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Ann Hum Genet. 2008 Mar;72(Pt 2):178-83. doi: 10.1111/j.1469-1809.2007.00417.x. Epub 2008 Jan 20.

Genetic Polymorphism of CYP2C19 gene in the Stanislas cohort. A link with inflammation.

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  • 1INSERM U525, Faculté de Pharmacie, 30 rue Lionnois, Nancy, France.

Abstract

CYP2C19, a member of the cytochrome P450 family, metabolises arachidonic acid to produce epoxyeicosanoid acids, which are involved in vascular tone and inflammation. Thus, this study describes the possible relationship between a CYP2C19 polymorphism (681G>A) and three inflammatory markers: interleukin (IL)-6, tumor necrosis factor-alpha (TNF-alpha) and high sensitivity C-reactive protein (hs-CRP) in healthy individuals. In a sub-sample of 178 men and 181 women from the Stanislas study, we quantified plasma IL-6 and TNF-alpha concentrations by using an enzyme-linked immunosorbent assay, and serum hs-CRP concentration by immunonephelometry. The CYP2C19 681G>A polymorphism was genotyped using the kinetic thermocycling allele specific PCR method. In the Stanislas cohort, the frequency of the allele CYP2C19*2 (681A) was 17.8%. Circulating levels of inflammatory factors were increased in individuals homozygous for the defective allele CYP2C19*2 (A) notably IL-6 in the whole sample (P= 0.0008) and hs-CRP only in women (P= 0.008), with a significant interaction with sex (P= 0.005), in comparison to carriers of one copy or more of the wild type allele CYP2C19*1 (G). Only a trend of association (P= 0.089) was found between this polymorphism and TNF-alpha concentration in the whole sample. The association between CYP2C19*2 polymorphism and inflammatory markers' concentrations could suggest that CYP2C19 may be considered as a new candidate gene for cardiovascular risks via inflammation.

PMID:
18205890
[PubMed - indexed for MEDLINE]
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