Abstract
Elevated homocysteine has been shown to be associated with coronary heart disease,
stroke, peripheral arterial occlusion and venous thromboembolism. High serum concentrations
are found in individuals with genetic variants (e.g. MTHFR polymorphism), in folic
acid deficiency, vitamin B12 -, and vitamin B6-deficiency, hypothyreosis, alcoholism,
malignancy, and due to special drug therapy. Recent data from clinical trials demonstrated
a significant decrease in serum concentrations of homocysteine during treatment with
folic acid, vitamin B12 and vitamin B6, but there were no effects on clinical outcomes,
like coronary artery disease, stroke, or peripheral vascular disease. Therefore, at
present, elevated homocysteine should have the following practical implications: Hyperhomocysteinemia
may be a marker of vitamin deficiency. Hence the causes of elevated homocysteine should
be identified. Lowering homocysteine for the purpose of reducing cardiovascular risk
cannot be recommended so far. Therefore, in the case of elevated homocysteine, the
therapeutic focus should concentrate on the classical, modifiable risk factors (e.g.
LDL-cholesterin, blood pressure).
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Dr. med. univ. Tanja B. Grammer
Synlab Medizinisches Versorgungszentrum für Labordiagnostik Heidelberg
Postfach 104129
69031 Heidelberg
eMail: tanja.grammer@synlab.de
