Homocysteine Levels in Parkinson's Disease: Is Entacapone Effective?

Bilge Kocer,Hayat Guven,Selim Selcuk Comoglu

doi:10.1155/2016/7563705

Abstract

Plasma homocysteine (Hcy) levels may increase in levodopa-treated patients with Parkinson's disease (PD) as a consequence of levodopa methylation via catechol-O-methyltransferase (COMT). Results from previous studies that assessed the effect of COMT inhibitors on levodopa-induced hyperhomocysteinemia are conflicting. We aimed to evaluate the effects of levodopa and entacapone on plasma Hcy levels. A hundred PD patients were enrolled to the study and divided into three treatment groups (group I: levodopa and/or dopamine agonists; group II: levodopa, entacapone, and/or a dopamine agonist; and group III: dopamine agonist alone). We measured the serum B12, folic acid, and Hcy levels in all patients. There were no statistically significant differences between groups in terms of modified Hoehn and Yahr stages, Unified Parkinson's Disease Rating Scale II/III, Standardized Mini-Mental Test scores, and serum vitamin B12 and folic acid levels. Plasma median Hcy levels were found above the normal laboratory values in groups I and II, but they were normal in group III. However, there was no statistically significant difference in plasma Hcy levels between groups. Our results showed that levodopa treatment may cause a slight increase in the Hcy levels in PD compared with dopamine agonists and that COMT inhibitors may not have a significant effect on preventing hyperhomocysteinemia.

Highlights

High levels of homocysteine (Hcy) are a known risk factor for vascular diseases and dementia in the general population [1, 2]
We evaluated the effects of various treatment options on plasma Hcy levels in idiopathic Parkinson’s disease (PD) and investigated whether the addition of entacapone to the treatment contributed to a reduction in plasma Hcy levels
There were no differences between groups in terms of mHY stages, Unified Parkinson’s Disease Rating Scale” (UPDRS) Part II/III scores, and Standardized Mini-Mental Test” (SMMT) scores (Table 2)

Summary

Introduction

High levels of homocysteine (Hcy) are a known risk factor for vascular diseases and dementia in the general population [1, 2]. Plasma Hcy levels may increase as a result of genetic and acquired causes [3]. In terms of the genetic causes, a gene mutation exists that encodes the methylenetetrahydrofolate reductase (MTHFR) enzyme and is commonly encountered in the general population [3]. Plasma Hcy levels can be affected by severe metabolic disorders, vitamin B12 and folic acid deficiency, and the use of vitamins and certain medications [3]. An increase in plasma Hcy levels has been reported in Parkinson’s disease (PD) patients who were using levodopa. The catalysis of levodopa with the catechol-O-methyltransferase (COMT) enzyme results in the formation of S-adenosylhomocysteine (SAH), which hydrolyses to form Hcy [3]

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Conclusion