Endothelial dysfunction and hyperhomocysteinemia in Parkinson's disease: flow-mediated dilation study

Abstract

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.

Keywords: Parkinson's disease; endothelial dysfunction; flow-mediated dilation; hyperhomocysteinemia.