使用Statin與巴金森氏症風險增加有關


  【24drs.com】來自大型國家理賠資料庫的新研究發現顯示,使用statin類降膽固醇藥物與巴金森氏症(PD)風險增加有關,與以前的研究(認為該類藥物對於PD有保護效果)相反。
  
  資深作者、賓州賓州醫學院研究副主席Xuemei Huang醫師表示,我們檢視了20,000名巴金森氏症患者,探討使用statin類藥物是否與風險增加或降低有關,我們發現,使用statin類藥物者的PD風險比較高,所以,這和之前的假設相反。
  
  雖然高膽固醇曾顯示對於PD風險有保護效果,使用statin類藥物的角色一直是爭論所在。
  
  2012年線上發表於神經學誌、支持具有效益的研究顯示,使用statin類藥物適度減少巴金森氏症。
  
  Huang醫師等人探討他們自己之前的一篇研究時發現,事實上,使用statin類藥物與風險增加有關,他們想在新研究中對更大型的研究對象進一步探討這項關聯。
  
  為了發表於美國神經科協會(ANA)2016年會的這篇新研究,研究者轉為使用MarketScan商業理賠與遭遇資料庫的數據,介於2008年1月1日至2012年12月31日間的30,343,035名40-65歲者的資料。
  
  這些研究對象中,根據原發性或次發性診斷、使用巴金森氏症治療藥物,進行了深部腦刺激手術,共有21,559人被認為患有PD。
  
  在橫斷面分析中,校正年齡、性別、其他共病症,如高血脂症、糖尿病、高血壓與冠狀動脈疾病之後,使用降膽固醇藥物—包括statin類或非statin類,都與巴金森氏症風險盛行率顯著較高有關(勝算比[OR], 1.61 - 1.67; P < .0001)。
  
  至於對比的神經退化組,研究者也探討了使用statin與阿茲海默氏症的關聯,但是僅發現極小的關聯(OR, 1.01 - 1.12;P = .055)。
  
  高血脂患者的降膽固醇藥物與PD之關聯最強,對PD風險的影響上,親脂性或親水性statin類藥物之間並無顯著差異,其他非statin類降膽固醇藥物也是(沒有差異)。
  
  Huang醫師解釋,我們知道,文獻的整體價值有利於高膽固醇與巴金森氏症的有益結果相關,所以,statin類藥物可能是因為治療了高膽固醇而減少了保護效果。
  
  另一個可能是,statin類藥物不只可以阻斷膽固醇合成,也阻斷了細胞功能所必須之輔酶Q10的合成。
  
  研究者也根據治療期間將研究對象分類,將2,458組PD案例與對照組進行滯後配對案例控制分析。
  
  橫斷面分析中,statin類和非statin類降膽固醇藥物都與PD有關,但是在治療期間的滯後案例控制分析中,只有statin類藥物與PD風險有顯著關聯。
  
  開始使用statin類藥物後最初幾年的風險最高(使用小於1年:OR, 1.93;使用1-2.5年:OR ,1.83 ;2.5年以上:OR, 1.37;趨勢P < .0001)。
  
  Huang醫師表示,當開始使用statin類藥物時,巴金森氏症的風險增加,所以,我們認為可能是statin類藥物未遮蔽巴金森氏症,也就是說,人們可能已處於發生巴金森氏症的狀態,當他們使用statin類藥物控制高膽固醇時,推了巴金森氏症一把、使它發生臨床症狀。
  
  根據這個資料,我們認為,在倡導statin類藥物對巴金森氏症有保護力之前,應小心謹慎。因為,這些資料還不完全清楚。
  
  今年初發表於藥物流行病學與藥物安全期刊的一篇統合分析認為,statin類藥物角色不一致之原因的證據之一是,許多研究無法校正膽固醇值。
  
  在這篇報告中,沒有校正的這些研究顯示statin的保護效果(相對風險:0.75),但是,有校正膽固醇或高脂血症的研究則顯示沒有保護效果:校正高脂血症之研究的相對風險為0.91,校正膽固醇之研究的相對風險是1.04。
  
  作者們表示,statin類藥物對於巴金森氏症風險的明顯保護效果,至少有一部份可由statin適應症的混雜性來解釋。
  
  此外,2013年發表於神經學期刊的另一篇統合分析認為,最近的文獻關於statin類藥物對PD的保護效果有明顯的發表偏見。
  
  Huang醫師指出,目前這篇研究是少數報導statin類藥物對帕金森氏症之可能負面影響的研究之一。
  
  資料來源: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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