title: [The apolipoprotein E-CI-CII gene cluster polymorphisms and coronary artery disease].
abstract: OBJECTIVE
  To investigate associations between the apolipoprotein E-CI-CII gene cluster polymorphisms and coronary artery disease (CAD).
  
  
  METHODS
  apoE genotypes were identified by multiplex amplification refractory mutation system (multi-ARMS) and the polymorphisms of both apoCI and apoCII genes were detected by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 203 cases of CAD and 365 controls. Pairwise linkage disequilibrium coefficients (D, D') were estimated by the LINKAGE program.
  
  
  RESULTS
  The frequencies of apoE E3/4 genotype (0.259) and epsilon4 (0.139) in CAD group were significantly higher than that in control group (0.125, 0.069), (P<0.05). The significant difference was also found for the apoCI locus, the frequencies of H2 allele were 0. 205 in the CAD and 0.113 in the control. Linkage disequilibrium coefficient D' was 0.672 (P<0.01) between apoE and apoCI genes. Significant differences for a deficit of epsilon3-H1-T1 and excess of epsilon4-H2-T1 were found in the CAD by estimation of the haplotype frequencies. After adjustment for possible confounding factors, the multivariate Logistic analysis showed a significant interaction among epsilon4, H2 and smoking, OR value was 18.3 (95%CI:2.35-150.81, P<0.05), attributable proportions of interaction (API) was 57.3%, it was a multiplicative model. An additive model was shown among epsilon4, H2 and bibulosity; the odds ratio (OR) (95%CI) and API of their interaction were 12.7(2.8-58.6, P<0.05) and 43.5%, respectively.
  
  
  CONCLUSIONS
  The results suggested that both apoE and apoCI on chromosome 19 were the susceptibility loci for CAD, their linkage disequilibrium should be responsible for the development of CAD. Smoking and bibulosity can significantly increase the risk of CAD.
authors.affiliation: Department of Hygiene, School of Medicine, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, 430071 P. R. China. chwang027@yahoo.com.cn
authors.forename: Chunhong
authors.initials: C
authors.lastname: Wang
authors.forename: Xin
authors.initials: X
authors.lastname: Zhou
authors.forename: Fang
authors.initials: F
authors.lastname: Zheng
authors.forename: Dingfen
authors.initials: D
authors.lastname: Han
authors.forename: Qun
authors.initials: Q
authors.lastname: Shi
authors.forename: Fang
authors.initials: F
authors.lastname: Liu
mesh_terms: D000368:Aged; D000428:Alcohol Drinking; D053302:Apolipoprotein C-I / Q000235:genetics*; D053304:Apolipoprotein C-II / Q000235:genetics*; D001057:Apolipoproteins E / Q000235:genetics*; D003324:Coronary Artery Disease / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D006239:Haplotypes; D006801:Humans; D015810:Linkage Disequilibrium; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D005810:Multigene Family / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D012307:Risk Factors; D012907:Smoking
chemical_list: D053302:Apolipoprotein C-I; D053304:Apolipoprotein C-II; D001057:Apolipoproteins E; C054300:apolipoprotein C-II (St Michael)