Homocysteine,
MTHFR 677C [flecha diestra] T polymorphism, and risk of ischemic stroke: results of a meta-analysis.
Genotyping assays for F2 c.*97G>A, F5 c.1601G>A,
MTHFR c.665C>T, and
MTHFR c.1286A>C were performed.
In this study, the polymorphisms of the
MTHFR genes (
MTHFR C677T and
MTHFR A1298C), MTR (MTR A2756G), and MTRR (MTRR A66G) were determined in malaria patients in Burkina Faso.
The
MTHFR primer sequences were as follows: F: 5-GGCTGACCTGAAGCACTTGAA-3' and R: 5'-AGAAAAGCTGCGTGATGATGAA-3'.
MTHFR gene mutations could not be assayed at our hospital at that time.
Biochemical analyses performed on our patient revealed hyperhomocysteinemia, and genetic analysis demonstrated a homozygous (T/T) mutation of
MTHFR (C677T).
Deficiency of folic acid or mutation in
MTHFR enzyme can result in raised serum homocysteine level.
Also,
MTHFR C 677 T could be frequently encountered (Albayrak et al 2011).
However, results from studies examining the relationship between
MTHFR rs1801133 and rs1801131 polymorphisms and CHD risk have been inconsistent (Zhang et al., 2018; Asim et al., 2017; Yu et al., 2017; Guo et al., 2017).
After adjustment for baseline homocysteine concentrations, the homocysteine-lowering effect of folic acid was significantly greater in patients who were homozygous for the 677C[right arrow]T genotype of the methylenetetrahydrofolate reductase (
MTHFR) gene than in those with the CC or CT genotype.