Summary
The correlation between homocysteine and vascular disease has been assessed in several
clinical studies that demonstrated that elevation of plasma total homocysteine (tHcy)
was an independent risk factor for atheriosclerotic disease. Major advances of homocysteine
metabolism disorders have been made during the last few years, encompassing the rare
homozygous enzyme deficiencies, as well as more common milder abnormalities. In experimental
and clinical studies, a homocysteine-mediated oxidant stress has been shown to trigger
platelet activation, in turn leading to a tendency to thrombosis, in patients with
severe hyperhomocysteinaemia. Likewise, the hypomethylation hypothesis on acquired
hyperhomocysteinaemia (chronic renal disease) and the interrelationship between hyperhomocysteinaemia
and impaired fibrinolysis, have added further biological plausibility to the role
for hyperhomocysteinaemia in vascular medicine. However, whether hyperhomocysteinaemia
is causal or a marker of vascular disease, and whether plasma tHcy is only an indicator
of the metabolic status remains to be clarified. The role of the intake of some vitamins
(folic acid, vit.B12, vit.B6) on cardiovascular disease (CVD) is poorly understood: in spite of the lowering of
homocysteine (Hcy) levels, vitamin supplementation failed to exert significant effects
on cardiovascular risk. On the other hand, although some lipid-modifying treatments
increase Hcy levels in diabetics, there is no evidence that this attenuates the beneficial
effects of such treatments on the cardiovascular risk. Because of these uncertainties
in the area, the data available do not provide support for routine screening and treatment
for elevated Hcy to prevent CVD.
Keywords
Homocysteine - arterial thrombosis - folate
