title: Reduced plasma homocysteine levels in levodopa/entacapone treated Parkinson patients.
abstract: Hyperhomocysteinemia is not only a major risk factor for atherothrombotic disease, but is also strongly associated with an increased risk of dementia and cognitive impairment, both of which are common in the course of Parkinson's disease (PD). Previous work has found that levodopa increases plasma homocysteine concentrations. Animal studies have indicated that the catechol-O-methyltransferase (COMT) inhibitors can prevent levodopa-induced elevation of homocysteine concentrations by reducing the O-methylation of levodopa. The objective of our study was to assess the impact of entacapone, a COMT inhibitor, on plasma levels of homocysteine, serum folate, and vitamin B12 in levodopa-treated PD patients. Nineteen PD patients receiving only levodopa and 21 PD patients on a combination of levodopa and entacapone participated in the cross-sectional study. The control group consisted of 17 subjects on dopamine agonists. The mean plasma homocysteine concentration in the subjects on only levodopa was higher than that in the subjects on a combination of levodopa and entacapone (P=0.001) or in the control group (P=0.0001). Concentrations of serum vitamin B12 and serum folate were on average normal in all groups, but levodopa-treated subjects (with or without entacapone therapy) were more prone to have hypovitaminosis B12 (45%) than controls on dopamine agonists (6%). We suggest that the COMT inhibition may play a promising role in successfully controlling levodopa-induced hyperhomocysteinemia and in reducing the risk of pathologies probably linked to it. These preliminary findings and postulated hypotheses must now be confirmed in prospective studies.
authors.affiliation: Department of Neurology, Derer's University Hospital, Limbová 5, Bratislava 83305, Slovak Republic. valkovicpeter@hotmail.com
authors.forename: Peter
authors.initials: P
authors.lastname: Valkovic
authors.forename: Ján
authors.initials: J
authors.lastname: Benetin
authors.forename: Pavol
authors.initials: P
authors.lastname: Blazícek
authors.forename: L'udmila
authors.initials: L
authors.lastname: Valkovicová
authors.forename: Karin
authors.initials: K
authors.lastname: Gmitterová
authors.forename: Peter
authors.initials: P
authors.lastname: Kukumberg
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000978:Antiparkinson Agents / Q000627:therapeutic use*; D002394:Catechol O-Methyltransferase / Q000378:metabolism; D065098:Catechol O-Methyltransferase Inhibitors; D002396:Catechols / Q000627:therapeutic use*; D003430:Cross-Sectional Studies; D004359:Drug Therapy, Combination; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D005260:Female; D005492:Folic Acid / Q000097:blood; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000188:drug therapy / Q000517:prevention & control; D007980:Levodopa / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009570:Nitriles; D010300:Parkinson Disease / Q000097:blood / Q000188:drug therapy*; D014805:Vitamin B 12 / Q000097:blood
chemical_list: D000978:Antiparkinson Agents; D065098:Catechol O-Methyltransferase Inhibitors; D002396:Catechols; D004791:Enzyme Inhibitors; D009570:Nitriles; D006710:Homocysteine; D007980:Levodopa; C071192:entacapone; D005492:Folic Acid; D002394:Catechol O-Methyltransferase; D014805:Vitamin B 12