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Homocysteine elevation with fibrates: is it a class effect?
D Harats1, O Yodfat, R Doolman
1Institute of Lipid and Atherosclerosis Research, Sheba Medical Center, Tel-Hashomer, Israel. dharats@post.tau.ac.il
Insights
Ciprofibrate significantly increases plasma homocysteine levels, while bezafibrate reduces them. This homocysteine elevation is reversible after stopping ciprofibrate treatment, indicating it
Area of Science:
- Pharmacology and Cardiovascular Medicine
- Lipid Metabolism and Atherosclerosis Research
Background:
- Elevated plasma homocysteine is a significant risk factor for atherosclerotic vascular diseases.
- Certain medications, including some lipid-lowering drugs, can influence homocysteine levels.
- Previous studies suggest interactions between fibrates and homocysteine plasma levels.
Purpose of the Study:
- To investigate the impact of different fibrate medications on plasma homocysteine levels.
- To assess the reversibility of observed changes in homocysteine following fibrate treatment cessation.
Main Methods:
- Evaluated ciprofibrate and bezafibrate effects on homocysteine in hyperlipidemia patients.
- Measured homocysteine levels during 12 weeks of treatment and after a 6-week cessation period.
Main Results:
- Ciprofibrate treatment led to a 57% increase in plasma homocysteine levels.
- Bezafibrate treatment resulted in a 17% reduction in plasma homocysteine levels.
- The homocysteine increase with ciprofibrate was sustained and partially reversible post-treatment.
Conclusions:
- Fibrates do not uniformly affect homocysteine levels; the magnitude of change varies by drug.
- The observed increase in plasma homocysteine with ciprofibrate is reversible upon drug discontinuation.
Background:
Case-control and prospective studies indicate that an elevated plasma homocysteine level is a powerful risk factor for atherosclerotic vascular diseases. Certain medications can induce hyperhomocystinemia, such as methotrexate, trimethoprim and anti-epileptic drugs. There are few reports indicating an interaction between lipid-lowering drugs (cholestyramine and niacin) and homocysteine. Recently, an interaction was shown between fenofibrate and benzafibrates (a fibric acid derivative) and homocysteine plasma levels.
Objectives:
To evaluate the effects of different fibrates on plasma homocysteine levels and to measure the reversibility of this effect.
Methods And Results:
We investigated the effects of ciprofibrate and bezafibrate on homocysteine levels in patients with type IV hyperlipidemia and/or low high density lipoprotein levels. While a 57% increase in homocysteine was detected in the ciprofibrate-treated group (n = 26), a 17% reduction in homocysteine was detected in the group treated with bezafibrate (n = 12). The increase in homocysteine in the ciprofibrate-treated group was sustained for the 12 weeks of treatment and was partially reversible after 6 weeks of discontinuing the ciprofibrate therapy.
Conclusions:
These results indicate that an increase in plasma homocysteine levels following administration of fibrates is not a class effect, at least in its magnitude. Moreover, it is reversible upon discontinuation of the treatment.