HLA antigens in drug-induced parkinsonism.
Identifieur interne : 004F94 ( PubMed/Corpus ); précédent : 004F93; suivant : 004F95HLA antigens in drug-induced parkinsonism.
Auteurs : W S Metzer ; J E Newton ; R W Steele ; M. Claybrook ; S R Paige ; D E Mcmillan ; S. HaysSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1989.
English descriptors
- KwdEn :
- Adult, Antipsychotic Agents (adverse effects), Antipsychotic Agents (therapeutic use), Dyskinesia, Drug-Induced (genetics), HLA Antigens (genetics), Humans, Male, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (genetics), Risk Factors, Schizophrenia (drug therapy), Schizophrenia (genetics).
- MESH :
- chemical , adverse effects : Antipsychotic Agents.
- chemical , genetics : HLA Antigens.
- chemical , therapeutic use : Antipsychotic Agents.
- chemically induced : Parkinson Disease, Secondary.
- drug therapy : Schizophrenia.
- genetics : Dyskinesia, Drug-Induced, Parkinson Disease, Secondary, Schizophrenia.
- Adult, Humans, Male, Risk Factors.
Abstract
The results of two epidemiological studies suggest a hereditary predisposition to develop drug-induced parkinsonism. We investigated human leukocyte antigen (HLA) antigen prevalence rates in patients with neuroleptic-induced parkinsonism. Fifty-two male, white, neuroleptic-treated, chronic in-patients with DSM-III-diagnosed schizophrenia were examined for the presence of parkinsonism. Subjects were tested for 23 type A, 43 type B, 4 type C, and 10 type DR HLA antigens. The group of schizophrenic patients with parkinsonism (n = 29) was compared with the group of schizophrenic patients without parkinsonism (n = 23). There were no significant differences between the two groups with respect to age, duration of neuroleptic exposure, or anticholinergic drug exposure. One HLA antigen, B44, was significantly more prevalent in the group with parkinsonism than in the group without parkinsonism. We derived a relative risk of 7.16 for drug-induced parkinsonism with HLA-B44 present in this group of schizophrenic patients. These data indicate that HLA-B44 may play a role in genetic or immunologic susceptibility to develop drug-induced parkinsonism in white schizophrenic individuals.
DOI: 10.1002/mds.870040203
PubMed: 2567491
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pubmed:2567491Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">HLA antigens in drug-induced parkinsonism.</title><author><name sortKey="Metzer, W S" sort="Metzer, W S" uniqKey="Metzer W" first="W S" last="Metzer">W S Metzer</name><affiliation><nlm:affiliation>Department of Neurology, University of Arkansas for Medical Sciences, Little Rock.</nlm:affiliation></affiliation></author><author><name sortKey="Newton, J E" sort="Newton, J E" uniqKey="Newton J" first="J E" last="Newton">J E Newton</name></author><author><name sortKey="Steele, R W" sort="Steele, R W" uniqKey="Steele R" first="R W" last="Steele">R W Steele</name></author><author><name sortKey="Claybrook, M" sort="Claybrook, M" uniqKey="Claybrook M" first="M" last="Claybrook">M. Claybrook</name></author><author><name sortKey="Paige, S R" sort="Paige, S R" uniqKey="Paige S" first="S R" last="Paige">S R Paige</name></author><author><name sortKey="Mcmillan, D E" sort="Mcmillan, D E" uniqKey="Mcmillan D" first="D E" last="Mcmillan">D E Mcmillan</name></author><author><name sortKey="Hays, S" sort="Hays, S" uniqKey="Hays S" first="S" last="Hays">S. Hays</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1989">1989</date><idno type="RBID">pubmed:2567491</idno><idno type="pmid">2567491</idno><idno type="doi">10.1002/mds.870040203</idno><idno type="wicri:Area/PubMed/Corpus">004F94</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">HLA antigens in drug-induced parkinsonism.</title><author><name sortKey="Metzer, W S" sort="Metzer, W S" uniqKey="Metzer W" first="W S" last="Metzer">W S Metzer</name><affiliation><nlm:affiliation>Department of Neurology, University of Arkansas for Medical Sciences, Little Rock.</nlm:affiliation></affiliation></author><author><name sortKey="Newton, J E" sort="Newton, J E" uniqKey="Newton J" first="J E" last="Newton">J E Newton</name></author><author><name sortKey="Steele, R W" sort="Steele, R W" uniqKey="Steele R" first="R W" last="Steele">R W Steele</name></author><author><name sortKey="Claybrook, M" sort="Claybrook, M" uniqKey="Claybrook M" first="M" last="Claybrook">M. Claybrook</name></author><author><name sortKey="Paige, S R" sort="Paige, S R" uniqKey="Paige S" first="S R" last="Paige">S R Paige</name></author><author><name sortKey="Mcmillan, D E" sort="Mcmillan, D E" uniqKey="Mcmillan D" first="D E" last="Mcmillan">D E Mcmillan</name></author><author><name sortKey="Hays, S" sort="Hays, S" uniqKey="Hays S" first="S" last="Hays">S. Hays</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1989" type="published">1989</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Antipsychotic Agents (adverse effects)</term><term>Antipsychotic Agents (therapeutic use)</term><term>Dyskinesia, Drug-Induced (genetics)</term><term>HLA Antigens (genetics)</term><term>Humans</term><term>Male</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (genetics)</term><term>Risk Factors</term><term>Schizophrenia (drug therapy)</term><term>Schizophrenia (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antipsychotic Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>HLA Antigens</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antipsychotic Agents</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Schizophrenia</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease, Secondary</term><term>Schizophrenia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Humans</term><term>Male</term><term>Risk Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The results of two epidemiological studies suggest a hereditary predisposition to develop drug-induced parkinsonism. We investigated human leukocyte antigen (HLA) antigen prevalence rates in patients with neuroleptic-induced parkinsonism. Fifty-two male, white, neuroleptic-treated, chronic in-patients with DSM-III-diagnosed schizophrenia were examined for the presence of parkinsonism. Subjects were tested for 23 type A, 43 type B, 4 type C, and 10 type DR HLA antigens. The group of schizophrenic patients with parkinsonism (n = 29) was compared with the group of schizophrenic patients without parkinsonism (n = 23). There were no significant differences between the two groups with respect to age, duration of neuroleptic exposure, or anticholinergic drug exposure. One HLA antigen, B44, was significantly more prevalent in the group with parkinsonism than in the group without parkinsonism. We derived a relative risk of 7.16 for drug-induced parkinsonism with HLA-B44 present in this group of schizophrenic patients. These data indicate that HLA-B44 may play a role in genetic or immunologic susceptibility to develop drug-induced parkinsonism in white schizophrenic individuals.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">2567491</PMID><DateCreated><Year>1989</Year><Month>07</Month><Day>17</Day></DateCreated><DateCompleted><Year>1989</Year><Month>07</Month><Day>17</Day></DateCompleted><DateRevised><Year>2007</Year><Month>11</Month><Day>14</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>4</Volume><Issue>2</Issue><PubDate><Year>1989</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>HLA antigens in drug-induced parkinsonism.</ArticleTitle><Pagination><MedlinePgn>121-8</MedlinePgn></Pagination><Abstract><AbstractText>The results of two epidemiological studies suggest a hereditary predisposition to develop drug-induced parkinsonism. We investigated human leukocyte antigen (HLA) antigen prevalence rates in patients with neuroleptic-induced parkinsonism. Fifty-two male, white, neuroleptic-treated, chronic in-patients with DSM-III-diagnosed schizophrenia were examined for the presence of parkinsonism. Subjects were tested for 23 type A, 43 type B, 4 type C, and 10 type DR HLA antigens. The group of schizophrenic patients with parkinsonism (n = 29) was compared with the group of schizophrenic patients without parkinsonism (n = 23). There were no significant differences between the two groups with respect to age, duration of neuroleptic exposure, or anticholinergic drug exposure. One HLA antigen, B44, was significantly more prevalent in the group with parkinsonism than in the group without parkinsonism. We derived a relative risk of 7.16 for drug-induced parkinsonism with HLA-B44 present in this group of schizophrenic patients. These data indicate that HLA-B44 may play a role in genetic or immunologic susceptibility to develop drug-induced parkinsonism in white schizophrenic individuals.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Metzer</LastName><ForeName>W S</ForeName><Initials>WS</Initials><AffiliationInfo><Affiliation>Department of Neurology, University of Arkansas for Medical Sciences, Little Rock.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Newton</LastName><ForeName>J E</ForeName><Initials>JE</Initials></Author><Author ValidYN="Y"><LastName>Steele</LastName><ForeName>R W</ForeName><Initials>RW</Initials></Author><Author ValidYN="Y"><LastName>Claybrook</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Paige</LastName><ForeName>S R</ForeName><Initials>SR</Initials></Author><Author ValidYN="Y"><LastName>McMillan</LastName><ForeName>D E</ForeName><Initials>DE</Initials></Author><Author ValidYN="Y"><LastName>Hays</LastName><ForeName>S</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>RR05350-23</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</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="D014150">Antipsychotic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006680">HLA Antigens</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000328">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014150">Antipsychotic Agents</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000009">adverse effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004409">Dyskinesia, Drug-Induced</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006680">HLA Antigens</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010302">Parkinson Disease, Secondary</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000139">chemically induced</QualifierName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012307">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012559">Schizophrenia</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1989</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1989</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1989</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">2567491</ArticleId><ArticleId IdType="doi">10.1002/mds.870040203</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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