Significantly elevated plasma levels of homocysteine, but not cysteine and cysteinylglycine, were found in treated parkinsonian patients compared to controls. Elevated levels of homocysteine may be either caused by an unknown endogenous metabolic disturbance or by antiparkinsonian treatment, because no association to severity or duration of disease was found. Based on the results of this study one may speculate that homocysteine may be an independent risk factor for vascular disease in Parkinson’s disease.

Sirs: A significant increased hazard ratio for both ischaemic heart and cerebrovascular disease was found in a cohort of 220 parkinsonian patients [2]. Mild hyperhomocysteinaemia has been suggested as a risk factor for atherosclerosis and vascular disease [9]. A significant elevation of plasma homocysteine in parkinsonian patients was found in comparison with controls [1]. However, a major drawback of that study was the insufficient clinical information given on total levodopa dosage, severity of disease and age of subjects. The aim of our study reported here was to evaluate a possible relationship between hyperhomocysteinaemia and Parkinson's disease (PD).We determined plasma levels of homocysteine in 22 parkinsonian patients treated with levodopa/decarboxylase inhibitor and in age-and sex-matched controls. Characteristics of the patients and controls and homocysteine levels are given in Table 1. Excluded as controls were subjects with neurodegenerative diseases, current smokers and individuals with a known history of alcohol abuse or metabolic disturbances such as hypercholesterolaemia, diabetes mellitus, hypertension or hypovitaminosis. Matching was done within an age range of 4 years. Blood samples were drawn in the morning between 8 and 9 a.m. after 10 h of fasting, from a peripheral vein drop-wise in plastic vacuum tubes containing EDTA for estimating plasma levels of homocysteine. Within 10 min the samples were centrifuged for 15 min, 300 × g av at 10°C. The resulting supernatant (plasma) was decanted and stored at -80°C. The time period between freezing and evaluation of the plasma samples was no longer than 3 months. Levels of homocysteine were measured by an automated high-performance liquid chromatography (HPLC) method with reverse phase separation and fluorescent detection, by NaBH 4 /monobromobimane (mBrB) reduction followed by mBrB derivation [8].We compared homocysteine levels for all patients and controls and stratified by age and gender using Student's t test. Additionally, we evaluated the association between disease severity and homocysteine levels among cases using Spearman's rank correlation coefficient and linear regression. Finally, a multivariate linear regression model was built and residuals analysed for normal distribution.Patients had a median Hoehn and Yahr Score (HYS) of 3.25 and a Unified Parkinson's Disease Rating Scale (UPDRS) score of 48. Twentyone patients received conventional pharmacotherapy including levodopa/benserazide or carbidopa preparations and various other antiparkinsonian drugs (amantadine: n =1, bromocriptine: n = 9, budipine: n = 4; pergolide: n = 5, selegiline n = 11 mg). In univariate linear regression, significant positive associations between plasma levels of homocysteine and age were found in patients [β-coefficient: 0.41; 95% confidence interval (CI) 0.11-0.71] and (borderline) in controls (β = 0.20; 95% CI 0.002-0.39). Mean total homocysteine was significantly elevated (mean difference 3.7 µmol/l; 95% CI 0.5-6.9) in parkinsonian patients compared with contro...

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