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Methylenetetrahydrofolate reductase gene rs1801133 polymorphism and essential hypertension risk from a comprehensive analysis

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Abstract Background Essential hypertension (EH) is common and multifactorial disorders likely to be influenced by multiple genes. The methylenetetrahydrofolate reductase (MTHFR) gene rs1801133 polymorphism is related to MTHFR enzyme activity and to plasma homocysteine concentration. In addition, variations in MTHFR functions likely play roles in the etiology of EH. So far, larger number of studies between MTHFR rs1801133 polymorphism and EH have provided controversial or inconclusive results. To better assess the purported relationship, we performed a comprehensive analysis of 50 publications. Methods Eligible studies were identified by searching the PubMed, Wanfang and CNKI databases. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to assess this association. Results Overall, increased significant associations were detected between MTHFR rs1801133 polymorphism and EH risk (such as T vs. C: OR = 1.37, 95%CI = 1.24–1.52, P = 0.000), the same as in race subgroup (Asian: T vs. C: OR = 1.46, 95%CI = 1.29–1.67, P = 0.000; China: T vs. C: OR = 1.51, 95%CI = 1.30–1.74, P = 0.000). Similar associations were also found in source of control and genotype methods subgroups. Conclusions Our study showed evidence that MTHFR rs1801133 null genotype may increase EH risk. Future studies with larger sample size are warranted to further evaluate this association in more detail.
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Title: Methylenetetrahydrofolate reductase gene rs1801133 polymorphism and essential hypertension risk from a comprehensive analysis
Description:
Abstract Background Essential hypertension (EH) is common and multifactorial disorders likely to be influenced by multiple genes.
The methylenetetrahydrofolate reductase (MTHFR) gene rs1801133 polymorphism is related to MTHFR enzyme activity and to plasma homocysteine concentration.
In addition, variations in MTHFR functions likely play roles in the etiology of EH.
So far, larger number of studies between MTHFR rs1801133 polymorphism and EH have provided controversial or inconclusive results.
To better assess the purported relationship, we performed a comprehensive analysis of 50 publications.
Methods Eligible studies were identified by searching the PubMed, Wanfang and CNKI databases.
Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to assess this association.
Results Overall, increased significant associations were detected between MTHFR rs1801133 polymorphism and EH risk (such as T vs.
C: OR = 1.
37, 95%CI = 1.
24–1.
52, P = 0.
000), the same as in race subgroup (Asian: T vs.
C: OR = 1.
46, 95%CI = 1.
29–1.
67, P = 0.
000; China: T vs.
C: OR = 1.
51, 95%CI = 1.
30–1.
74, P = 0.
000).
Similar associations were also found in source of control and genotype methods subgroups.
Conclusions Our study showed evidence that MTHFR rs1801133 null genotype may increase EH risk.
Future studies with larger sample size are warranted to further evaluate this association in more detail.

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