Association of ABCB1 gene variants, plasma antidepressant concentration, and treatment response: Results from a randomized clinical study.
Identifieur interne : 000172 ( PubMed/Curation ); précédent : 000171; suivant : 000173Association of ABCB1 gene variants, plasma antidepressant concentration, and treatment response: Results from a randomized clinical study.
Auteurs : Barbara Breitenstein [Allemagne] ; Sandra Scheuer [Allemagne] ; Tanja Maria Brückl [Allemagne] ; Jobst Meyer [Allemagne] ; Marcus Ising [Allemagne] ; Manfred Uhr [Allemagne] ; Florian Holsboer [Allemagne]Source :
- Journal of psychiatric research [ 1879-1379 ] ; 2016.
English descriptors
- KwdEn :
- Adult, Alleles, Analysis of Variance, Antidepressive Agents (blood), Antidepressive Agents (therapeutic use), Chromatography, High Pressure Liquid, Depression (blood), Depression (drug therapy), Depression (genetics), Dose-Response Relationship, Drug, Double-Blind Method, Female, Follow-Up Studies, Genotype, Humans, Male, Middle Aged, P-Glycoproteins (genetics), Pharmacogenetics, Polymorphism, Single Nucleotide (genetics), Psychiatric Status Rating Scales, Tandem Mass Spectrometry, Time Factors, Treatment Outcome.
- MESH :
- chemical , blood : Antidepressive Agents.
- chemical , genetics : P-Glycoproteins.
- chemical , therapeutic use : Antidepressive Agents.
- blood : Depression.
- drug therapy : Depression.
- genetics : Depression, Polymorphism, Single Nucleotide.
- Adult, Alleles, Analysis of Variance, Chromatography, High Pressure Liquid, Dose-Response Relationship, Drug, Double-Blind Method, Female, Follow-Up Studies, Genotype, Humans, Male, Middle Aged, Pharmacogenetics, Psychiatric Status Rating Scales, Tandem Mass Spectrometry, Time Factors, Treatment Outcome.
Abstract
P-glycoprotein, encoded by the ABCB1 gene, functions as an ATP-driven efflux pump in the blood-brain barrier, extruding its substrates and thereby limiting their passage into the brain. ABCB1 polymorphisms predicted antidepressant drug response: Minor allele carriers of SNPs rs2032583 and rs2235015 had higher remission rates than major allele homozygotes. The aim of the current study was to evaluate an ABCB1 genotype-dependent efficacy of a quick dose escalation strategy. Depressed inpatients (n = 73) treated with antidepressants that are P-glycoprotein substrates were randomly assigned to a standard or high dose condition for 28 days. HAM-D scores, adverse effects and plasma antidepressant concentration were measured weekly and tested among two intronic SNPs rs2032583 and rs2235015. A treatment as usual control sample (n = 128) was retrospectively matched to the study group by gender, age, and diagnosis. There was a significant interaction of genotype x plasma antidepressant concentration: Minor allele carriers of rs2032583 [F(1,65) = 7.221, p = 0.009] and rs2235015 [F(1,65) = 4.939, p = 0.030] whose plasma drug concentration were within recommended range had a greater symptom reduction at study endpoint which exceeded the therapeutic benefit of the treatment as usual group [for rs2032583: F(1,163) = 4.366, p = 0.038]. Minor allele carriers of rs2032583 with high plasma drug levels had more sleep-related side effects than major allele homozygotes with high plasma drug levels. The treatment of MDD can be optimized by ABCB1 genotyping combined with monitoring of plasma drug concentrations: For minor allele carriers of rs2032583 and rs2235015, plasma antidepressant levels should not exceed the recommended range in order to obtain optimal treatment outcome.
DOI: 10.1016/j.jpsychires.2015.11.010
PubMed: 26704739
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Electronic address: barbara.breitenstein@hmnc.de.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>HMNC GmbH, Maximilianstr. 34, 80539 Munich, Germany; Max Planck Institute of Psychiatry, Kraepelinstr. 2 - 10, 80804 Munich, Germany; Department of Neurobehavioral Genetics, Institute of Psychobiology, University of Trier, Johanniterufer 15, 54290 Trier</wicri:regionArea></affiliation></author><author><name sortKey="Scheuer, Sandra" sort="Scheuer, Sandra" uniqKey="Scheuer S" first="Sandra" last="Scheuer">Sandra Scheuer</name><affiliation wicri:level="1"><nlm:affiliation>Max Planck Institute of Psychiatry, Kraepelinstr. 2 - 10, 80804 Munich, Germany. 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Electronic address: florian.holsboer@hmnc.de.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>HMNC GmbH, Maximilianstr. 34, 80539 Munich, Germany; Max Planck Institute of Psychiatry, Kraepelinstr. 2 - 10, 80804 Munich</wicri:regionArea></affiliation></author></analytic><series><title level="j">Journal of psychiatric research</title><idno type="eISSN">1879-1379</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Alleles</term><term>Analysis of Variance</term><term>Antidepressive Agents (blood)</term><term>Antidepressive Agents (therapeutic use)</term><term>Chromatography, High Pressure Liquid</term><term>Depression (blood)</term><term>Depression (drug therapy)</term><term>Depression (genetics)</term><term>Dose-Response Relationship, Drug</term><term>Double-Blind Method</term><term>Female</term><term>Follow-Up Studies</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>P-Glycoproteins (genetics)</term><term>Pharmacogenetics</term><term>Polymorphism, Single Nucleotide (genetics)</term><term>Psychiatric Status Rating Scales</term><term>Tandem Mass Spectrometry</term><term>Time Factors</term><term>Treatment Outcome</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Antidepressive Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>P-Glycoproteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antidepressive Agents</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Depression</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Depression</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Depression</term><term>Polymorphism, Single Nucleotide</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Alleles</term><term>Analysis of Variance</term><term>Chromatography, High Pressure Liquid</term><term>Dose-Response Relationship, Drug</term><term>Double-Blind Method</term><term>Female</term><term>Follow-Up Studies</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Pharmacogenetics</term><term>Psychiatric Status Rating Scales</term><term>Tandem Mass Spectrometry</term><term>Time Factors</term><term>Treatment Outcome</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">P-glycoprotein, encoded by the ABCB1 gene, functions as an ATP-driven efflux pump in the blood-brain barrier, extruding its substrates and thereby limiting their passage into the brain. ABCB1 polymorphisms predicted antidepressant drug response: Minor allele carriers of SNPs rs2032583 and rs2235015 had higher remission rates than major allele homozygotes. The aim of the current study was to evaluate an ABCB1 genotype-dependent efficacy of a quick dose escalation strategy. Depressed inpatients (n = 73) treated with antidepressants that are P-glycoprotein substrates were randomly assigned to a standard or high dose condition for 28 days. HAM-D scores, adverse effects and plasma antidepressant concentration were measured weekly and tested among two intronic SNPs rs2032583 and rs2235015. A treatment as usual control sample (n = 128) was retrospectively matched to the study group by gender, age, and diagnosis. There was a significant interaction of genotype x plasma antidepressant concentration: Minor allele carriers of rs2032583 [F(1,65) = 7.221, p = 0.009] and rs2235015 [F(1,65) = 4.939, p = 0.030] whose plasma drug concentration were within recommended range had a greater symptom reduction at study endpoint which exceeded the therapeutic benefit of the treatment as usual group [for rs2032583: F(1,163) = 4.366, p = 0.038]. Minor allele carriers of rs2032583 with high plasma drug levels had more sleep-related side effects than major allele homozygotes with high plasma drug levels. The treatment of MDD can be optimized by ABCB1 genotyping combined with monitoring of plasma drug concentrations: For minor allele carriers of rs2032583 and rs2235015, plasma antidepressant levels should not exceed the recommended range in order to obtain optimal treatment outcome.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26704739</PMID><DateCreated><Year>2016</Year><Month>02</Month><Day>02</Day></DateCreated><DateCompleted><Year>2016</Year><Month>10</Month><Day>20</Day></DateCompleted><DateRevised><Year>2016</Year><Month>12</Month><Day>30</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-1379</ISSN><JournalIssue CitedMedium="Internet"><Volume>73</Volume><PubDate><Year>2016</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Journal of psychiatric research</Title><ISOAbbreviation>J Psychiatr Res</ISOAbbreviation></Journal><ArticleTitle>Association of ABCB1 gene variants, plasma antidepressant concentration, and treatment response: Results from a randomized clinical study.</ArticleTitle><Pagination><MedlinePgn>86-95</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jpsychires.2015.11.010</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0022-3956(15)30010-8</ELocationID><Abstract><AbstractText>P-glycoprotein, encoded by the ABCB1 gene, functions as an ATP-driven efflux pump in the blood-brain barrier, extruding its substrates and thereby limiting their passage into the brain. ABCB1 polymorphisms predicted antidepressant drug response: Minor allele carriers of SNPs rs2032583 and rs2235015 had higher remission rates than major allele homozygotes. The aim of the current study was to evaluate an ABCB1 genotype-dependent efficacy of a quick dose escalation strategy. Depressed inpatients (n = 73) treated with antidepressants that are P-glycoprotein substrates were randomly assigned to a standard or high dose condition for 28 days. HAM-D scores, adverse effects and plasma antidepressant concentration were measured weekly and tested among two intronic SNPs rs2032583 and rs2235015. A treatment as usual control sample (n = 128) was retrospectively matched to the study group by gender, age, and diagnosis. There was a significant interaction of genotype x plasma antidepressant concentration: Minor allele carriers of rs2032583 [F(1,65) = 7.221, p = 0.009] and rs2235015 [F(1,65) = 4.939, p = 0.030] whose plasma drug concentration were within recommended range had a greater symptom reduction at study endpoint which exceeded the therapeutic benefit of the treatment as usual group [for rs2032583: F(1,163) = 4.366, p = 0.038]. Minor allele carriers of rs2032583 with high plasma drug levels had more sleep-related side effects than major allele homozygotes with high plasma drug levels. The treatment of MDD can be optimized by ABCB1 genotyping combined with monitoring of plasma drug concentrations: For minor allele carriers of rs2032583 and rs2235015, plasma antidepressant levels should not exceed the recommended range in order to obtain optimal treatment outcome.</AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Breitenstein</LastName><ForeName>Barbara</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>HMNC GmbH, Maximilianstr. 34, 80539 Munich, Germany; Max Planck Institute of Psychiatry, Kraepelinstr. 2 - 10, 80804 Munich, Germany; Department of Neurobehavioral Genetics, Institute of Psychobiology, University of Trier, Johanniterufer 15, 54290 Trier, Germany. Electronic address: barbara.breitenstein@hmnc.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Scheuer</LastName><ForeName>Sandra</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Max Planck Institute of Psychiatry, Kraepelinstr. 2 - 10, 80804 Munich, Germany. Electronic address: sandra_scheuer@psych.mpg.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brückl</LastName><ForeName>Tanja Maria</ForeName><Initials>TM</Initials><AffiliationInfo><Affiliation>Max Planck Institute of Psychiatry, Kraepelinstr. 2 - 10, 80804 Munich, Germany. Electronic address: brueckl@psych.mpg.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meyer</LastName><ForeName>Jobst</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Neurobehavioral Genetics, Institute of Psychobiology, University of Trier, Johanniterufer 15, 54290 Trier, Germany. Electronic address: meyerjo@uni-trier.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ising</LastName><ForeName>Marcus</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Max Planck Institute of Psychiatry, Kraepelinstr. 2 - 10, 80804 Munich, Germany. Electronic address: ising@psych.mpg.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Uhr</LastName><ForeName>Manfred</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Max Planck Institute of Psychiatry, Kraepelinstr. 2 - 10, 80804 Munich, Germany. Electronic address: uhr@psych.mpg.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Holsboer</LastName><ForeName>Florian</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>HMNC GmbH, Maximilianstr. 34, 80539 Munich, Germany; Max Planck Institute of Psychiatry, Kraepelinstr. 2 - 10, 80804 Munich, Germany. Electronic address: florian.holsboer@hmnc.de.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>11</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Psychiatr Res</MedlineTA><NlmUniqueID>0376331</NlmUniqueID><ISSNLinking>0022-3956</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C513055">ABCB1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000928">Antidepressive Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018435">P-Glycoproteins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000483" MajorTopicYN="N">Alleles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000704" MajorTopicYN="N">Analysis of Variance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000928" MajorTopicYN="N">Antidepressive Agents</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="Y">blood</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002851" MajorTopicYN="N">Chromatography, High Pressure Liquid</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003863" MajorTopicYN="Y">Depression</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004305" MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004311" MajorTopicYN="N">Double-Blind Method</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018435" MajorTopicYN="N">P-Glycoproteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010597" MajorTopicYN="N">Pharmacogenetics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020641" MajorTopicYN="N">Polymorphism, Single Nucleotide</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011569" MajorTopicYN="N">Psychiatric Status Rating Scales</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053719" MajorTopicYN="N">Tandem Mass Spectrometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ABCB1</Keyword><Keyword MajorTopicYN="N">Antidepressant treatment</Keyword><Keyword MajorTopicYN="N">MDR1</Keyword><Keyword MajorTopicYN="N">Major depressive disorder</Keyword><Keyword MajorTopicYN="N">P-glycoprotein</Keyword><Keyword MajorTopicYN="N">Side effects</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>07</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>11</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>11</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>12</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>12</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd \
| NlmPubMed2Wicri -a UnivTrevesV1
| This area was generated with Dilib version V0.6.31. |  |