Homocysteine: a novel risk factor in vascular disease |
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| Affiliation: | 2. Department of Rehabilitation, Toyama Prefectural Rehabilitation Hospital and Support Center for Children with Disabilities, Toyama, Japan;3. Department of Rehabilitation, University of Toyama, Toyama, Japan;1. School of Public Health, Key Laboratory of Public Health Safety of the Ministry of Education and Key Laboratory of Health Technology Assessment of the Ministry of Health, Fudan University, Shanghai, China;3. Shanghai Key Laboratory of Meteorology and Health, Shanghai, China;4. Department of Epidemiology, College of Public Health and Health Professions and College of Medicine, University of Florida, Gainesville, FL, USA;1. Department of Biomedicine, Neuroscience and Advanced Diagnostics (Bi.N.D.), University of Palermo, Palermo, Italy;2. Department of Experimental Medicine, TOR, University of Rome “Tor Vergata”, Rome, Italy;3. Istituto Dermopatico dell''Immacolata, IRCCS, Rome, Italy;4. Department of Internal Medicine and Cardiovascular Disease, Division of Cardiology and Cardiovascular Rehabilitation, University Hospital Paolo Giaccone, Palermo, Italy;5. Cardiac Surgery Unit, Department of Surgical Science, Tor Vergata University Hospital, Rome, Italy;6. MRC-Toxicology Unit, University of Cambridge, UK |
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| Abstract: | Homocysteine is a sulphydryl-containing aminoacid derived from the metabolic demethylation of methionine. Moderately raised concentrations of total homocysteine (tHcy) have been correlated with an increased risk of atherothrombotic vascular events. The prevalence of hyperhomocysteinaemia has been estimated to be about 5% in the general population, and 13–47% among patients with symptomatic atherosclerotic vascular disease. Nutritional deficiencies in the vitamin cofactors (folate, vitamin B12, and vitamin B6) required for homocysteine metabolism may promote hyperhomocysteinaemia. Clinical and experimental studies suggest that high homocysteine concentrations may cause the atherogenic and thrombotic tendencies of homocystinuric and hyperhomocysteinaemic patients. Experimental evidence suggests that the atherogenic propensity associated with hyperhomocysteinaemia results from endothelial dysfunction and injury followed by platelet activation and thrombus formation. The treatment of hyperhomocysteinaemia varies with the underlying cause; however, vitamin supplementation (with folic acid, pyridoxine [vitamin B6], and vitamin B12) is generally effective in reducing homocysteine concentrations. Before advocating widespread screening of patients with atherosclerotic vascular disease, we must have a clearer understanding of the clinical efficacy of potential therapeutic interventions. Prospective, randomized clinical trials, however, will be necessary to determine the effect of vitamin supplementation on cardiovascular morbidity and mortality. |
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