Neuropathy as a potential complication of levodopa use in Parkinson's disease.
Identifieur interne : 000956 ( Ncbi/Merge ); précédent : 000955; suivant : 000957Neuropathy as a potential complication of levodopa use in Parkinson's disease.
Auteurs : Cory Toth [Canada] ; Martin Sutton Brown ; Sarah Furtado ; Oksana Suchowersky ; Douglas ZochodneSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2008.
English descriptors
- KwdEn :
- Analysis of Variance, Antiparkinson Agents (adverse effects), Female, Homocysteine (blood), Humans, Levodopa (adverse effects), Male, Methylmalonic Acid (blood), Parkinson Disease (complications), Parkinson Disease (drug therapy), Peripheral Nervous System Diseases (etiology), Retrospective Studies, Vitamin B 12 (blood).
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , blood : Homocysteine, Methylmalonic Acid, Vitamin B 12.
- complications : Parkinson Disease.
- drug therapy : Parkinson Disease.
- etiology : Peripheral Nervous System Diseases.
- Analysis of Variance, Female, Humans, Male, Retrospective Studies.
Abstract
The presence and potential etiologies of peripheral neuropathy (PN) in patients with Parkinson's Disease (PD) is unknown. We examined for presence of PN in patients with PD. From a PD patient population of 500 patients screened for features of symptomatic PN, patients were further selected for clinical, electrophysiological, and laboratory studies related to PN. This PD patient population with idiopathic PN (PD-IPN) was compared to a group of PD patients without PN (PD-only), and a large group of patients without PD with idiopathic PN (IPN) for abnormalities in Cbl, fasting homocysteine (Hcy), and fasting methylmalonic acid (MMA) levels. PD-IPN and IPN patients identified with abnormalities in Cbl, Hcy, or MMA levels were treated with intramuscular Cbl for 1 to 2 years. Of 49 PD patients with symptomatic PN, 34 patients (69%) had PD-IPN, and 32/34 (94%) had abnormal Hcy or MMA levels as compared to 26/258 (10%) of IPN patients. Cumulative lifetime L-dopa dosage and fasting MMA levels were associated with PN severity. Cbl therapy led to improvements in Hcy and MMA levels in all groups, and PN in PD-IPN patients stabilized during therapy. PN in PD patients may be associated with iatrogenic Cbl metabolic abnormalities. Alternatively PN may be a peripheral nervous system manifestation of PD.
DOI: 10.1002/mds.22137
PubMed: 18785232
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uniqKey="Furtado S" first="Sarah" last="Furtado">Sarah Furtado</name></author><author><name sortKey="Suchowersky, Oksana" sort="Suchowersky, Oksana" uniqKey="Suchowersky O" first="Oksana" last="Suchowersky">Oksana Suchowersky</name></author><author><name sortKey="Zochodne, Douglas" sort="Zochodne, Douglas" uniqKey="Zochodne D" first="Douglas" last="Zochodne">Douglas Zochodne</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2008">2008</date><idno type="RBID">pubmed:18785232</idno><idno type="pmid">18785232</idno><idno type="doi">10.1002/mds.22137</idno><idno type="wicri:Area/PubMed/Corpus">000F40</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000F40</idno><idno type="wicri:Area/PubMed/Curation">000F40</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000F40</idno><idno type="wicri:Area/PubMed/Checkpoint">000F40</idno><idno type="wicri:explorRef" 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last="Brown">Martin Sutton Brown</name></author><author><name sortKey="Furtado, Sarah" sort="Furtado, Sarah" uniqKey="Furtado S" first="Sarah" last="Furtado">Sarah Furtado</name></author><author><name sortKey="Suchowersky, Oksana" sort="Suchowersky, Oksana" uniqKey="Suchowersky O" first="Oksana" last="Suchowersky">Oksana Suchowersky</name></author><author><name sortKey="Zochodne, Douglas" sort="Zochodne, Douglas" uniqKey="Zochodne D" first="Douglas" last="Zochodne">Douglas Zochodne</name></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="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Analysis of Variance</term><term>Antiparkinson Agents (adverse effects)</term><term>Female</term><term>Homocysteine (blood)</term><term>Humans</term><term>Levodopa (adverse effects)</term><term>Male</term><term>Methylmalonic Acid (blood)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (drug therapy)</term><term>Peripheral Nervous System Diseases (etiology)</term><term>Retrospective Studies</term><term>Vitamin B 12 (blood)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Homocysteine</term><term>Methylmalonic Acid</term><term>Vitamin B 12</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Peripheral Nervous System Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term><term>Female</term><term>Humans</term><term>Male</term><term>Retrospective Studies</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The presence and potential etiologies of peripheral neuropathy (PN) in patients with Parkinson's Disease (PD) is unknown. We examined for presence of PN in patients with PD. From a PD patient population of 500 patients screened for features of symptomatic PN, patients were further selected for clinical, electrophysiological, and laboratory studies related to PN. This PD patient population with idiopathic PN (PD-IPN) was compared to a group of PD patients without PN (PD-only), and a large group of patients without PD with idiopathic PN (IPN) for abnormalities in Cbl, fasting homocysteine (Hcy), and fasting methylmalonic acid (MMA) levels. PD-IPN and IPN patients identified with abnormalities in Cbl, Hcy, or MMA levels were treated with intramuscular Cbl for 1 to 2 years. Of 49 PD patients with symptomatic PN, 34 patients (69%) had PD-IPN, and 32/34 (94%) had abnormal Hcy or MMA levels as compared to 26/258 (10%) of IPN patients. Cumulative lifetime L-dopa dosage and fasting MMA levels were associated with PN severity. Cbl therapy led to improvements in Hcy and MMA levels in all groups, and PN in PD-IPN patients stabilized during therapy. PN in PD patients may be associated with iatrogenic Cbl metabolic abnormalities. Alternatively PN may be a peripheral nervous system manifestation of PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18785232</PMID><DateCreated><Year>2008</Year><Month>11</Month><Day>04</Day></DateCreated><DateCompleted><Year>2009</Year><Month>04</Month><Day>08</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>13</Issue><PubDate><Year>2008</Year><Month>Oct</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Neuropathy as a potential complication of levodopa use in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>1850-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.22137</ELocationID><Abstract><AbstractText>The presence and potential etiologies of peripheral neuropathy (PN) in patients with Parkinson's Disease (PD) is unknown. We examined for presence of PN in patients with PD. From a PD patient population of 500 patients screened for features of symptomatic PN, patients were further selected for clinical, electrophysiological, and laboratory studies related to PN. This PD patient population with idiopathic PN (PD-IPN) was compared to a group of PD patients without PN (PD-only), and a large group of patients without PD with idiopathic PN (IPN) for abnormalities in Cbl, fasting homocysteine (Hcy), and fasting methylmalonic acid (MMA) levels. PD-IPN and IPN patients identified with abnormalities in Cbl, Hcy, or MMA levels were treated with intramuscular Cbl for 1 to 2 years. Of 49 PD patients with symptomatic PN, 34 patients (69%) had PD-IPN, and 32/34 (94%) had abnormal Hcy or MMA levels as compared to 26/258 (10%) of IPN patients. Cumulative lifetime L-dopa dosage and fasting MMA levels were associated with PN severity. Cbl therapy led to improvements in Hcy and MMA levels in all groups, and PN in PD-IPN patients stabilized during therapy. PN in PD patients may be associated with iatrogenic Cbl metabolic abnormalities. Alternatively PN may be a peripheral nervous system manifestation of PD.</AbstractText><CopyrightInformation>(c) 2008 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Toth</LastName><ForeName>Cory</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada. corytoth@shaw.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brown</LastName><ForeName>Martin Sutton</ForeName><Initials>MS</Initials></Author><Author ValidYN="Y"><LastName>Furtado</LastName><ForeName>Sarah</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Suchowersky</LastName><ForeName>Oksana</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Zochodne</LastName><ForeName>Douglas</ForeName><Initials>D</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0LVT1QZ0BA</RegistryNumber><NameOfSubstance UI="D006710">Homocysteine</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>8LL8S712J7</RegistryNumber><NameOfSubstance UI="D008764">Methylmalonic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>P6YC3EG204</RegistryNumber><NameOfSubstance UI="D014805">Vitamin B 12</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Mov Disord. 2010 Apr 15;25(5):660-1</RefSource><PMID Version="1">20213824</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000704" MajorTopicYN="N">Analysis of Variance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006710" MajorTopicYN="N">Homocysteine</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008764" MajorTopicYN="N">Methylmalonic Acid</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010523" MajorTopicYN="N">Peripheral Nervous System Diseases</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014805" 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Martin Sutton" sort="Brown, Martin Sutton" uniqKey="Brown M" first="Martin Sutton" last="Brown">Martin Sutton Brown</name><name sortKey="Furtado, Sarah" sort="Furtado, Sarah" uniqKey="Furtado S" first="Sarah" last="Furtado">Sarah Furtado</name><name sortKey="Suchowersky, Oksana" sort="Suchowersky, Oksana" uniqKey="Suchowersky O" first="Oksana" last="Suchowersky">Oksana Suchowersky</name><name sortKey="Zochodne, Douglas" sort="Zochodne, Douglas" uniqKey="Zochodne D" first="Douglas" last="Zochodne">Douglas Zochodne</name></noCountry><country name="Canada"><region name="Alberta"><name sortKey="Toth, Cory" sort="Toth, Cory" uniqKey="Toth C" first="Cory" last="Toth">Cory Toth</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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