained by confounding by statin indication," the authors said.

In addition, a separate meta-analysis published in the Journal of Neurology in 2013 suggested that there is a significant publication bias in recent literature toward reporting protective effects of statins in PD.

"The current study is one of very few studies reporting potential negative effects of statin in Parkinson's disease," Dr Huang noted.

The study was funded by grants from the National Institutes of Health, Pennsylvania State University College of Medicine-Milton S. Hershey Medical Center, General Clinical Research Center (GCRC), GCRC Construction, and the Center for Applied Studies in Health Economics. The authors have disclosed no relevant financial relationships.

American Neurological Association (ANA) 2016 Annual Meeting. Abstract S137. Presented October 16, 2016.

    
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