Journal
EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY
Volume 58, Issue 1, Pages 1-5Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00228-001-0421-6
Keywords
folate; homocysteine; coagulation
Categories
Ask authors/readers for more resources
Objective: To determine whether folate treatment, besides decreasing homocysteine (tHcy), improves coagulation status, oxidative stress and endothelial dysfunction and whether these depend on genetic polymorphism of the enzyme methylenetetrahydrofolate reductase (MTHFR). Methods: Fifty-seven volunteers (males 30, females 27, mean age 61.2 years) with high coronary risk or manifest atherosclerotic disease and tHcy concentration of at least 20 mumol/l participated in an open, prospective study 1 month of placebo period, followed by 2 months of treatment with folate 10 mg daily. Concentrations of tHcy were measured using high-pressure liquid chromatography with fluorescence detection. Other variables were measured using commercial kits, and polymorphisim of MTHFR was detected using a polymerase chain reaction. Results: Folate treatment resulted in a significant decrease of tHcy and fibrinogen, while plasminogen and antithrombin III significantly increased. Glutathione peroxidase, glutathione and superoxide dismutase significantly increased after the folate treatment; moreover, malonyldialdehyde and von Willebrand factor decreased concomitantly. The individual MTHFR polymorphism did not influence the outcomes of folate treatment. Conclusion: Folate treatment resulted not only in tHcy decrease, but also in an improvement of hypercoagulation, oxidative stress and endothelial dysfunction. The sufficiently high dose of folate seems to be able to decrease plasma tHcy in all three individual MTHFR polymorphism groups, to almost the same post-treatment concentrations.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available