Statins and cancer risk - A meta-analysis

被引:486
作者
Dale, KM
Coleman, CI
Henyan, NN
Kluger, J
White, CM
机构
[1] Hartford Hosp, Div Drug Informat, Hartford, CT 06102 USA
[2] Hartford Hosp, Div Cardiol, Hartford, CT 06102 USA
[3] Univ Connecticut, Sch Med, Farmington, CT USA
来源
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION | 2006年 / 295卷 / 01期
关键词
D O I
10.1001/jama.295.1.74
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Context Statins are cholesterol - lowering drugs that have been proven in randomized controlled trials to prevent cardiac events. Recent retrospective analyses have suggested that statins also prevent cancer. Objectives To investigate the effect of statin therapy on cancer incidence and cancer death and to analyze the effect of statins on specific cancers and the effect of statin lipophilicity or derivation. Data Sources A systematic literature search of MEDLINE, EMBASE, CINAHL, Web of Science, CANCERLIT, and the Cochrane Systematic Review Database through July 2005 was conducted using specific search terms. A review of cardiology and cancer abstracts and manual review of references was also performed. Study Selection Twenty-seven of the 8943 articles (n = 86 936 participants) initially identified met the inclusion criteria, reporting 26 randomized controlled trials of statins, with a mean duration of follow-up of at least 1 year, enrolling a minimum of 100 patients, and reporting data on either cancer incidence (n = 20 studies) or cancer death (n = 22 studies). Data Extraction All data were independently extracted by 3 investigators using a standardized data abstraction tool. Weighted averages were reported as odds ratios (ORs) with 95% confidence intervals (CIs) using a random-effects model (DerSimonian and Laird methods). Statistical heterogeneity scores were assessed with the Q statistic. Data Synthesis In meta-analyses including 6662 incident cancers and 2407 cancer deaths, statins did not reduce the incidence of cancer (OR, 1.02; 95% Cl, 0.97-1.07) or cancer deaths (OR, 1.01; 95% Cl, 0.93-1.09). No reductions were noted for any individual cancer type. This null effect on cancer incidence persisted when only hydrophilic, lipophilic, naturally derived, or synthetically derived statins were evaluated. Conclusions Statins have a neutral effect on cancer and cancer death risk in randomized controlled trials.. We found that no type of cancer was affected by statin use and no subtype of statin affected the risk of cancer.
引用
收藏
页码:74 / 80
页数:7
相关论文
共 48 条
[1]  
[Anonymous], 2000, J Atheroscler Thromb, V7, P110
[2]  
[Anonymous], 2002, JAMA
[3]  
[Anonymous], 2000, ITAL HEART J
[4]   Two-year statin therapy does not alter the progression of intima-media thickness in patients with type 2 diabetes without manifest cardiovascular disease [J].
Beishuizen, ED ;
Van de Ree, MA ;
Jukema, JW ;
Tamsma, JT ;
Van der Vijver, JCM ;
Meinders, AE ;
Putter, H ;
Huisman, MV .
DIABETES CARE, 2004, 27 (12) :2887-2892
[5]  
Bestehorn HP, 1997, EUR HEART J, V18, P226
[6]   Do statins cause cancer? A meta-analysis of large randomized clinical trials [J].
Bjerre, LM ;
LeLorier, J .
AMERICAN JOURNAL OF MEDICINE, 2001, 110 (09) :716-723
[7]   3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors and the risk of cancer -: A nested case-control study [J].
Blais, L ;
Desgagné, A ;
LeLorier, J .
ARCHIVES OF INTERNAL MEDICINE, 2000, 160 (15) :2363-2368
[8]   CORONARY ANGIOGRAPHIC CHANGES WITH LOVASTATIN THERAPY - THE MONITORED ATHEROSCLEROSIS REGRESSION STUDY (MARS) [J].
BLANKENHORN, DH ;
AZEN, SP ;
KRAMSCH, DM ;
MACK, WJ ;
CASHINHEMPHILL, L ;
HODIS, HN ;
DEBOER, LWV ;
MAHRER, PR ;
MASTELLER, MJ ;
VAILAS, LI ;
ALAUPOVIC, P ;
HIRSCH, LJ .
ANNALS OF INTERNAL MEDICINE, 1993, 119 (10) :969-976
[9]   The association between 3-hydroxy-3-methylglutaryl conenzyme A inhibitor use and breast carcinoma risk among postmenopausal women - A case-control study [J].
Boudreau, DM ;
Gardner, JS ;
Malone, KE ;
Heckbert, SR ;
Blough, DK ;
Daling, JR .
CANCER, 2004, 100 (11) :2308-2316
[10]   Statins activate the mitochondrial pathway of apoptosis in human lymphoblasts and myeloma cells [J].
Cafforio, P ;
Dammacco, F ;
Gernone, A ;
Silvestris, F .
CARCINOGENESIS, 2005, 26 (05) :883-891