HYPERHOMOCYST(E)INEMIA - AN INDEPENDENT R ISK FACTOR FOR STROKE

The total of free and protein-bound homocysteine including its derivat ives is usually summarised as ''homocyst(e)ine [H(e)]''. Several conge nital enzyme deficiencies may cause markedly elevated H(e) plasma leve ls, leading to the well-known clinical syndromes of homocystinuria. Re cently, mild hyperhomocyst(e)inemia has been recognised as an independ ent risk factor for ischaemic cerebrovascular disease, coronary heart disease, and peripheral artery disease. H(e) levels are also related t o the extent of atherosclerotic vessel wall alterations. The role of m ild hyperhomocyst(e)inemia in venous thromboembolic disease, however, is not yet clear. A considerable proportion of patients with mild hype rhomocyst(e)inemia suffers from a deficiency of folate, vitamin B-12, and/or vitamin B-6. Supplementation of these agents - alone or combine d with betain - leads to a decrease or even to a normalisation of elev ated H(e) levels in the majority of such patients. Hitherto, no prospe ctive randomised studies dealing with the clinical efficacy of such a - probably innocuous - supplementation have been performed. In the mea ntime, adequate alimentary intake of folate should be ensured.