The effect of l-dopa administration and folate deficiency on plasma homocysteine concentrations in rats

Daly, Deborah; Miller, Joshua W.; Nadeau, Marie; Selhub, Jacob

doi:10.1016/s0955-2863(97)00110-1

Cited by 25 publications

(29 citation statements)

References 30 publications

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“…It is also possible that L-dopa treatment for several years may result in greater Hcy elevations than seen after a few months of therapy, although the only empiric data on this point suggests L-dopa-induced hyperhomocysteinemia in rats attenuates with chronic use. 6 This issue requires further study. The L-dopa-induced elevation of tHcy was inversely related to the baseline tHcy.…”

Section: Discussionmentioning

confidence: 97%

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Modest increase in plasma homocysteine follows levodopa initiation in Parkinson's disease

et al. 2004

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Levodopa, typically ingested chronically at high daily doses, is predictably methylated by means of a series of reactions using B vitamins, which convert methionine to homocysteine. Elevated total plasma homocysteine (tHcy), a risk factor for dementia, has been found in PD patients using levodopa. We prospectively measured the effects on plasma tHcy and B vitamins of levodopa initiation, and measured the effects of dose changes and of treatment with dopamine agonists and entacapone. We collected paired plasma samples, at baseline and again after several months treatment, from patients initiating levodopa (n = 30), from patients whose levodopa dose was doubled (n = 15), halved or stopped (n = 14), from patients starting or stopping entacapone (n = 15) and from patients initiating or doubling dopamine agonist monotherapy (n = 16). Vitamin B12, folate, and tHcy concentrations were measured. Baseline tHcy concentration of 8.7 (2.8) micromol/L increased to 10.1 (3.1) micromol/L (P = 0.004) an average of 94 (range 36 to 200) days after initiation of 604 (240 to 1050) mg/day of L-dopa. Average concentration of vitamin B12 fell from 380 to 291 pmol/ L (P = 0.01). Patients who doubled their daily levodopa dose experienced tHcy elevations from 9.5 to 11.1 micromol/L (P = 0.05). Levodopa reduction, agonist treatment, and entacapone treatment did not have significant effects. Levodopa elevates tHcy and lowers vitamin B12 concentration to modest degrees. The clinical implications, if any, have not yet been determined.

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Section: Discussionmentioning

confidence: 97%

“…5,6 Previous cross-sectional studies in humans have found that tHcy was higher among L-dopa using compared to non-using PD patients. [7][8][9] A recent prospective study reported elevation in tHcy among 20 Japanese patients after L-dopa treatment.…”

mentioning

confidence: 99%

Modest increase in plasma homocysteine follows levodopa initiation in Parkinson's disease

et al. 2004

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“…A common acquired cause of elevated plasma Hcy levels is represented by L-dopa (3,4-dihydroxyphenylalanine) therapy (Daly et al 1997, Zoccolella et al 2005a). L-dopa is metabolized by catechol-O-methyltransferase (COMT) in both brain and peripheral tissues.…”

Section: Effect Of Levodopa Treatment On Plasma Hcy Levelsmentioning

confidence: 99%

“…Other pathways involved in L-dopa-induced hyperHcy, are represented by: (1) decreased re-methylation of Hcy, which may result from exhaustion of the pool of methyl groups, also induced by deficiency of folate and vitamin B12 levels, or by genetically determined inefficiency of MS or MTHFR; and (2) dysfunction in transsulfuration pathway, induced by deficiency of vitamin B6, by lack of allosteric activation in CBS by SAM, or by genetic inefficiency of CBS. Experimental studies demonstrated a significant increase in Hcy concentration after L-dopa treatment (Daly et al 1997); this effect is related to a significant decrease in SAM and increase in SAH concentrations in brain and peripheral tissues (Ordez and Wurtman 1974, Taufek and Bone, 1980, Fuller et al 1984, Daly et al 1997. These effects could be prevented by COMT inhibitors treatment and accentuated during folate deficiency (Daly et al 1997).…”

Section: Effect Of Levodopa Treatment On Plasma Hcy Levelsmentioning

confidence: 99%

“…Experimental studies demonstrated a significant increase in Hcy concentration after L-dopa treatment (Daly et al 1997); this effect is related to a significant decrease in SAM and increase in SAH concentrations in brain and peripheral tissues (Ordez and Wurtman 1974, Taufek and Bone, 1980, Fuller et al 1984, Daly et al 1997. These effects could be prevented by COMT inhibitors treatment and accentuated during folate deficiency (Daly et al 1997).…”

Section: Effect Of Levodopa Treatment On Plasma Hcy Levelsmentioning

confidence: 99%

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Role of lifestyle factors on plasma homocysteine levels in Parkison's disease patients treated with levodopa

Siniscalchi

Gallelli²,

Mercuri

et al. 2006

Nutritional Neuroscience

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Many papers documented that Parkinson's disease (PD) patients treated with levodopa (L-dopa) shows elevated plasma homocysteine (Hcy) levels. Several lifestyle factors are able to influence plasma Hcy levels. We review the evidence that L-dopa therapy is related with an increase in plasma Hcy levels and that several behaviours could be able to cause changes in plasma Hcy concentrations. Therefore, there are reasons to suggest that a healthy lifestyle lowering Hcy may prevent this potential iatrogenic complication during L-dopa therapy. Moreover, at present, no controlled prospective studies have evaluated this phenomenon.

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Levodopa, methylmalonic acid, and neuropathy in idiopathic Parkinson disease

Toth

Breithaupt

et al. 2010

Annals of Neurology

179

137

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The effect of l-dopa administration and folate deficiency on plasma homocysteine concentrations in rats

Cited by 25 publications

References 30 publications

Modest increase in plasma homocysteine follows levodopa initiation in Parkinson's disease

Modest increase in plasma homocysteine follows levodopa initiation in Parkinson's disease

Role of lifestyle factors on plasma homocysteine levels in Parkison's disease patients treated with levodopa

Levodopa, methylmalonic acid, and neuropathy in idiopathic Parkinson disease

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