Pharmacogenetic study of antipsychotic induced acute extrapyramidal symptoms in a first episode psychosis cohort: role of dopamine, serotonin and glutamate candidate genes
This study investigated whether the risk of presenting antipsychotic (AP)-induced extrapyramidal symptoms (EPS) could be related to single-nucleotide polymorphisms (SNPs) in a naturalistic cohort of first episode psychosis (FEP) patients. Two hundred and two SNPs in 31 candidate genes (involved in d...
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| Veröffentlicht in: | The pharmacogenomics journal 2016-10, Vol.16 (5), p.439-445 |
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| creator | Mas, S Gassó, P Lafuente, A Bioque, M Lobo, A Gonzàlez-Pinto, A Olmeda, M S Corripio, I Llerena, A Cabrera, B Saiz-Ruiz, J Bernardo, M |
| description | This study investigated whether the risk of presenting antipsychotic (AP)-induced extrapyramidal symptoms (EPS) could be related to single-nucleotide polymorphisms (SNPs) in a naturalistic cohort of first episode psychosis (FEP) patients. Two hundred and two SNPs in 31 candidate genes (involved in dopamine, serotonin and glutamate pathways) were analyzed in the present study. One hundred and thirteen FEP patients (43 presenting EPS and 70 non-presenting EPS) treated with high-potency AP (amisulpride, paliperidone, risperidone and ziprasidone) were included in the analysis. The statistical analysis was adjusted by age, gender, AP dosage, AP combinations and concomitant treatments as covariates. Four SNPs in different genes (
DRD2
,
SLC18A2
,
HTR2A
and
GRIK3
) contributed significantly to the risk of EPS after correction for multiple testing (
P |
| doi_str_mv | 10.1038/tpj.2016.44 |
| format | Article |
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DRD2
,
SLC18A2
,
HTR2A
and
GRIK3
) contributed significantly to the risk of EPS after correction for multiple testing (
P
<1 × 10
−4
). These findings support the involvement of dopamine, serotonin and glutamate pathways in AP-induced EPS.</description><identifier>ISSN: 1470-269X</identifier><identifier>EISSN: 1473-1150</identifier><identifier>DOI: 10.1038/tpj.2016.44</identifier><identifier>PMID: 27272046</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>45/77 ; 631/208/205 ; 692/53/2423 ; 692/699/476/1799 ; Adolescent ; Adult ; Antipsychotic agents ; Antipsychotic Agents - adverse effects ; Antipsychotics ; Basal Ganglia Diseases - chemically induced ; Basal Ganglia Diseases - genetics ; Basal Ganglia Diseases - metabolism ; Basal Ganglia Diseases - physiopathology ; Biomedical and Life Sciences ; Biomedicine ; Case-Control Studies ; Child ; Dopamine ; Dopamine - metabolism ; Dopamine D2 receptors ; Dopamine receptors ; Dosage and administration ; Drug therapy ; Extrapyramidal system ; Female ; Follow-Up Studies ; Gene Expression ; Genetic aspects ; Genetic Association Studies ; Genetic Predisposition to Disease ; GluK3 Kainate Receptor ; Glutamate ; Glutamic Acid - metabolism ; Haplotypes ; Human Genetics ; Humans ; Longitudinal Studies ; Male ; Oncology ; original-article ; Pharmacogenetics ; Pharmacogenomic Variants ; Pharmacotherapy ; Phenotype ; Polymorphism, Single Nucleotide ; Prospective Studies ; Psychopharmacology ; Psychosis ; Psychotic Disorders - diagnosis ; Psychotic Disorders - drug therapy ; Psychotic Disorders - physiopathology ; Psychotropic drugs ; Receptor, Serotonin, 5-HT2A - genetics ; Receptors, Dopamine D2 - genetics ; Receptors, Kainic Acid - genetics ; Risk Assessment ; Risk Factors ; Risperidone ; Serotonin ; Serotonin - metabolism ; Single nucleotide polymorphisms ; Single-nucleotide polymorphism ; Spain ; Statistical analysis ; Treatment Outcome ; Vesicular Monoamine Transport Proteins - genetics ; Young Adult ; Ziprasidone</subject><ispartof>The pharmacogenomics journal, 2016-10, Vol.16 (5), p.439-445</ispartof><rights>Macmillan Publishers Limited 2016</rights><rights>COPYRIGHT 2016 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Oct 2016</rights><rights>Macmillan Publishers Limited 2016.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-6d723f02129b235f74ccc607bed065feb25567dfb1d0771869a94fa5c8b20b9f3</citedby><cites>FETCH-LOGICAL-c482t-6d723f02129b235f74ccc607bed065feb25567dfb1d0771869a94fa5c8b20b9f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27272046$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mas, S</creatorcontrib><creatorcontrib>Gassó, P</creatorcontrib><creatorcontrib>Lafuente, A</creatorcontrib><creatorcontrib>Bioque, M</creatorcontrib><creatorcontrib>Lobo, A</creatorcontrib><creatorcontrib>Gonzàlez-Pinto, A</creatorcontrib><creatorcontrib>Olmeda, M S</creatorcontrib><creatorcontrib>Corripio, I</creatorcontrib><creatorcontrib>Llerena, A</creatorcontrib><creatorcontrib>Cabrera, B</creatorcontrib><creatorcontrib>Saiz-Ruiz, J</creatorcontrib><creatorcontrib>Bernardo, M</creatorcontrib><creatorcontrib>PEPs GROUP</creatorcontrib><title>Pharmacogenetic study of antipsychotic induced acute extrapyramidal symptoms in a first episode psychosis cohort: role of dopamine, serotonin and glutamate candidate genes</title><title>The pharmacogenomics journal</title><addtitle>Pharmacogenomics J</addtitle><addtitle>Pharmacogenomics J</addtitle><description>This study investigated whether the risk of presenting antipsychotic (AP)-induced extrapyramidal symptoms (EPS) could be related to single-nucleotide polymorphisms (SNPs) in a naturalistic cohort of first episode psychosis (FEP) patients. Two hundred and two SNPs in 31 candidate genes (involved in dopamine, serotonin and glutamate pathways) were analyzed in the present study. One hundred and thirteen FEP patients (43 presenting EPS and 70 non-presenting EPS) treated with high-potency AP (amisulpride, paliperidone, risperidone and ziprasidone) were included in the analysis. The statistical analysis was adjusted by age, gender, AP dosage, AP combinations and concomitant treatments as covariates. Four SNPs in different genes (
DRD2
,
SLC18A2
,
HTR2A
and
GRIK3
) contributed significantly to the risk of EPS after correction for multiple testing (
P
<1 × 10
−4
). These findings support the involvement of dopamine, serotonin and glutamate pathways in AP-induced EPS.</description><subject>45/77</subject><subject>631/208/205</subject><subject>692/53/2423</subject><subject>692/699/476/1799</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Antipsychotic agents</subject><subject>Antipsychotic Agents - adverse effects</subject><subject>Antipsychotics</subject><subject>Basal Ganglia Diseases - chemically induced</subject><subject>Basal Ganglia Diseases - genetics</subject><subject>Basal Ganglia Diseases - metabolism</subject><subject>Basal Ganglia Diseases - physiopathology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Case-Control Studies</subject><subject>Child</subject><subject>Dopamine</subject><subject>Dopamine - metabolism</subject><subject>Dopamine D2 receptors</subject><subject>Dopamine receptors</subject><subject>Dosage and administration</subject><subject>Drug therapy</subject><subject>Extrapyramidal system</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Gene Expression</subject><subject>Genetic aspects</subject><subject>Genetic Association Studies</subject><subject>Genetic Predisposition to Disease</subject><subject>GluK3 Kainate Receptor</subject><subject>Glutamate</subject><subject>Glutamic Acid - metabolism</subject><subject>Haplotypes</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Longitudinal Studies</subject><subject>Male</subject><subject>Oncology</subject><subject>original-article</subject><subject>Pharmacogenetics</subject><subject>Pharmacogenomic Variants</subject><subject>Pharmacotherapy</subject><subject>Phenotype</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Prospective Studies</subject><subject>Psychopharmacology</subject><subject>Psychosis</subject><subject>Psychotic Disorders - diagnosis</subject><subject>Psychotic Disorders - drug therapy</subject><subject>Psychotic Disorders - physiopathology</subject><subject>Psychotropic drugs</subject><subject>Receptor, Serotonin, 5-HT2A - genetics</subject><subject>Receptors, Dopamine D2 - genetics</subject><subject>Receptors, Kainic Acid - genetics</subject><subject>Risk Assessment</subject><subject>Risk Factors</subject><subject>Risperidone</subject><subject>Serotonin</subject><subject>Serotonin - metabolism</subject><subject>Single nucleotide polymorphisms</subject><subject>Single-nucleotide polymorphism</subject><subject>Spain</subject><subject>Statistical analysis</subject><subject>Treatment Outcome</subject><subject>Vesicular Monoamine Transport Proteins - genetics</subject><subject>Young Adult</subject><subject>Ziprasidone</subject><issn>1470-269X</issn><issn>1473-1150</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kk2LFDEQhhtR3HX15F0CXgR3xiSdTrq9Lcv6AQt6UPAW0kllJkN30iZpsH-Tf3LTzvrJInVIpfK8VZWiquopwVuC6_ZVng5bignfMnavOiVM1BtCGnz_h483lHdfTqpHKR1wgYhoH1YnVBTDjJ9W3z_uVRyVDjvwkJ1GKc9mQcEi5bOb0qL3YQ07b2YNBik9Z0DwLUc1LVGNzqgBpWWcchhToZBC1sWUEUwuBQPomCK5hHTYh5hfoxgGWAuYMBW9h3OUIIYc_Kr2Bu2GOatRlTK6XEuB4q3dpcfVA6uGBE9uz7Pq85urT5fvNtcf3r6_vLjeaNbSvOFG0NpiSmjX07qxgmmtORY9GMwbCz1tGi6M7YnBQpCWd6pjVjW67SnuO1ufVS-OeacYvs6Qshxd0jAMykOYkyQtFR2hZeYFff4Peghz9KU7STkjgtCW1_-jSq7SFOMd_U3t1ADSeRvKkPVaWl6wFtcdboko1PYOqpiB0engwboS_0vw8ijQMaQUwcopulHFRRIs1wWSZYHkukCSsUI_u2117kcwv9ifG1OA8yOQypPfQfzjL3fkuwGFENFw</recordid><startdate>20161001</startdate><enddate>20161001</enddate><creator>Mas, S</creator><creator>Gassó, P</creator><creator>Lafuente, A</creator><creator>Bioque, M</creator><creator>Lobo, A</creator><creator>Gonzàlez-Pinto, A</creator><creator>Olmeda, M S</creator><creator>Corripio, I</creator><creator>Llerena, A</creator><creator>Cabrera, B</creator><creator>Saiz-Ruiz, J</creator><creator>Bernardo, M</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope></search><sort><creationdate>20161001</creationdate><title>Pharmacogenetic study of antipsychotic induced acute extrapyramidal symptoms in a first episode psychosis cohort: role of dopamine, serotonin and glutamate candidate genes</title><author>Mas, S ; Gassó, P ; Lafuente, A ; Bioque, M ; Lobo, A ; Gonzàlez-Pinto, A ; Olmeda, M S ; Corripio, I ; Llerena, A ; Cabrera, B ; Saiz-Ruiz, J ; Bernardo, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-6d723f02129b235f74ccc607bed065feb25567dfb1d0771869a94fa5c8b20b9f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>45/77</topic><topic>631/208/205</topic><topic>692/53/2423</topic><topic>692/699/476/1799</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Antipsychotic agents</topic><topic>Antipsychotic Agents - adverse effects</topic><topic>Antipsychotics</topic><topic>Basal Ganglia Diseases - chemically induced</topic><topic>Basal Ganglia Diseases - genetics</topic><topic>Basal Ganglia Diseases - metabolism</topic><topic>Basal Ganglia Diseases - physiopathology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Case-Control Studies</topic><topic>Child</topic><topic>Dopamine</topic><topic>Dopamine - metabolism</topic><topic>Dopamine D2 receptors</topic><topic>Dopamine receptors</topic><topic>Dosage and administration</topic><topic>Drug therapy</topic><topic>Extrapyramidal system</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Gene Expression</topic><topic>Genetic aspects</topic><topic>Genetic Association Studies</topic><topic>Genetic Predisposition to Disease</topic><topic>GluK3 Kainate Receptor</topic><topic>Glutamate</topic><topic>Glutamic Acid - metabolism</topic><topic>Haplotypes</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Longitudinal Studies</topic><topic>Male</topic><topic>Oncology</topic><topic>original-article</topic><topic>Pharmacogenetics</topic><topic>Pharmacogenomic Variants</topic><topic>Pharmacotherapy</topic><topic>Phenotype</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Prospective Studies</topic><topic>Psychopharmacology</topic><topic>Psychosis</topic><topic>Psychotic Disorders - diagnosis</topic><topic>Psychotic Disorders - drug therapy</topic><topic>Psychotic Disorders - physiopathology</topic><topic>Psychotropic drugs</topic><topic>Receptor, Serotonin, 5-HT2A - genetics</topic><topic>Receptors, Dopamine D2 - genetics</topic><topic>Receptors, Kainic Acid - genetics</topic><topic>Risk Assessment</topic><topic>Risk Factors</topic><topic>Risperidone</topic><topic>Serotonin</topic><topic>Serotonin - metabolism</topic><topic>Single nucleotide polymorphisms</topic><topic>Single-nucleotide polymorphism</topic><topic>Spain</topic><topic>Statistical analysis</topic><topic>Treatment Outcome</topic><topic>Vesicular Monoamine Transport Proteins - genetics</topic><topic>Young Adult</topic><topic>Ziprasidone</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mas, S</creatorcontrib><creatorcontrib>Gassó, P</creatorcontrib><creatorcontrib>Lafuente, A</creatorcontrib><creatorcontrib>Bioque, M</creatorcontrib><creatorcontrib>Lobo, A</creatorcontrib><creatorcontrib>Gonzàlez-Pinto, A</creatorcontrib><creatorcontrib>Olmeda, M S</creatorcontrib><creatorcontrib>Corripio, I</creatorcontrib><creatorcontrib>Llerena, A</creatorcontrib><creatorcontrib>Cabrera, B</creatorcontrib><creatorcontrib>Saiz-Ruiz, J</creatorcontrib><creatorcontrib>Bernardo, M</creatorcontrib><creatorcontrib>PEPs GROUP</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><jtitle>The pharmacogenomics journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mas, S</au><au>Gassó, P</au><au>Lafuente, A</au><au>Bioque, M</au><au>Lobo, A</au><au>Gonzàlez-Pinto, A</au><au>Olmeda, M S</au><au>Corripio, I</au><au>Llerena, A</au><au>Cabrera, B</au><au>Saiz-Ruiz, J</au><au>Bernardo, M</au><aucorp>PEPs GROUP</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pharmacogenetic study of antipsychotic induced acute extrapyramidal symptoms in a first episode psychosis cohort: role of dopamine, serotonin and glutamate candidate genes</atitle><jtitle>The pharmacogenomics journal</jtitle><stitle>Pharmacogenomics J</stitle><addtitle>Pharmacogenomics J</addtitle><date>2016-10-01</date><risdate>2016</risdate><volume>16</volume><issue>5</issue><spage>439</spage><epage>445</epage><pages>439-445</pages><issn>1470-269X</issn><eissn>1473-1150</eissn><abstract>This study investigated whether the risk of presenting antipsychotic (AP)-induced extrapyramidal symptoms (EPS) could be related to single-nucleotide polymorphisms (SNPs) in a naturalistic cohort of first episode psychosis (FEP) patients. Two hundred and two SNPs in 31 candidate genes (involved in dopamine, serotonin and glutamate pathways) were analyzed in the present study. One hundred and thirteen FEP patients (43 presenting EPS and 70 non-presenting EPS) treated with high-potency AP (amisulpride, paliperidone, risperidone and ziprasidone) were included in the analysis. The statistical analysis was adjusted by age, gender, AP dosage, AP combinations and concomitant treatments as covariates. Four SNPs in different genes (
DRD2
,
SLC18A2
,
HTR2A
and
GRIK3
) contributed significantly to the risk of EPS after correction for multiple testing (
P
<1 × 10
−4
). These findings support the involvement of dopamine, serotonin and glutamate pathways in AP-induced EPS.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27272046</pmid><doi>10.1038/tpj.2016.44</doi><tpages>7</tpages></addata></record> |
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| language | eng |
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| source | MEDLINE; Alma/SFX Local Collection |
| subjects | 45/77 631/208/205 692/53/2423 692/699/476/1799 Adolescent Adult Antipsychotic agents Antipsychotic Agents - adverse effects Antipsychotics Basal Ganglia Diseases - chemically induced Basal Ganglia Diseases - genetics Basal Ganglia Diseases - metabolism Basal Ganglia Diseases - physiopathology Biomedical and Life Sciences Biomedicine Case-Control Studies Child Dopamine Dopamine - metabolism Dopamine D2 receptors Dopamine receptors Dosage and administration Drug therapy Extrapyramidal system Female Follow-Up Studies Gene Expression Genetic aspects Genetic Association Studies Genetic Predisposition to Disease GluK3 Kainate Receptor Glutamate Glutamic Acid - metabolism Haplotypes Human Genetics Humans Longitudinal Studies Male Oncology original-article Pharmacogenetics Pharmacogenomic Variants Pharmacotherapy Phenotype Polymorphism, Single Nucleotide Prospective Studies Psychopharmacology Psychosis Psychotic Disorders - diagnosis Psychotic Disorders - drug therapy Psychotic Disorders - physiopathology Psychotropic drugs Receptor, Serotonin, 5-HT2A - genetics Receptors, Dopamine D2 - genetics Receptors, Kainic Acid - genetics Risk Assessment Risk Factors Risperidone Serotonin Serotonin - metabolism Single nucleotide polymorphisms Single-nucleotide polymorphism Spain Statistical analysis Treatment Outcome Vesicular Monoamine Transport Proteins - genetics Young Adult Ziprasidone |
| title | Pharmacogenetic study of antipsychotic induced acute extrapyramidal symptoms in a first episode psychosis cohort: role of dopamine, serotonin and glutamate candidate genes |
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