Association study of the CTH 1364 G>T polymorphism with coronary artery disease in the Greek population.
Drug Metab Pers Ther
; 34(1)2019 03 12.
Article
em En
| MEDLINE
| ID: mdl-30860977
Background Cystathionine γ-lyase enzyme, which is encoded by the CTH gene, is responsible for hydrogen sulfide (H2S) production in the endothelium. The CTH 1364 G>T polymorphism may alter the CTH expression and H2S bioavailability, thus leading to atherosclerosis and coronary artery disease (CAD). We examined the potential association of the CTH 1364 G>T polymorphism with CAD. Methods The CTH 1364 G>T polymorphism was determined in 178 coronary artery bypass grafting (CABG) patients and 156 non-atherosclerotic controls of Greek Caucasian origin using the PCR-RFLP method. Results No significant difference in the frequency of the CTH 1364 G>T genotypes (p = 0.281) and alleles (p = 0.265) was found between the CABG patients and controls. After conducting stratification according to sex, analysis showed a numerical difference in the CTH 1364 TT genotype frequency in female participants that did not reach statistical significance (16.3% and 8.5% in the CABG and controls, respectively, p = 0.26). The frequency of the CTH 1364 TT genotype between the male CABG patients and controls did not differ (p = 0.507). Conclusions The CTH 1364 G>T polymorphism was not associated with CAD in the studied population. However, interestingly, a higher - if not significantly so - CTH 1364 TT genotype frequency was present in female CABG patients compared with female controls. Larger studies are necessary to conclude on the potential overall or gender-driven association between CTH 1364 G>T gene polymorphism and CAD.
Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Doença da Artéria Coronariana
/
Polimorfismo de Nucleotídeo Único
/
Cistationina gama-Liase
Tipo de estudo:
Observational_studies
/
Risk_factors_studies
Limite:
Aged
/
Female
/
Humans
/
Male
/
Middle aged
País como assunto:
Europa
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article