Levodopa therapy for Parkinson's disease: Pharmacokinetics and pharmacodynamics.
Identifieur interne : 000195 ( Main/Exploration ); précédent : 000194; suivant : 000196Levodopa therapy for Parkinson's disease: Pharmacokinetics and pharmacodynamics.
Auteurs : Peter A. Lewitt [États-Unis]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2015.
English descriptors
- KwdEn :
- MESH :
- chemical , pharmacokinetics : Antiparkinson Agents, Levodopa.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- drug effects : Brain.
- drug therapy : Parkinson Disease.
- metabolism : Brain, Parkinson Disease.
- pathology : Parkinson Disease.
- Humans.
Abstract
For all its imperfections at treating Parkinson's disease (PD), orally-administered levodopa (l-dopa) can be regarded as the "platinum" standard of PD therapeutics for its impact on disability and discomfort and its cost-effectiveness. The past half-century has confirmed that the typical l-dopa-treated patient gains improvement for most Parkinsonian features, presumably by conversion of this amino acid into dopamine in the striatum. However, fundamental questions remain as to its full mechanism of action and how adverse reactions evolve. Various aspects of clinical phenomenology associated with chronic l-dopa use (such as dyskinesias and the long-duration anti-Parkinsonian response) present a continuing challenge for better understanding of its pharmacology. The pharmacokinetics of l-dopa tend to predict some of problems that can emerge during chronic therapy, which can be linked with its irregular uptake and marked dose-by-dose variability in plasma concentrations. Several new pharmaceutical approaches are targeted at the unique physiology of l-dopa uptake and are likely to improve the consistency of its anti-Parkinsonian effect.
DOI: 10.1002/mds.26082
PubMed: 25449210
Affiliations:
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Le document en format XML
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Lewitt</name><affiliation wicri:level="2"><nlm:affiliation>Parkinson's Disease and Movement Disorders Center, Henry Ford Hospital, West Bloomfield, Michigan, and the Department of Neurology, Wayne State University School of Medicine, Detroit, Michigan, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Parkinson's Disease and Movement Disorders Center, Henry Ford Hospital, West Bloomfield, Michigan, and the Department of Neurology, Wayne State University School of Medicine, Detroit, Michigan</wicri:regionArea><placeName><region type="state">Michigan</region></placeName></affiliation></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiparkinson Agents (pharmacokinetics)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Brain (drug effects)</term><term>Brain (metabolism)</term><term>Humans</term><term>Levodopa (pharmacokinetics)</term><term>Levodopa (therapeutic use)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">For all its imperfections at treating Parkinson's disease (PD), orally-administered levodopa (l-dopa) can be regarded as the "platinum" standard of PD therapeutics for its impact on disability and discomfort and its cost-effectiveness. The past half-century has confirmed that the typical l-dopa-treated patient gains improvement for most Parkinsonian features, presumably by conversion of this amino acid into dopamine in the striatum. However, fundamental questions remain as to its full mechanism of action and how adverse reactions evolve. Various aspects of clinical phenomenology associated with chronic l-dopa use (such as dyskinesias and the long-duration anti-Parkinsonian response) present a continuing challenge for better understanding of its pharmacology. The pharmacokinetics of l-dopa tend to predict some of problems that can emerge during chronic therapy, which can be linked with its irregular uptake and marked dose-by-dose variability in plasma concentrations. Several new pharmaceutical approaches are targeted at the unique physiology of l-dopa uptake and are likely to improve the consistency of its anti-Parkinsonian effect.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Michigan</li></region></list><tree><country name="États-Unis"><region name="Michigan"><name sortKey="Lewitt, Peter A" sort="Lewitt, Peter A" uniqKey="Lewitt P" first="Peter A" last="Lewitt">Peter A. Lewitt</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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