Normal fasting homocysteine plasma levels average 5–15 µmol/l. Elevated homocysteine plasma levels are caused by genetic variants, malnutrition, drugs or renal failure, among other causes. A relatively frequent point mutation of the N5,N10-methylenetetrahydrofolate-reductase (MTHFR) gene codes for a thermolabile variant of MTHFR with reduced enzymatic activity. The prevalence of mild hyperhomocysteinemia in the general population is 5–7%; severe hyperhomocysteinemia is rare. In contrast to severe hyperhomocysteinemia, mild hyperhomocysteinemia often remains asymptomatic until the fourth decade, then causing premature atherosclerotic vascular disease. So far, several studies have shown that the association between coronary artery disease and hyperhomocysteinemia is not confined to the rare inborn homocystinuria but also exists in the general population. In fact, there is a positive correlation between homocysteine plasma levels above 10 µmol/l and mortality. Homocysteine plasma levels can be lowered by intake of folic acid and vitamins B6 and B12. However, until the results of randomized controlled studies investigating the effects of homocysteine-lowering therapy are available, general screening for hyperhomocysteinemia is not recommended. In patients with hyperhomocysteinemia and a high risk for cardiovascular events (i.e. patients with multiple risk factors or established atherosclerotic vascular disease), the dietary intake of folic acid and vitamins B6 and B12 should be optimized. Persistently elevated homocysteine plasma levels may be treated with dietary supplementation of these vitamins, i.e. folic acid 0.4 mg/day, vitamin B6 2 mg, and vitamin B12 6 µg/day.

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