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Hyperhomocysteinemia is typically managed with vitamin B 6, vitamin B 9 and vitamin B 12 supplementation. [4] Hyperhomocysteinemia is a risk factor for cardiovascular disease; supplements of these vitamins may slightly reduce stroke outcome but not myocardial infarction, death from any cause or adverse events.
Defects in variants of MTHFR can therefore lead to hyperhomocysteinemia. [9] There are two common variants of MTHFR deficiency. In the more significant of the two, the individual is homozygous for the 677T polymorphism. This variant in particular is the most common genetic cause of hyperhomocysteinemia. [9]
Homocystinuria (HCU) [2] is an inherited disorder of the metabolism of the amino acid methionine due to a deficiency of cystathionine beta synthase or methionine synthase. [3] It is an inherited autosomal recessive trait, which means a child needs to inherit a copy of the defective gene from both parents to be affected.
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Hyperhomocysteinemia has been correlated with the occurrence of blood clots, heart attacks, and strokes, although it is unclear whether hyperhomocysteinemia is an independent risk factor for these conditions. [6] Hyperhomocysteinemia has also been associated with early-term spontaneous abortions [7] and with neural tube defects. [8]
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Treatment with other drugs or vitamins is unsupported by clinical evidence, "but trials evaluating the effect of folate and vitamin B 12 on hyperhomocysteinemia, a putative vascular risk factor, are near completion". [74]