Elevation of total homocysteine levels in patients with Parkinson’s disease treated with duodenal levodopa/carbidopa gel

Abstract

Levodopa/carbidopa (LD/CD) application elevates total plasma homocysteine (thcys). We determined thcys-, LD- and 3-O-methyldopa (3-OMD) concentrations in 28 patients with Parkinson's disease (PD) on a LD/CD duodenal gel treatment. We found a distinct thcys increase (29.52 ± 28.98 μmol/l [median ± SD]) above the 15 μmol/l threshold and a significant (R = 0.7) correlation between LD and 3-OMD. thcys ascent was observed in relation with the onset of atherosclerosis, non-motor symptoms and polyneuropathy in PD patients in the long term.

Electrophysiological features of lower motor neuron involvement in progressive supranuclear palsy

“…Findings suggesting neurogenic abnormalities in skeletal muscles, were found in one third of our MSA patients, so more rarely than in PSP (mean age in MSA group was 60.6±8.1 yrs, and in PSP 67.6± 5.7 yrs). As the involvement of peripheral nerves is very rare in patients with PSP, also in patients with PSP treated with levodopa, we could not confirm recent reports [22] that levodopa may cause polyneuropathy in patients with Parkinson's disease.…”

Is peripheral neuron degeneration involved in multiple system atrophy? A clinical and electrophysiological study

“…Recent reports indicate that levodopa may cause polyneuropathy in patients with Parkinson's disease by increasing homocysteine level [16][17][18][19]. A similar mechanism of neuropathy has not been considered in MSA.…”

Inhibition of catechol-O-methyltransferase modifies acute homocysteine rise during repeated levodopa application in patients with Parkinson’s disease

“…The period between freezing and work up of the plasma samples was no longer than 3 months. Reversed-phase highperformance liquid chromatography (HPLC) was employed in combination with electrochemical detection for the measurement of levodopa/3-O-methyldopa levels in plasma, which was diluted with a factor of 1:1.95 before assessment (Muller et al 2011). Homocysteine was measured by an automated HPLC with reverse phase separation and fluorescent detection, by NaBH 4 /mBrB reduction followed by monobromobimane derivatization (Muller et al 2011).…”

“…This is common practice, as the short plasma half-life of levodopa/DDI limits its efficacy on motor symptoms of PD patients. Repeated levodopa/DDI intake or duodenal levodopa/CD infusion caused an up to tenfold elevation of homocysteine above the generally accepted threshold of 15 μmol/l in plasma (Nevrly et al 2010;Muller et al 2011). Vitamin supplementation decreases homocysteine generation, as B 12 or folic acid catalyze the reversible degradation of homocysteine to methionine and B 6 the irreversible turnover of homocysteine to cysteine (Cacciapuoti 2011).…”