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Interleukin-1 (IL-1) gene polymorphisms: Risk of coronary arterial disease

Dewberry, RM; Camp, NJ; Gunn, J; Burton, AJ; Carter, ND; Jeffery, S; Syrris, P; ... Francis, SE; + view all (1998) Interleukin-1 (IL-1) gene polymorphisms: Risk of coronary arterial disease. Heart , 79 (SUPPL. 1)

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An inflammatory component has been established in coronary artery disease (CAD). We analysed allele frequencies for IL-1 and TNFα gene variants in a Sheffield population with angiographically characterised single vessel disease (SVD) n= 103, multivessel disease (MVD) n=324 and normal coronary arteries (controls) n=129. Genotyping was performed for interleukin-1 receptor antagonist (IL-1RN), IL-1β, IL-1α and TNFα variants using polymerase chain reaction (PCR). There were no significant differences in genotypic distributions at the IL-1A (-889), IL-1B (+3953) and TNFA (-308) loci. Allele 2 (2*) of the IL-1RN gene was increased in patients with SVD : 34% vs 23% in controls. Genotype distribution analysis indicated a significant bias towards the IL-1RN (*2/*2) genotype (χ 2 carriage = 7.579, p=0.0059, Or hom =3.67, 95%CI 1.42-9.47). This effect was less marked in the London population (SVD 57, MVD 191, NCA, 102)(χ 2 carriage = 3.53, p=0.06). No significant bias towards IL-1RN *2/*2 was observed in the MVD populations. Carriage of allele 2 (*2) at IL-1β (-511) was significantly raised in SVD and MVD populations (χ 2 carriage = 4.92, p=0.027) mostly due to heterozygotes. In London SVD, a trend with *2 at IL-1B (-511) was also observed (χ 2 trend = 2.02, p =0.15). Allele 2 of IL-1B (-511) is a weak genetic risk factor for CAD. Possession of allele 2 at IL-1RN (especially homozygosity (*2/*2) may confer susceptibility to SVD. These data support a role for the IL-1 family of cytokines in the pathogenesis of CAD.

Type: Article
Title: Interleukin-1 (IL-1) gene polymorphisms: Risk of coronary arterial disease
UCL classification: UCL > School of Life and Medical Sciences
UCL > School of Life and Medical Sciences > Faculty of Population Health Sciences > Institute of Cardiovascular Science
URI: http://discovery.ucl.ac.uk/id/eprint/1298634
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