Related Experiment Video
Updated: Apr 25, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Endothelial dysfunction and hyperhomocysteinemia in Parkinson's disease: flow-mediated dilation study
Jung Han Yoon1, Jin Soo Lee, Seok Woo Yong
1Department of Neurology, Ajou University School of Medicine, Suwon, South Korea.
Insights
Levodopa (l-dopa) therapy for Parkinson's disease (PD) may cause endothelial dysfunction by increasing homocysteine levels. This study found impaired flow-mediated dilation in PD patients on l-dopa, suggesting a link to treatment.
Area of Science:
- Neurology
- Cardiovascular Science
- Pharmacology
Background:
- Parkinson's disease (PD) treatment with levodopa (l-dopa) is associated with elevated serum homocysteine.
- Elevated homocysteine is a potential risk factor for endothelial dysfunction.
Purpose of the Study:
- To investigate the association between levodopa treatment, homocysteine levels, and endothelial function in Parkinson's disease patients.
- To compare endothelial function (flow-mediated dilation) across different PD treatment groups and controls.
Main Methods:
- Cross-sectional study comparing flow-mediated dilation (FMD) in four groups: PD patients on l-dopa, PD patients on l-dopa/entacapone, untreated PD patients, and healthy controls.
- Serum homocysteine levels were measured and correlated with FMD.
Main Results:
- PD patients on l-dopa exhibited significantly lower FMD compared to those on l-dopa/entacapone, untreated PD patients, and controls.
- Higher homocysteine levels were observed in PD patients treated with l-dopa.
- Elevated homocysteine was an independent predictor of reduced flow-mediated dilation.
Conclusions:
- Chronic levodopa treatment in Parkinson's disease may be linked to endothelial dysfunction.
- Increased homocysteine levels during levodopa therapy could contribute to endothelial impairment in PD patients.
Background:
Levodopa (l-dopa) therapy in Parkinson's disease (PD) increases serum homocysteine levels because of its metabolism via catechol O-methyltransferase, which may lead to endothelial dysfunction.
Method:
We enrolled 40 PD patients treated with l-dopa, 33 PD patients treated with l-dopa/entacapone, 22 untreated PD and 30 controls, and compared the flow-mediated dilation in these subjects.
Results:
The flow-mediated dilation was significantly lower in PD patients with l-dopa (6.0 ± 1.8%) than in those with l-dopa/entacapone (7.2 ± 1.1%, P = 0.03), untreated PD patients (7.8 ± 1.2%, P < 0.05), and controls (8.5 ± 2.9%, P < 0.05). The homocysteine level was significantly higher in PD patients with l-dopa than in other groups. In a multivariate logistic regression model, the uppermost homocysteine quartile was an independent predictor of the lowest tertile of flow-mediated dilation (odds ratio, 6.33; 95% confidence interval, 1.61-26.65; P = 0.012).
Conclusions:
Our findings indicate that endothelial dysfunction may be associated with chronic l-dopa treatment in patients with PD.
Related Concept Videos
Parkinson Disease ll: Pathophysiology
Hypertension II: Pathophysiology
Parkinson's Disease: Overview
Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation

