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The treatment of hyperhomocysteinemia
Bradley A Maron1, Joseph Loscalzo
1Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. bmaron@partners.org
Annual Review of Medicine
|August 30, 2008
Summary
High homocysteine levels increase risks for cardiovascular and cognitive diseases. While B-vitamin therapy lowers homocysteine, its effectiveness in trials has been limited, suggesting a need for targeted patient selection.
Area of Science:
- Biochemistry
- Cardiovascular Science
- Neurology
Background:
- Homocysteine's reactivity contributes to oxidant stress and cellular toxicity.
- Hyperhomocysteinemia is an established risk factor for cardiovascular, cerebrovascular, and cognitive disorders.
- B-vitamin therapy effectively reduces homocysteine levels.
Purpose of the Study:
- To evaluate the clinical utility of homocysteine reduction in specific patient populations.
- To address limitations of previous trials that focused on mildly elevated homocysteine levels.
Main Methods:
- Review of epidemiological data and randomized controlled trials.
- Analysis of clinical scenarios where homocysteine reduction may be beneficial.
Main Results:
- Despite B-vitamin therapy reducing homocysteine, clinical trial outcomes have often been disappointing.
- Previous trials typically included patients with only mild hyperhomocysteinemia.
- Effectiveness in primary prevention or severe hyperhomocysteinemia remains underexplored.
Conclusions:
- Current evidence does not fully support widespread homocysteine monitoring for all patients.
- Further research is needed to identify patient subgroups (e.g., primary prevention, severe hyperhomocysteinemia) who may benefit from homocysteine reduction therapy.
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