title: Evaluation of the contribution of renin angiotensin system polymorphisms to the risk of coronary artery disease among Tunisians.
abstract: Recent studies have identified genetic markers that may directly influence the risk of the coronary artery disease (CAD), in particular the renin angiotensin system genes. Since there are no existing data for the Tunisian population, we investigated the association between these polymorphisms (angiotensin-converting enzyme [ACE] insertion/deletion [Ins/Del]; the angiotensinogen T174M and M235T; and the angiotensin II type 1 receptor A1166C polymorphisms) and CAD in Tunisians. Study subjects comprised 341 cases and 316 age- and sex-matched healthy individuals. Clinical characteristics and other biochemical and environmental risk factors were collected for both. The distribution of the Ins/Del genotypes was significantly different between cases and controls (p = 0.049) with the genotype Ins/Ins identified as a risk, p = 0.02. Similarly, the distributions of the T174M and M235T genotypes were significantly different between cases and controls (p = 0.037 and 0.047, respectively) with 174 M/M and 235 T/T as the risky genotypes (p = 0.001 and 0.026, respectively). However, A1166C genotype frequencies were not significantly different between patients and controls. In conclusion, our results suggest that a significantly higher risk of CAD was associated with the Ins/Del, the M235T, and T174M polymorphisms; other environmental variables such as body mass index; and biochemical variables such as cholesterol.
authors.affiliation: Research Unit of Hematological and Autoimmune Diseases, Faculty of Pharmacy, University of Monastir, Monastir, Tunisia. aness_21@yahoo.fr
authors.forename: Nesrine
authors.initials: N
authors.lastname: Abboud
authors.forename: Lakhder
authors.initials: L
authors.lastname: Ghazouani
authors.forename: Belhassen
authors.initials: B
authors.lastname: Kaabi
authors.forename: Sonia
authors.initials: S
authors.lastname: Ben-Hadj-Khalifa
authors.forename: Fawzi
authors.initials: F
authors.lastname: Addad
authors.forename: Mahjoub
authors.initials: M
authors.lastname: Marwen
authors.forename: Wassim Y
authors.initials: WY
authors.lastname: Almawi
authors.forename: Touhami
authors.initials: T
authors.lastname: Mahjoub
mesh_terms: D000328:Adult; D000368:Aged; D000808:Angiotensinogen / Q000235:genetics*; D001483:Base Sequence; D016022:Case-Control Studies; D003327:Coronary Disease / Q000453:epidemiology / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006239:Haplotypes / Q000235:genetics; D006801:Humans; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D016254:Mutagenesis, Insertional; D020125:Mutation, Missense; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D017354:Point Mutation; D011110:Polymorphism, Genetic; D020641:Polymorphism, Single Nucleotide; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics*; D012084:Renin-Angiotensin System / Q000235:genetics*; D012306:Risk; D017384:Sequence Deletion; D014416:Tunisia / Q000453:epidemiology
chemical_list: C544065:AGTR1 protein, human; D044140:Receptor, Angiotensin, Type 1; D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A