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Homocysteine and vascular disease
C S Berwanger1, J Y Jeremy, G Stansby
1Academic Surgical Unit, St Mary's Hospital Medical School, London, UK.
Insights
High homocysteine (HC) levels are a risk factor for premature atherosclerosis, especially in young individuals. Lowering HC with vitamins B6, B12, folate, or betaine is a potential treatment, though its effectiveness is still under investigation.
Area of Science:
- Cardiovascular Medicine
- Genetics
- Biochemistry
Background:
- Elevated blood homocysteine (HC) is increasingly recognized as a risk factor for premature atherosclerosis.
- The genetic prevalence of conditions leading to high HC suggests it may be more common than previously estimated.
- High HC should be suspected in young patients lacking other atherosclerosis risk factors.
Purpose of the Study:
- To review the evidence linking elevated homocysteine levels to premature vascular disease.
- To discuss diagnostic methods for identifying hyperhomocysteinemia.
- To outline current treatment strategies aimed at reducing homocysteine levels.
Main Methods:
- Review of existing scientific literature on homocysteine and atherosclerosis.
- Analysis of studies demonstrating elevated plasma HC in patients with premature vascular diseases.
- Examination of proposed mechanisms of HC-induced vascular damage.
Main Results:
- Significantly increased homocysteine levels were observed in patients with premature coronary, peripheral, and cerebrovascular diseases.
- Endothelial injury is considered a likely mechanism through which HC contributes to vascular damage.
- Diagnostic approaches include measuring basal or post-methionine-load plasma HC levels.
Conclusions:
- Hyperhomocysteinemia is a significant risk factor for premature atherosclerosis, particularly in younger individuals.
- Treatment involves lowering blood HC levels using vitamin B6, vitamin B12, folate, or betaine.
- The clinical efficacy of homocysteine-lowering therapy in preventing vascular complications requires further research.
Abstract:
There is increasing evidence that a raised blood level of homocysteine (HC) is a risk factor for premature atherosclerosis. With a gene frequency between one in 70 and one in 200 this condition may be more common than previously thought. It should be suspected especially in young patients in whom other risk factors are absent. The diagnosis may be made by demonstrating raised plasma HC levels, either basally or after methionine loading. Studies have shown significantly increased levels of HC in patients with premature coronary artery, peripheral vascular and cerebrovascular disease. The mechanisms by which HC produces vascular damage are, as yet, not completely understood but endothelial injury is probably a central factor. The principle of treatment is to lower HC levels in the blood by administration of vitamin B6, vitamin B12, folate or betaine. How effective this strategy will be in preventing complications is not yet known.