Vohnout Branislav, Di Castelnuovo Augusto, Trotta Roberto, D'Orazi Andria, Panniteri Gaetano, Montali Anna, Donati Maria Benedetta, Arca Marcello, Iacoviello Licia
Angela Valenti Laboratory of Genetic and Environmental Risk Factors for Thrombotic Disease, Consorzio Mario Negri Sud, via Nazionale 1, 66030 Santa Maria Imbaro, Italy.
Haematologica. 2003 Jan;88(1):54-60.
The pro-inflammatory cytokine interleukin (IL)-1 has been suggested to play a role in atherosclerosis. Several genetic polymorphisms have been described in the genes of the IL-1 cluster and associations with coronary artery disease (CAD) have been reported, although with contrasting results.
The associations of a variable number tandem repeat (86 bp) polymorphism in intron 2 of interleukin-1 receptor antagonist (IL1-RA) and of the 511 C/T polymorphism of IL-1b with the risk of CAD were studied. Three hundred and thirty-five case (CAD+) patients with angiographically documented CAD (stenosis >50% in at least one major coronary artery) were compared with 205 unrelated individuals free of CAD signs at angiogram (CAD- controls). One hundred and two (30.5%) CAD+ patients had single-vessel disease (SVD) and 233 (69.5%) multiple-vessel disease (MVD).
There was no statistically significant difference in either genotype distribution or allele frequency of both IL-1 RA and IL-1b 511 C/T polymorphisms between CAD+ cases and CAD- controls. Moreover in multivariate analysis, adjusting for multiple comparisons and confounding factors, no difference was found in IL-1 RA genotype distribution between patients with SVD or MVD.
Our study does not support the association between IL-1 RA intron 2 VNTR and IL-1b 511 C/T polymorphisms and the risk of CAD in individuals undergoing coronary angiography.