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Homocysteine-lowering treatment: an overview
C van Guldener1, C D Stehouwer
1Department of Internal Medicine, University Hospital and Institute of Cardiovascular Research, Vrije Universiteit, Amsterdam, The Netherlands.
Expert Opinion on Pharmacotherapy
|October 5, 2001
Summary
High homocysteine levels are linked to cardiovascular disease. Supplementing with folic acid and pyridoxine can effectively lower homocysteine, especially in at-risk patients.
Area of Science:
- Biochemistry
- Cardiovascular Medicine
- Nutritional Science
Background:
- Elevated fasting plasma homocysteine is prevalent in cardiovascular disease patients.
- Hyperhomocysteinaemia is associated with increased atherothrombotic risk.
- Causes include genetic defects (e.g., cystathionine-beta-synthase deficiency), vitamin deficiencies, and renal failure.
Purpose of the Study:
- To review the causes and management of hyperhomocysteinaemia.
- To evaluate homocysteine-lowering therapies for cardiovascular disease prevention.
Main Methods:
- Review of existing literature on homocysteine metabolism and treatment.
- Analysis of treatment strategies for specific causes of hyperhomocysteinaemia.
- Consideration of ongoing clinical trials for secondary prevention.
Main Results:
- Genetic defects (CBS deficiency) treated with pyridoxine, folic acid, and betaine.
- Vitamin B12 and folic acid deficiencies corrected by supplementation.
- Dietary folate increases lower homocysteine in some individuals.
- Renal failure patients show partial improvement with folic acid.
- Primary hyperhomocysteinaemia treated with folic acid.
- Post-methionine loading hyperhomocysteinaemia managed with pyridoxine and folic acid.
Conclusions:
- Folic acid and pyridoxine offer effective, safe, and inexpensive treatment options.
- Screening and treating high-risk patients is recommended pending further clinical trial results.
- Homocysteine-lowering therapy's role in secondary prevention requires further investigation in large trials.