Plasma concentration of levodopa in Parkinsonism before and after inhibition of peripheral decarboxylase

Reid, John L.; Calne, D. B.; Vakil, S. D.; Allen, John G.; Davies, Carolina

doi:10.1016/0022-510x(72)90021-4

Cited by 22 publications

(6 citation statements)

References 20 publications

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“…4a, b). In contrast to the findings of Rinne et al (1973b) and Reid et al (1972), Tolosa found no significant correlation between plasma levodopa and dyskinesia for the entire group of patients, considered together. Woods et al (1973) observed in three parkinsonian patients that peak plasma levels of levodopa achieved following oral administration coincided with maximum suppression of parkinsonian symptoms and the appearance of abnormal involuntary movements.…”

Section: Studies That Find Positive Correlation Between Plasma Levodocontrasting

confidence: 79%

Clinical Pharmacokinetics of Levodopa in Parkinson??s Disease

Bianchine¹,

Shaw²

1976

Clinical Pharmacokinetics

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Although levodopa has provided a major advance in the treatment of parkinsonism, its maximum benefits have not yet been realised, in part because of its complicated pharmacokinetics. This review summarises that available pharmacokinetic data involving levodopa, especially as it relates to therapeutic response of parkinsonian patients. A large number of factors, including protein intake, gastric emptying time, pyridoxine ingestion, and dopa decarboxylase activity, affect plasma levels of levodopa attained following oral administration of this drug. Other variables influence the rate of brain uptake of levodopa from the blood. Even so, plasma levodopa concentration correlates significantly with dosage size in a large parkinsonian population and also coincides with therapeutic response in many, but not all, patients. Therefore, in certain instances, valuable information may be derived by correlating clinical response with plasma levodopa concentration. Cerebrospinal fluid levels of homovanillic acid, a major metabolite of dopamine, may have some value in predicting clinical response to levodopa. This relationship, however, has not been firmly established. Concentration of homovanillic acid or levodopa in body fluids may also be closely related to certain adverse side-effects, including abnormal involuntary movements, gastric discomfort and psychiatric disturbances. Evidence indicates that a clearer understanding of levodopa pharmacokinetics may improve the clinical management of parkinsonism.

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Section: Studies That Find Positive Correlation Between Plasma Levodocontrasting

confidence: 79%

Clinical Pharmacokinetics of Levodopa in Parkinson??s Disease

Bianchine¹,

Shaw²

1976

Clinical Pharmacokinetics

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“…L-dopa itself is one possible candidate for this role. Comparison of plasma levels of L-dopa in patients on maximum tolerated dosage with and without a decarboxylase inhibitor indicates that while peak plasma concentrations are similar, blockade of decarboxylation leads to more sustained levels of L-dopa (Reid et al, 1972); the areas under the plasma concentration curves, representing the quantity of levodopa in the blood, are increased.…”

Section: Discussionmentioning

confidence: 99%

Gout induced by L-dopa and decarboxylase inhibitors

Calne

Fermaglich

1976

Postgraduate Medical Journal

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“…The blood was centrifuged in tubes containing heparin and sodium metabisulphite. The amino-acid fraction was separated on a Dowex column, oxidized to hydroxy-indole derivatives, and assayed fluorimetrically for levodopa as described by Reid et al (1972).…”

Section: Patient and Methodsmentioning

confidence: 99%