Key result
MTHFR C677T polymorphism linked to ~6-fold higher risk of carotid artery atherosclerosis.
Why the study?
The MTHFR C677T polymorphism has been linked to hypertension and coronary heart disease, but its relationship with carotid artery atherosclerosis remained unknown.
Is the C677T polymorphism of the MTHFR gene associated with an increased risk of carotid artery atherosclerosis?
Case-Control (n=420)
No
Is the C677T polymorphism of the MTHFR gene associated with an increased risk of carotid artery atherosclerosis?
Effect estimate: OR 6.143 (95% CI 3.872-11.526)
p-value: p=0.001
The C677T polymorphism of the MTHFR gene is a significant risk factor for carotid artery atherosclerosis, alongside elevated systolic blood pressure, total cholesterol, and LDL-C.
Does not justify MTHFR testing in practice; leaves open prospective validation of its added predictive value.
BACKGROUND The C677T polymorphism of the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene polymorphism has been associated with hypertension and coronary heart disease, but its relationship with carotid artery remains unknown. This study aimed to investigate the association between the C677T polymorphism of the MTHFR gene in patients with confirmed carotid artery atherosclerosis. MATERIAL AND METHODS This retrospective study included 210 patients with carotid artery atherosclerosis (the patient group) and 210 controls (the control group). Color Doppler ultrasound was used to identify carotid artery intimo-medial thickness and atherosclerotic plaques. Sanger sequencing using the polymerase chain reaction (PCR) was used to detect the MTHFR C677T gene polymorphism. Systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting plasma glucose (FPG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglyceride (TG), glycosylated hemoglobin (HbA1c), and other laboratory indicators were measured. RESULTS SBP, DBP, FPG, TC, LDL-C, HbA1c, and intimo-medial thickness were significantly increased in the patient group compared with the control group, and HDL-C was significantly lower. The allele frequencies of the C667T locus of MTHFR gene were significantly different between the two groups (P<0.05), and the TT genotype and the T allele frequencies in the patient group were higher than in the control group. Logistic regression analysis showed that SBP, TC, LDL-C, and the C667T MTHFR gene polymorphism were risk factors for carotid artery atherosclerosis. CONCLUSIONS The C677T polymorphism of the MTHFR gene was expressed in patients with carotid artery atherosclerosis.
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Li et al. (2020) conducted a case-control in Carotid artery atherosclerosis (n=420). MTHFR C677T polymorphism vs. Healthy controls was evaluated on Carotid artery atherosclerosis (OR 6.143, 95% CI 3.872-11.526, p=0.001). The MTHFR gene C677T polymorphism was an independent risk factor for carotid artery atherosclerosis, increasing the risk by 6.143 times.
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