title: Apolipoprotein E polymorphism in Omani dyslipidemic patients with and without coronary artery disease.
abstract: Apolipoprotein E (APOE) polymorphism is a predictor of interindividual variability in plasma levels of lipids and lipoproteins and a predictor of risk of coronary artery disease (CAD). We studied the relationship between APOE polymorphism and lipid profiles and risk of CAD in Omani dyslipidemic patients. This retrospective study included 244 dyslipidemic patients, of whom 67 had CAD. Fasting blood glucose, lipids, and plasma lipoprotein levels were measured using standard methods, and APOE genotypes were detected by PCR-RFLP. The dyslipidemic patients had the following APOE allele frequencies: APOE*2, 0.030; APOE*3, 0.894; and APOE*4, 0.076. APOE allele frequencies between patients with and without CAD showed no significant differences. Compared to APOE*3/*3 homozygotes, APOE*4 allele patients had higher mean levels of low-density lipoprotein (LDL) cholesterol (p = 0.014), apoB (p = 0.031), lower mean levels of apoA1 (p = 0.043), and a trend of higher mean level of total cholesterol (p = 0.084). Thirty-one percent of patients with CAD had the APOE*4 allele compared to 26% with the APOE*3 allele, but this difference was not significant. Compared with APOE*3/*3 homozygotes, patients with the APOE*4 allele had 1.3 times higher risk for CAD after ignoring dyslipidemia, but this risk was modified after adjusting for dyslipidemia. In conclusion, among dyslipidemic patients, carriers of APOE*4 compared to homozygous carriers of APOE*3 had significantly higher levels of LDL cholesterol and apoB, but no relationship with CAD was found.
authors.affiliation: Department of Biochemistry, College of Medicine and Health Sciences, Sultan Qaboos University, P.O. Box 35, Al-Khoud 123, Sultanate of Oman.
authors.forename: Said Ali S
authors.initials: SA
authors.lastname: Al-Yahyaee
authors.forename: Shyam Sundar
authors.initials: SS
authors.lastname: Ganguly
authors.forename: Mohammed Nasser
authors.initials: MN
authors.lastname: Al Kindi
authors.forename: Ali Ihassan
authors.initials: AI
authors.lastname: Al-Bahrani
mesh_terms: D000328:Adult; D000368:Aged; D053329:Apolipoprotein E2 / Q000235:genetics; D053318:Apolipoprotein E3 / Q000235:genetics*; D053327:Apolipoprotein E4 / Q000235:genetics*; D003327:Coronary Disease / Q000235:genetics; D050171:Dyslipidemias / Q000150:complications / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D005828:Genetics, Population / Q000379:methods; D006720:Homozygote; D006801:Humans; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D009850:Oman; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D012189:Retrospective Studies
chemical_list: D053329:Apolipoprotein E2; D053318:Apolipoprotein E3; D053327:Apolipoprotein E4; D008055:Lipids