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Statements

Subject Item
n2:RIV%2F00023001%3A_____%2F11%3A00002479%21RIV12-MZ0-00023001
rdf:type
n9:Vysledek skos:Concept
dcterms:description
Background The MTHFR 677C -> T polymorphism has been associated with raised homocysteine concentration and increased risk of stroke. A previous overview showed that the effects were greatest in regions with low dietary folate consumption, but differentiation between the effect of folate and small-study bias was difficult. A meta-analysis of randomised trials of homocysteine-lowering interventions showed no reduction in coronary heart disease events or stroke, but the trials were generally set in populations with high folate consumption. We aimed to reduce the effect of small-study bias and investigate whether folate status modifies the association between MTHFR 677C -> T and stroke in a genetic analysis and meta-analysis of randomised controlled trials. Methods We established a collaboration of genetic studies consisting of 237 datasets including 59 995 individuals with data for homocysteine and 20 885 stroke events. We compared the genetic findings with a meta-analysis of 13 randomised trials of homocysteine-lowering treatments and stroke risk (45 549 individuals, 2314 stroke events, 269 transient ischaemic attacks). Findings The effect of the MTHFR 677C -> T variant on homocysteine concentration was larger in low folate regions (Asia; difference between individuals with TT versus CC genotype, 3.12 mu mol/L, 95% CI 2.23 to 4.01) than in areas with folate fortification (America, Australia, and New Zealand, high; 0.13 mu mol/L, -0.85 to 1.11). The odds ratio (OR) for stroke was also higher in Asia (1.68, 95% CI 1.44 to 1.97) than in America, Australia, and New Zealand, high (1.03, 0.84 to 1.25). Most randomised trials took place in regions with high or increasing population folate concentrations. The summary relative risk (RR) of stroke in trials of homocysteine-lowering interventions (0 94, 95% CI 085 to 1.04) was similar to that predicted for the same extent of homocysteine reduction in large genetic studies in populations with similar folate status (pre Background The MTHFR 677C -> T polymorphism has been associated with raised homocysteine concentration and increased risk of stroke. A previous overview showed that the effects were greatest in regions with low dietary folate consumption, but differentiation between the effect of folate and small-study bias was difficult. A meta-analysis of randomised trials of homocysteine-lowering interventions showed no reduction in coronary heart disease events or stroke, but the trials were generally set in populations with high folate consumption. We aimed to reduce the effect of small-study bias and investigate whether folate status modifies the association between MTHFR 677C -> T and stroke in a genetic analysis and meta-analysis of randomised controlled trials. Methods We established a collaboration of genetic studies consisting of 237 datasets including 59 995 individuals with data for homocysteine and 20 885 stroke events. We compared the genetic findings with a meta-analysis of 13 randomised trials of homocysteine-lowering treatments and stroke risk (45 549 individuals, 2314 stroke events, 269 transient ischaemic attacks). Findings The effect of the MTHFR 677C -> T variant on homocysteine concentration was larger in low folate regions (Asia; difference between individuals with TT versus CC genotype, 3.12 mu mol/L, 95% CI 2.23 to 4.01) than in areas with folate fortification (America, Australia, and New Zealand, high; 0.13 mu mol/L, -0.85 to 1.11). The odds ratio (OR) for stroke was also higher in Asia (1.68, 95% CI 1.44 to 1.97) than in America, Australia, and New Zealand, high (1.03, 0.84 to 1.25). Most randomised trials took place in regions with high or increasing population folate concentrations. The summary relative risk (RR) of stroke in trials of homocysteine-lowering interventions (0 94, 95% CI 085 to 1.04) was similar to that predicted for the same extent of homocysteine reduction in large genetic studies in populations with similar folate status (pre
dcterms:title
Effect modification by population dietary folate on the association between MTHFR genotype, homocysteine, and stroke risk: a meta-analysis of genetic studies and randomised trials Effect modification by population dietary folate on the association between MTHFR genotype, homocysteine, and stroke risk: a meta-analysis of genetic studies and randomised trials
skos:prefLabel
Effect modification by population dietary folate on the association between MTHFR genotype, homocysteine, and stroke risk: a meta-analysis of genetic studies and randomised trials Effect modification by population dietary folate on the association between MTHFR genotype, homocysteine, and stroke risk: a meta-analysis of genetic studies and randomised trials
skos:notation
RIV/00023001:_____/11:00002479!RIV12-MZ0-00023001
n9:predkladatel
n16:ico%3A00023001
n3:aktivita
n19:Z
n3:aktivity
Z(MZ0IKEM2005)
n3:cisloPeriodika
9791
n3:dodaniDat
n6:2012
n3:domaciTvurceVysledku
n5:6513832
n3:druhVysledku
n11:J
n3:duvernostUdaju
n12:S
n3:entitaPredkladatele
n17:predkladatel
n3:idSjednocenehoVysledku
196157
n3:idVysledku
RIV/00023001:_____/11:00002479
n3:jazykVysledku
n15:eng
n3:klicovaSlova
coronary heart disease; methylenetetrahydrofolate reductase gene; folic acid supplementation; stage renal disease; cardiovascular disease; B-vitamins; ischemic stroke; plasma homocysteine; C677T polymorphism; vascular disease
n3:klicoveSlovo
n4:folic%20acid%20supplementation n4:vascular%20disease n4:plasma%20homocysteine n4:B-vitamins n4:C677T%20polymorphism n4:stage%20renal%20disease n4:cardiovascular%20disease n4:coronary%20heart%20disease n4:ischemic%20stroke n4:methylenetetrahydrofolate%20reductase%20gene
n3:kodStatuVydavatele
GB - Spojené království Velké Británie a Severního Irska
n3:kontrolniKodProRIV
[BF7EA6206A7C]
n3:nazevZdroje
Lancet
n3:obor
n10:EB
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
46
n3:rokUplatneniVysledku
n6:2011
n3:svazekPeriodika
378
n3:tvurceVysledku
Szolnaki, Z. Singleton, A. B. Holmes, M. V. Bobak, M. Humphries, S. E. Breteler, MMB. Linnebank, M. Meschia, J. F. Cooper, J. Hubáček, Jaroslav Rich, S. S. Ricketts, S. L. van Bockxmeer, F. M. Whittaker, J. C. Ferrucci, L. Shimokata, H. Smeeth, L. Shmeleva, V. Talmud, P. J. Roest, M. Fowkes, FGR. van Dujin, C. Algra, A. Hingorani, A. D. Norman, P. E. Worrall, BB. Lawlor, D. A. Sterne, JAC. Matarin, M. Hardy, J. Ebrahim, S. Almeida, OP. Wareham, N. J. Zacho, J. Sofat, R. Smith, G. D. Khaw, K-T. Nalls, M. A. Flicker, L. Bautista, L. E. Sharma, P. Sandhu, M. S. Newcombe, P. Casas, J. P. Hankey, G. J. Price, J. F.
n3:wos
000294319500030
n3:zamer
n18:MZ0IKEM2005
s:issn
0140-6736
s:numberOfPages
11
n8:doi
10.1016/S0140-6736(11)60872-6