A clinical and pharmacokinetic case study of an interaction of levodopa and antituberculous therapy in Parkinson's disease
Identifieur interne : 005961 ( Main/Exploration ); précédent : 005960; suivant : 005962A clinical and pharmacokinetic case study of an interaction of levodopa and antituberculous therapy in Parkinson's disease
Auteurs : G. K. Wenning [Royaume-Uni] ; M. T. O'Connell [Royaume-Uni] ; P. N. Patsalos [Royaume-Uni] ; Quinn [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 1995-09.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Antibiotique, Homme.
English descriptors
- KwdEn :
- 3,4-Dihydroxyphenylacetic Acid (metabolism), Agonist, Antibiotic, Antiparkinson agent, Antitubercular Agents (pharmacokinetics), Antitubercular Agents (therapeutic use), Antituberculous agent, Antituberculous therapy, Case study, Dopa Decarboxylase (metabolism), Dopa decarboxylase, Dopamine, Drug interaction, Homovanillic Acid (metabolism), Human, Humans, Idiopathic, Isoniazid, Isoniazid (pharmacokinetics), Isoniazid (therapeutic use), Levodopa, Levodopa (blood), Levodopa (metabolism), Levodopa (therapeutic use), Lung, Male, Middle Aged, Parkinson Disease (complications), Parkinson Disease (drug therapy), Parkinson disease, Parkinson's disease, Pharmacokinetic interaction, Pharmacokinetics, Rifampin (pharmacokinetics), Rifampin (therapeutic use), Treatment, Tuberculosis, Tuberculosis, Pulmonary (complications), Tuberculosis, Pulmonary (drug therapy).
- MESH :
- chemical , blood : Levodopa.
- chemical , metabolism : 3,4-Dihydroxyphenylacetic Acid, Dopa Decarboxylase, Homovanillic Acid, Levodopa.
- chemical , pharmacokinetics : Antitubercular Agents, Isoniazid, Rifampin.
- chemical , therapeutic use : Antitubercular Agents, Isoniazid, Levodopa, Rifampin.
- complications : Parkinson Disease, Tuberculosis, Pulmonary.
- drug therapy : Parkinson Disease, Tuberculosis, Pulmonary.
- Humans, Male, Middle Aged.
Abstract
We studied the relationship between levodopa response and antituberculous treatment in a patient with idiopathic Parkinson's disease whose parkinsonism deteriorated when treatment with rifampicin and isoniazid (Rifinah) for pulmonary tuberculosis was started. A levodopa challenge test with regular recording of motor function was performed during, and again after stopping, antituberculous treatment. Plasma levodopa and levodopa metabolite pharmacokinetic profiles were determined using standard techniques. “On” period duration was 75% longer after antituberculous treatment had been stopped. These clinical findings correlated with a 37% increase in area under the concentration versus time curve (AUC), a 103% increase in apparent elimination half‐life (t1/2), a 41% increase in time to maximum concentration (Tmax), and a 33% decrease in maximum concentration (Cmax) of levodopa. A concurrent increase in plasma 3‐O‐methyldopa (3‐OMD) and a decrease in plasma 3,4‐dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), the three major metabolites of levodopa, suggests an inhibition of the enzyme dopa decarboxylase, probably by isoniazid.
Url:
DOI: 10.1002/mds.870100521
Affiliations:
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Le document en format XML
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1995-09">1995-09</date><biblScope unit="vol">10</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="664">664</biblScope><biblScope unit="page" to="667">667</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">2B182C53071FAD8B27970D365F3CFD62535276F4</idno><idno type="DOI">10.1002/mds.870100521</idno><idno type="ArticleID">MDS870100521</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>3,4-Dihydroxyphenylacetic Acid (metabolism)</term><term>Agonist</term><term>Antibiotic</term><term>Antiparkinson agent</term><term>Antitubercular Agents (pharmacokinetics)</term><term>Antitubercular Agents (therapeutic use)</term><term>Antituberculous agent</term><term>Antituberculous therapy</term><term>Case study</term><term>Dopa Decarboxylase (metabolism)</term><term>Dopa decarboxylase</term><term>Dopamine</term><term>Drug interaction</term><term>Homovanillic Acid (metabolism)</term><term>Human</term><term>Humans</term><term>Idiopathic</term><term>Isoniazid</term><term>Isoniazid (pharmacokinetics)</term><term>Isoniazid (therapeutic use)</term><term>Levodopa</term><term>Levodopa (blood)</term><term>Levodopa (metabolism)</term><term>Levodopa (therapeutic use)</term><term>Lung</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Pharmacokinetic interaction</term><term>Pharmacokinetics</term><term>Rifampin (pharmacokinetics)</term><term>Rifampin (therapeutic use)</term><term>Treatment</term><term>Tuberculosis</term><term>Tuberculosis, Pulmonary (complications)</term><term>Tuberculosis, Pulmonary (drug therapy)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>3,4-Dihydroxyphenylacetic Acid</term><term>Dopa Decarboxylase</term><term>Homovanillic Acid</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Antitubercular Agents</term><term>Isoniazid</term><term>Rifampin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antitubercular Agents</term><term>Isoniazid</term><term>Levodopa</term><term>Rifampin</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term><term>Tuberculosis, Pulmonary</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term><term>Tuberculosis, Pulmonary</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Agoniste</term><term>Antibiotique</term><term>Antiparkinsonien</term><term>Antituberculeux</term><term>Dopamine</term><term>Etude cas</term><term>Homme</term><term>Idiopathique</term><term>Interaction médicamenteuse</term><term>Isoniazide</term><term>Lévodopa</term><term>Mâle</term><term>Parkinson maladie</term><term>Pharmacocinétique</term><term>Poumon</term><term>Rifampicine</term><term>Traitement</term><term>Tuberculose</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Antibiotique</term><term>Homme</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We studied the relationship between levodopa response and antituberculous treatment in a patient with idiopathic Parkinson's disease whose parkinsonism deteriorated when treatment with rifampicin and isoniazid (Rifinah) for pulmonary tuberculosis was started. A levodopa challenge test with regular recording of motor function was performed during, and again after stopping, antituberculous treatment. Plasma levodopa and levodopa metabolite pharmacokinetic profiles were determined using standard techniques. “On” period duration was 75% longer after antituberculous treatment had been stopped. These clinical findings correlated with a 37% increase in area under the concentration versus time curve (AUC), a 103% increase in apparent elimination half‐life (t1/2), a 41% increase in time to maximum concentration (Tmax), and a 33% decrease in maximum concentration (Cmax) of levodopa. A concurrent increase in plasma 3‐O‐methyldopa (3‐OMD) and a decrease in plasma 3,4‐dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), the three major metabolites of levodopa, suggests an inhibition of the enzyme dopa decarboxylase, probably by isoniazid.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li></region></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Wenning, G K" sort="Wenning, G K" uniqKey="Wenning G" first="G. K." last="Wenning">G. K. Wenning</name></region><name sortKey="O Connell, M T" sort="O Connell, M T" uniqKey="O Connell M" first="M. T." last="O'Connell">M. T. O'Connell</name><name sortKey="Patsalos, P N" sort="Patsalos, P N" uniqKey="Patsalos P" first="P. N." last="Patsalos">P. N. Patsalos</name><name sortKey="Quinn" sort="Quinn" uniqKey="Quinn" last="Quinn">Quinn</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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