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Homocysteine--relevant for atherogenesis?
1Department of Nuclear Medicine, University of Vienna, Austria.
Insights
High homocysteine (hyperhomocysteinemia) is linked to early vascular disease. Vitamin B, particularly folic acid, can treat it, but more trials are needed to confirm benefits for atherosclerosis.
Area of Science:
- Cardiovascular Medicine
- Nutritional Science
- Genetics
Background:
- Hyperhomocysteinemia is strongly associated with premature atherosclerotic vascular disease.
- Causes include genetic defects and deficiencies in vitamin B12, folate, and B6.
- Elevated homocysteine levels are influenced by lifestyle, age, sex, illness, and medications.
Purpose of the Study:
- To review the causes, consequences, and management of hyperhomocysteinemia.
- To assess the role of hyperhomocysteinemia as a risk factor for atherosclerosis.
- To highlight the need for further clinical trials and standardized diagnostic methods.
Main Methods:
- Literature review of studies on hyperhomocysteinemia and atherosclerotic vascular disease.
- Analysis of etiological factors, including genetic and nutritional aspects.
- Evaluation of current treatment strategies and diagnostic challenges.
Main Results:
- Vitamin B supplementation, especially folic acid, effectively treats hyperhomocysteinemia.
- The definitive role of homocysteine as an independent risk factor for atherosclerosis remains unclear compared to established factors.
- Lack of standardized analytical methods complicates the interpretation of clinical data.
Conclusions:
- Diagnosis and treatment are currently recommended for high-risk patients with a family history of premature atherosclerosis.
- Further clinical trials are essential to validate the benefits of lowering homocysteine in preventing and managing atherosclerotic vascular disease.
- Standardization of homocysteine and folate assays is crucial for reliable clinical evaluation.
Abstract:
Numerous studies report strong associations between hyperhomocysteinemia and premature atherosclerotic vascular disease. Causes of hyperhomocysteinemia are hereditary heterozygous or, in very rare cases, homozygous defects, and quite frequently a lack of the coenzymes B6 and B12 and the cosubstrate folate. Lifestyle factors, age, sex, acute and chronic illness, vitamin deficiency and certain drugs may elevate homocysteine concentrations. Vitamin B supplementation, especially folic acid, is an effective treatment of hyperhomocysteinemia. Clinical trials are required to confirm the potential benefit of lowering homocysteine in regard of the development and progression of atherosclerotic vascular disease. The relevance of hyperhomocysteinemia as a risk factor for atherosclerosis, in contrast to the classical triad of risk factors, namely hypercholesterolemia, smoking and hypertension, is still unknown. Furthermore, a lack of standardized analytical methods for the determination of both homocysteine and blood folate renders the evaluation of studies and clinical data difficult. Therefore, at present, diagnosis and treatment is only recommended in high-risk patients (strong family history of premature atherosclerosis or arterial occlusive disease, especially in the absence of other risk factors, as well as in members of their families) with hyperhomocysteinemia.
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