Numerous studies report strong associations between hyperhomocysteinemia an
d premature atherosclerotic vascular disease. Causes of hyperhomocysteinemi
a are hereditary heterozygous or, in very rare cases, homozygous defects, a
nd quite frequently a lack of the coenzymes B6 and B12 and the cosubstrate
folate. Lifestyle factors, age, sex, acute and chronic illness, vitamin def
iciency and certain drugs may elevate homocysteine concentrations. Vitamin
B supplementation, especially folic acid, is an effective treatment of hype
rhomocysteinemia. Clinical trials are required to confirm the potential ben
efit of lowering homocysteine in regard of the development and progression
of atherosclerotic vascular disease. The relevance of hyperhomocysteinemia
as a risk factor for atherosclerosis, in contrast to the classical triad of
risk factors, namely hypercholesterolemia, smoking and hypertension, is st
ill unknown. Furthermore, a lack of standardized analytical methods for the
determination of both homocysteine and blood folate renders the evaluation
of studies and clinical data difficult. Therefore, at present, diagnosis a
nd treatment is only recommended in high-risk patients (strong family histo
ry of premature atherosclerosis or arterial occlusive disease, especially i
n the absence of other risk factors, as well as in members of their familie
s) with hyperhomocysteinemia.