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Original Article

Butyrylcholinesterase K variants increase the risk of coronary artery disease in the population of western Iran

, , , , , , , , & show all
Pages 123-129 | Received 13 Apr 2007, Accepted 15 Jul 2007, Published online: 08 Jul 2009
 

Abstract

The conflicting results of several studies suggest that there is an association between the butyrylcholinesterase‐K variant (BCHE‐K, G1615A/Ala539Thr) and the risk of developing coronary artery disease (CAD) in diabetes and non‐diabetic subjects. The objective of this study was to determine whether the presence of the BCHE‐K variant exacerbates the risk of CAD in patients from western Iran with and without type 2 diabetes mellitus (T2DM). This case‐control study comprised 464 subjects undergoing their first coronary angiography. They were matched and randomly assigned into four groups: CAD+T2DM+ (CAD/T2DM), CAD+DM (CAD/ND), CADDM+ (T2DM/NCAD) and CADDM(control). The BCHE‐K variant was detected by PCR‐RFLP. The BCHE‐K allele frequency in CAD patients with and without T2DM [total CAD (TCAD)] and separately for each group (CAD/T2DM and CAD/ND) was significantly higher than in the control group (21.1 % versus 13.3 % (p = 0.001), 22.4 % versus 13.3 % (p = 0.001) and 19.7 % versus 13.3 % (p = 0.015), respectively). The odds ratios (ORs) for the BCHE‐K heterozygous and homozygous variants in TCAD subjects were 1.65 (95 % CI 1.17–2.3; p = 0.004) and 4.3 (1.05–19.4; p = 0.048); for CAD/T2DM individuals 1.76 (1.2–2.6; p = 0.004) and 4.73 (0.96–23.3; p = 0.052); and for CAD/ND patients 1.53 (1.05–2.3; p = 0.029) and 3.88 (0.8–19.7; p = 0.7), respectively. The OR of the BCHE‐K allele was found to be 1.74 (1.1–2.4; p = 0.001) in TCAD subjects, 1.87 (1.12–1.48; p = 0.001) in the CAD/T2DM group and 1.59 (1.04–1.4; p = 0.016) in CAD/ND subjects. These data suggest that the BCHE‐K allele increases the risk of CAD in the population (with and without DM) in western parts of Iran, and its presence intensifies the risk of CAD in T2DM. The fact that the BCHE‐K allele, even in the heterozygous form, exacerbates the risk of CAD in this population, suggests that a specific therapeutic intervention should be considered for this particular group of patients.

Acknowledgement

This study was supported by a grant from the Kermanshah University of Medical Sciences, Kermanshah, Iran.

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