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Auer J et al.  
Homocysteine and Risk of Cardiovascular Disease

Journal of Clinical and Basic Cardiology 2001; 4 (4): 261-264

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Fig. 1: Homocystein - Metabolismus

Keywords: FolatHomocysteinkardiovaskuläre ErkrankungPathophysiologieTherapiecardiovascular diseasefolatehomocysteinepathophysiologytherapy

Homocysteine is a sulphydryl-containing aminoacid derived from demethylation of methionine. Nutritional deficiencies in the vitamin cofactors (folate, vitamin B12, and vitamin B6) required for homocysteine metabolism may promote hyper- homocysteinaemia. Multiple prospective and case-control studies suggested that a moderately elevated plasma homocysteine concentration is an independent risk factor for atherothrombotic vascular disease. Homocysteine concentrations are consistently higher in patients with peripheral, cerebrovascular, and coronary artery disease than in those without such diseases. Homocysteine seems to promote atherothrombogenesis by a variety of mechanisms; however, it is not yet clear whether homocysteine itself or a related metabolite or cofactor is primarily responsible for the atherothrombogenic effects of hyperhomocysteinaemia in vivo. Before advocating wide spread screening of patients with atherosclerotic vascular disease, we must have a clearer understanding of the clinical efficacy of potential therapeutic interventions. Vitamin supplementation decreases or even normalizes plasma homocysteine concentrations in most cases. Prospective, randomized clinical trials, however, will be necessary to determine the effect of vitamin supplementation on cardiovascular morbidity and mortality. The use of pills containing low dose B vitamins as a primary or secondary preventive measure against vascular disease remains unproved, although they are definitely cheap, probably innocuous, and may help prevent acute vascular episodes.
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