Journal
CLINICAL NEUROPHARMACOLOGY
Volume 29, Issue 3, Pages 106-111Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/01.WNF.0000220817.94102.95
Keywords
COMT inhibitors; entacapone; homocysteine; Parkinson disease; folate; B-12; vitamins
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Levodopa treatment of Parkinson disease results in hyperhomocysteinemia (HHcy) as a consequence of levodopa methylation by catechol-O-methyl-transferase (COMT). Although inhibition of COMT should theoretically prevent or reduce levodopa-induced HHcy, results from several prospective studies are conflicting. Our review of these studies suggests that the ability of COMT inhibition to reduce or prevent levodopa-induced HHcy in Parkinson disease patients may be attributed to differences in the vitamin status of the study participants. In patients with low or low-normal folate levels, levodopa administration is associated with a greater increase in homocysteine, and concomitant entacapone administration is associated with a greater reduction in homocysteine.
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