title: The effect of methylenetetrahydrofolate reductase C677T common variant on hypertensive risk is not solely explained by increased plasma homocysteine values.
abstract: The C677T transition of methylenetetrahydrofolate reductase (MTHFR) gene causes a moderate increase in total plasma homocysteine (tHcy). We studied the effect of MTHFR TT homozygosity and mild hyperhomocysteinemia on arterial hypertension. Normotensive controls (n = 223) and hypertensive subjects (n = 235) were matched for age, gender, and history of cardiovascular disease. Homocysteine levels were measured by a polarization immunoassay method. Methylenetetrahydrofolate reductase we determined by polymerase chain reaction and restriction fragment analysis. Hypertensives showed elevated tHcy compared to normotensive group in men (P = 0.039). Homocysteine values higher than 15 micromol/L were associated with increased hypertensive risk in the male population [odds ratios (OR) = 1.63; 95% confidence interval (CI) = 1.06-2.52; P = 0.027]. In multivariate analysis, TT genotype was associated with an increased risk of hypertension in males (OR = 2.27; 95% CI = 1.12-4.60; P = 0.022) An increased hypertensive risk was observed in those TT males with tHcy levels higher than 15 micromol/L (OR = 2.78; 95% CI = 1.05-7.3; P = 0.032) but not in those non-TT males with tHcy levels higher than 15 micromol/L (P = 0.33). Our findings do not support the possibility that mild hyperhomocysteinemia my solely account for the hypertensive risk associated to the TT genotype.
authors.affiliation: Research Unit, Hemodynamic-Cardiology Service, Hospital de Gran Canaria Dr. Negrín, Universidad de Las Palmas de Gran Canaria, Canary Islands, Spain.
authors.forename: Francisco
authors.initials: F
authors.lastname: Rodríguez-Esparragón
authors.forename: Octavio
authors.initials: O
authors.lastname: Hernández-Perera
authors.forename: José C
authors.initials: JC
authors.lastname: Rodríguez-Pérez
authors.forename: Aránzazu
authors.initials: A
authors.lastname: Anábitarte
authors.forename: Juan M
authors.initials: JM
authors.lastname: Díaz-Cremades
authors.forename: Antonio
authors.initials: A
authors.lastname: Losada
authors.forename: Dolores
authors.initials: D
authors.lastname: Fiuza
authors.forename: Enrique
authors.initials: E
authors.lastname: Hernández
authors.forename: Carla
authors.initials: C
authors.lastname: Yunis
authors.forename: Carlos M
authors.initials: CM
authors.lastname: Ferrario
mesh_terms: D000368:Aged; D001794:Blood Pressure / Q000235:genetics; D005260:Female; D020022:Genetic Predisposition to Disease / Q000453:epidemiology; D005838:Genotype; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood / Q000453:epidemiology / Q000235:genetics; D006973:Hypertension / Q000097:blood / Q000453:epidemiology* / Q000235:genetics*; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D008875:Middle Aged; D015999:Multivariate Analysis; D000587:Oxidoreductases Acting on CH-NH Group Donors / Q000235:genetics*; D017354:Point Mutation; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: D006710:Homocysteine; D000587:Oxidoreductases Acting on CH-NH Group Donors; D042965:Methylenetetrahydrofolate Reductase (NADPH2)