INFO - Treatment with folate to lower homocysteine

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Medscape

posted 07/29/04

Treatment With Folate to Lower Homocysteine

Question

What should be done about an elevated homocysteine level that persists

despite administration of high-dose folic acid and high blood levels of

folic acid?

Response from a Brownfield, MD

Assistant Professor of Medicine, Department of Medicine, Emory

University School of Medicine, Atlanta, Georgia; Staff Physician,

Department of Medicine, Grady Memorial Hospital, Atlanta, Georgia

High homocysteine levels are associated with an increased risk of

cardiovascular and cerebrovascular disease. Hyperhomocysteinemia can be

caused by several mechanisms: (1) genetic defects in the enzymes

involved in the metabolism of homocysteine, (2) nutritional deficiencies

in vitamin cofactors, or (3) some chronic medical conditions and drugs.

Smoking may increase homocysteine levels in the blood.

In the absence of known cardiovascular or cerebrovascular disease, it is

controversial whether or not to treat patients with elevated

homocysteine levels. There is no clear evidence for treating patients

who do not have severe hyperhomocysteinemia in the absence of

cardiovascular or thrombotic disease.[1] There are conflicting data on

the efficacy of supplementation aimed at lowering homocysteine levels to

prevent vascular events and death in patients with established vascular

disease.[2-4] For patients who are treated, the treatment should target

the underlying cause, if known.

In general, a diet rich in fruits, vegetables, and low-fat dairy

products as well as low in saturated and total fat can help to decrease

serum homocysteine. For patients with known cardiovascular disease, it

is generally recommended to treat with folic acid (1 mg/day), vitamin B6

(10 mg/day), and vitamin B12 (0.4 mg/day). Folic acid can be increased

up to 5 mg/day to reach a goal of lowering homocysteine levels below 15

mmol/L. In patients refractory to 5 mg/day of folic acid, 750 mg twice

daily of trimethylglycine have been used, but there are only limited

data demonstrating efficacy.[1] It is known that trimethylglycine

enhances the methylation metabolism of homocysteine.

Although treating hyperhomocysteinemia can be very important, it should

go without question that the more significant cardiovascular risk

factors, such as diabetes, hypertension, hypercholesterolemia, and

tobacco use, must also be addressed.

Posted 07/29/2004

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References

1. Rosen RS, Kang DS. Overview of homocysteine. UpToDate. April 2004.

2. Schnyder G, Roffi M, Flammer Y, Pin R, Hess OM. Effect of

homocysteine-lowering therapy with folic acid, vitamin B12, and vitamin

B6 on clinical outcome after percutaneous coronary intervention: the

Swiss Heart Study: a randomized controlled trial. JAMA.

2002;288:973-979. Abstract

3. Liem A, Reynierse-Buitenwerf GH, Zwinderman AH, Lukema JW, van

Veldhuisen DJ. Secondary prevention with folic acid: effects on clinical

outcomes. J Am Coll Cardiol. 2003;41:2105-2113. Abstract

4. Toole JF, Malinow MR, Chambless LE, et al. Lowering homocysteine

levels in patients with ischemic stroke to prevent recurrent stroke,

myocardial infarction, and death: the Vitamin Intervention for Stroke

Prevention randomized controlled trial. JAMA. 2004;291:565-575. Abstract

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