Levodopa treatment does not affect low‐dose apomorphine test in patients with Parkinson's disease
Identifieur interne : 003C68 ( Main/Exploration ); précédent : 003C67; suivant : 003C69Levodopa treatment does not affect low‐dose apomorphine test in patients with Parkinson's disease
Auteurs : Svenja Happe [Allemagne] ; Tobias Tings [Allemagne] ; Kathrin Helmschmied [Allemagne] ; Karin Neubert [Allemagne] ; Wolfgang Wuttke [Allemagne] ; Walter Paulus [Allemagne] ; Claudia Trenkwalder [Allemagne]Source :
- Movement Disorders [ 0885-3185 ] ; 2004-12.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Adult, Aged, Apomorphine (administration & dosage), Apomorphine (diagnostic use), Disability Evaluation, Dopamine (metabolism), Dopamine Agonists (administration & dosage), Dopamine Agonists (diagnostic use), Dopamine Agonists (therapeutic use), Drug Administration Schedule, Female, Human, Human Growth Hormone (blood), Human Growth Hormone (drug effects), Humans, Hydrocortisone (metabolism), Injections, Subcutaneous, Levodopa, Levodopa (therapeutic use), Low dose, Male, Middle Aged, Nervous system diseases, Parkinson Disease (drug therapy), Parkinson disease, Parkinson's disease, Severity of Illness Index, Treatment, apomorphine, cortisol, growth hormone (GH), hypothalamus.
- MESH :
- chemical , administration & dosage : Apomorphine, Dopamine Agonists.
- chemical , blood : Human Growth Hormone.
- chemical , diagnostic use : Apomorphine, Dopamine Agonists.
- chemical , drug effects : Human Growth Hormone.
- chemical , metabolism : Dopamine, Hydrocortisone.
- chemical , therapeutic use : Dopamine Agonists, Levodopa.
- drug therapy : Parkinson Disease.
- Adult, Aged, Disability Evaluation, Drug Administration Schedule, Female, Humans, Injections, Subcutaneous, Male, Middle Aged, Severity of Illness Index.
Abstract
Challenge with low‐dose apomorphine causes a significant rise in growth hormone (GH) in patients with Parkinson's disease (PD) compared to controls and patients with multiple system atrophy (MSA) who have not previously received dopaminergic treatment. To date, it has not been demonstrated whether an apomorphine‐induced rise in GH can still be detected in PD patients who are currently treated with levodopa. We investigated whether an ongoing treatment with levodopa influences the GH response to subcutaneously applied low‐dose apomorphine in PD patients. We studied 44 patients with idiopathic PD using the low‐dose apomorphine test. Twenty‐three patients were under treatment with levodopa and 21 patients were without any dopaminergic therapy. GH and cortisol levels were analyzed at time of injection and 45 minutes and 60 minutes after subcutaneous apomorphine injection. Forty‐five minutes after apomorphine injection, there was no significant difference between the mean rise in plasma GH in untreated PD patients compared with levodopa‐treated patients (P = 0.235). There was no increase of cortisol levels in each treatment group. Age, sex, duration, and severity of the disease did not show a covariate effect with GH levels. A small group of PD patients (n = 8) treated with dopamine agonists and a small group of patients with MSA (n = 5) as well as patients with vascular parkinsonism (n = 5) did not show any increase of GH. Our data suggest that the apomorphine‐induced rise in GH does not depend on previous levodopa treatment in PD patients but, as expected, is blocked by dopamine agonists and is not present in patients with other than idiopathic parkinsonian syndrome. Thus, the low‐dose apomorphine test may also be a useful biological marker in the early differential diagnosis of PD patients who have already received levodopa treatment. © 2004 Movement Disorder Society
Url:
DOI: 10.1002/mds.20244
Affiliations:
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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="2004-12">2004-12</date><biblScope unit="vol">19</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="1511">1511</biblScope><biblScope unit="page" to="1515">1515</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">21FBDAD91B290E934566EE298B8C9E51B20FCCB5</idno><idno type="DOI">10.1002/mds.20244</idno><idno type="ArticleID">MDS20244</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Apomorphine (administration & dosage)</term><term>Apomorphine (diagnostic use)</term><term>Disability Evaluation</term><term>Dopamine (metabolism)</term><term>Dopamine Agonists (administration & dosage)</term><term>Dopamine Agonists (diagnostic use)</term><term>Dopamine Agonists (therapeutic use)</term><term>Drug Administration Schedule</term><term>Female</term><term>Human</term><term>Human Growth Hormone (blood)</term><term>Human Growth Hormone (drug effects)</term><term>Humans</term><term>Hydrocortisone (metabolism)</term><term>Injections, Subcutaneous</term><term>Levodopa</term><term>Levodopa (therapeutic use)</term><term>Low dose</term><term>Male</term><term>Middle Aged</term><term>Nervous system diseases</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Severity of Illness Index</term><term>Treatment</term><term>apomorphine</term><term>cortisol</term><term>growth hormone (GH)</term><term>hypothalamus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Apomorphine</term><term>Dopamine Agonists</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Human Growth Hormone</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Apomorphine</term><term>Dopamine Agonists</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Human Growth Hormone</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Hydrocortisone</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Dopamine Agonists</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Disability Evaluation</term><term>Drug Administration Schedule</term><term>Female</term><term>Humans</term><term>Injections, Subcutaneous</term><term>Male</term><term>Middle Aged</term><term>Severity of Illness Index</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Apomorphine</term><term>Dose faible</term><term>Homme</term><term>Lévodopa</term><term>Parkinson maladie</term><term>Système nerveux pathologie</term><term>Traitement</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Challenge with low‐dose apomorphine causes a significant rise in growth hormone (GH) in patients with Parkinson's disease (PD) compared to controls and patients with multiple system atrophy (MSA) who have not previously received dopaminergic treatment. To date, it has not been demonstrated whether an apomorphine‐induced rise in GH can still be detected in PD patients who are currently treated with levodopa. We investigated whether an ongoing treatment with levodopa influences the GH response to subcutaneously applied low‐dose apomorphine in PD patients. We studied 44 patients with idiopathic PD using the low‐dose apomorphine test. Twenty‐three patients were under treatment with levodopa and 21 patients were without any dopaminergic therapy. GH and cortisol levels were analyzed at time of injection and 45 minutes and 60 minutes after subcutaneous apomorphine injection. Forty‐five minutes after apomorphine injection, there was no significant difference between the mean rise in plasma GH in untreated PD patients compared with levodopa‐treated patients (P = 0.235). There was no increase of cortisol levels in each treatment group. Age, sex, duration, and severity of the disease did not show a covariate effect with GH levels. A small group of PD patients (n = 8) treated with dopamine agonists and a small group of patients with MSA (n = 5) as well as patients with vascular parkinsonism (n = 5) did not show any increase of GH. Our data suggest that the apomorphine‐induced rise in GH does not depend on previous levodopa treatment in PD patients but, as expected, is blocked by dopamine agonists and is not present in patients with other than idiopathic parkinsonian syndrome. Thus, the low‐dose apomorphine test may also be a useful biological marker in the early differential diagnosis of PD patients who have already received levodopa treatment. © 2004 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Allemagne</li></country></list><tree><country name="Allemagne"><noRegion><name sortKey="Happe, Svenja" sort="Happe, Svenja" uniqKey="Happe S" first="Svenja" last="Happe">Svenja Happe</name></noRegion><name sortKey="Helmschmied, Kathrin" sort="Helmschmied, Kathrin" uniqKey="Helmschmied K" first="Kathrin" last="Helmschmied">Kathrin Helmschmied</name><name sortKey="Neubert, Karin" sort="Neubert, Karin" uniqKey="Neubert K" first="Karin" last="Neubert">Karin Neubert</name><name sortKey="Paulus, Walter" sort="Paulus, Walter" uniqKey="Paulus W" first="Walter" last="Paulus">Walter Paulus</name><name sortKey="Tings, Tobias" sort="Tings, Tobias" uniqKey="Tings T" first="Tobias" last="Tings">Tobias Tings</name><name sortKey="Trenkwalder, Claudia" sort="Trenkwalder, Claudia" uniqKey="Trenkwalder C" first="Claudia" last="Trenkwalder">Claudia Trenkwalder</name><name sortKey="Wuttke, Wolfgang" sort="Wuttke, Wolfgang" uniqKey="Wuttke W" first="Wolfgang" last="Wuttke">Wolfgang Wuttke</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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