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An HphI polymorphism in the E‐selectin gene is associated with premature coronary artery disease
Author(s) -
Zheng F,
Chevalier JA,
Zhang LQ,
Virgil D,
Ye SQ,
Kwiterovich PO
Publication year - 2001
Publication title -
clinical genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 102
eISSN - 1399-0004
pISSN - 0009-9163
DOI - 10.1034/j.1399-0004.2001.590110.x
Subject(s) - medicine , coronary artery disease , odds ratio , apolipoprotein b , gastroenterology , apolipoprotein e , exon , endocrinology , cholesterol , biology , gene , disease , genetics
An increased expression of E‐selectin has been observed in the arterial endothelium interacting with lymphocytes and macrophages in human atherosclerotic lesions. We examined whether a polymorphism in the E‐selectin gene, due to a G to T mutation (G98T) in the untranslated region of exon 2, was associated with premature coronary artery disease (CAD). Other lipid and nonlipid risk factors including a Ser to Arg (S128R) substitution in the E‐selectin gene were also assessed. In patients with premature CAD (men ≤45 years old and women ≤55 years old, N=51) who underwent an elective diagnostic coronary arteriography, the frequency of the mutation was significantly higher than in controls (N=50, 0.22 vs. 0.10, p=0.024). After controlling for other CAD risk factors (plasma total cholesterol, triglyceride, LDL‐apolipoprotein B, cigarette smoking and the S128R mutation) by multiple logistic analysis, the G98T mutation in the E‐selectin gene was still a significant predictor of premature CAD [p=0.022, odds ratio (95%, CI)=3.58 (1.20–10.67)].