Positive effects of methylphenidate on hyperactivity are moderated by monoaminergic gene variants in children with autism spectrum disorders
Methylphenidate (MPH) reduces hyperactive-impulsive symptoms common in children with autism spectrum disorders (ASDs), however, response and tolerability varies widely. We hypothesized monoaminergic gene variants may moderate MPH effects in ASD, as in typically developing children with attention-def...
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| Veröffentlicht in: | The pharmacogenomics journal 2014-06, Vol.14 (3), p.295-302 |
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| creator | McCracken, J T Badashova, K K Posey, D J Aman, M G Scahill, L Tierney, E Arnold, L E Vitiello, B Whelan, F Chuang, S Z Davies, M Shah, B McDougle, C J Nurmi, E L |
| description | Methylphenidate (MPH) reduces hyperactive-impulsive symptoms common in children with autism spectrum disorders (ASDs), however, response and tolerability varies widely. We hypothesized monoaminergic gene variants may moderate MPH effects in ASD, as in typically developing children with attention-deficit/hyperactivity disorder. Genotype data were available for 64 children with ASD and hyperactivity who were exposed to MPH during a 1-week safety/tolerability lead-in phase and 58 who went on to be randomized to placebo and three doses of MPH during a 4-week blinded, crossover study. Outcome measures included the Clinical Global Impression-Improvement (CGI-I) scale and the Aberrant Behavior Checklist (ABC-hyperactivity index). A total of 14 subjects discontinued the study because of MPH side effects. Subjects were genotyped for variants in
DRD1–DRD5
,
ADRA2A
,
SLC6A3
,
SLC6A4
,
MAOA
and
MAOB
, and
COMT
. Forty-nine percent of the sample met positive responder criteria. In this modest but relatively homogeneous sample, significant differences by
DRD1
(
P
=0.006),
ADRA2A
(
P |
| doi_str_mv | 10.1038/tpj.2013.23 |
| format | Article |
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DRD1–DRD5
,
ADRA2A
,
SLC6A3
,
SLC6A4
,
MAOA
and
MAOB
, and
COMT
. Forty-nine percent of the sample met positive responder criteria. In this modest but relatively homogeneous sample, significant differences by
DRD1
(
P
=0.006),
ADRA2A
(
P
<0.02),
COMT
(
P
<0.04),
DRD3
(
P
<0.05)
, DRD4
(
P
<0.05)
, SLC6A3
(
P
<0.05) and
SLC6A4
(
P
<0.05) genotypes were found for responders versus non-responders. Variants in
DRD2
(
P
<0.001) and
DRD3
(
P
<0.04) were associated with tolerability in the 14 subjects who discontinued the trial. For this first MPH pharmacogenetic study in children with ASD, multiple monoaminergic gene variants may help explain individual differences in MPH’s efficacy and tolerability.]]></description><identifier>ISSN: 1470-269X</identifier><identifier>ISSN: 1473-1150</identifier><identifier>EISSN: 1473-1150</identifier><identifier>DOI: 10.1038/tpj.2013.23</identifier><identifier>PMID: 23856854</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/154/436/108 ; 631/154/436/434 ; 631/208/726/649 ; 692/699/476/1312 ; Attention Deficit Disorder with Hyperactivity - complications ; Attention Deficit Disorder with Hyperactivity - drug therapy ; Attention Deficit Disorder with Hyperactivity - genetics ; Biogenic Monoamines - metabolism ; Biomedical and Life Sciences ; Biomedicine ; Care and treatment ; Central Nervous System Stimulants - therapeutic use ; Child ; Child Development Disorders, Pervasive - complications ; Child Development Disorders, Pervasive - genetics ; Dosage and administration ; Drug metabolism ; Gene Expression ; Genetic aspects ; Genetic variation ; Human Genetics ; Humans ; Identification and classification ; Methylphenidate ; Methylphenidate - therapeutic use ; Methylphenidate hydrochloride ; Oncology ; Original ; original-article ; Pervasive developmental disorders ; Pharmacotherapy ; Psychopharmacology</subject><ispartof>The pharmacogenomics journal, 2014-06, Vol.14 (3), p.295-302</ispartof><rights>The Author(s) 2014</rights><rights>COPYRIGHT 2014 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jun 2014</rights><rights>Copyright © 2014 Macmillan Publishers Limited 2014 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c546t-98e766e242521bc13e6e44472fffe5c55cdf5df4d1cb2cbfd1402e7c0a1f0f193</citedby><cites>FETCH-LOGICAL-c546t-98e766e242521bc13e6e44472fffe5c55cdf5df4d1cb2cbfd1402e7c0a1f0f193</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23856854$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McCracken, J T</creatorcontrib><creatorcontrib>Badashova, K K</creatorcontrib><creatorcontrib>Posey, D J</creatorcontrib><creatorcontrib>Aman, M G</creatorcontrib><creatorcontrib>Scahill, L</creatorcontrib><creatorcontrib>Tierney, E</creatorcontrib><creatorcontrib>Arnold, L E</creatorcontrib><creatorcontrib>Vitiello, B</creatorcontrib><creatorcontrib>Whelan, F</creatorcontrib><creatorcontrib>Chuang, S Z</creatorcontrib><creatorcontrib>Davies, M</creatorcontrib><creatorcontrib>Shah, B</creatorcontrib><creatorcontrib>McDougle, C J</creatorcontrib><creatorcontrib>Nurmi, E L</creatorcontrib><title>Positive effects of methylphenidate on hyperactivity are moderated by monoaminergic gene variants in children with autism spectrum disorders</title><title>The pharmacogenomics journal</title><addtitle>Pharmacogenomics J</addtitle><addtitle>Pharmacogenomics J</addtitle><description><![CDATA[Methylphenidate (MPH) reduces hyperactive-impulsive symptoms common in children with autism spectrum disorders (ASDs), however, response and tolerability varies widely. We hypothesized monoaminergic gene variants may moderate MPH effects in ASD, as in typically developing children with attention-deficit/hyperactivity disorder. Genotype data were available for 64 children with ASD and hyperactivity who were exposed to MPH during a 1-week safety/tolerability lead-in phase and 58 who went on to be randomized to placebo and three doses of MPH during a 4-week blinded, crossover study. Outcome measures included the Clinical Global Impression-Improvement (CGI-I) scale and the Aberrant Behavior Checklist (ABC-hyperactivity index). A total of 14 subjects discontinued the study because of MPH side effects. Subjects were genotyped for variants in
DRD1–DRD5
,
ADRA2A
,
SLC6A3
,
SLC6A4
,
MAOA
and
MAOB
, and
COMT
. Forty-nine percent of the sample met positive responder criteria. In this modest but relatively homogeneous sample, significant differences by
DRD1
(
P
=0.006),
ADRA2A
(
P
<0.02),
COMT
(
P
<0.04),
DRD3
(
P
<0.05)
, DRD4
(
P
<0.05)
, SLC6A3
(
P
<0.05) and
SLC6A4
(
P
<0.05) genotypes were found for responders versus non-responders. Variants in
DRD2
(
P
<0.001) and
DRD3
(
P
<0.04) were associated with tolerability in the 14 subjects who discontinued the trial. For this first MPH pharmacogenetic study in children with ASD, multiple monoaminergic gene variants may help explain individual differences in MPH’s efficacy and tolerability.]]></description><subject>631/154/436/108</subject><subject>631/154/436/434</subject><subject>631/208/726/649</subject><subject>692/699/476/1312</subject><subject>Attention Deficit Disorder with Hyperactivity - complications</subject><subject>Attention Deficit Disorder with Hyperactivity - drug therapy</subject><subject>Attention Deficit Disorder with Hyperactivity - genetics</subject><subject>Biogenic Monoamines - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Care and treatment</subject><subject>Central Nervous System Stimulants - therapeutic use</subject><subject>Child</subject><subject>Child Development Disorders, Pervasive - complications</subject><subject>Child Development Disorders, Pervasive - genetics</subject><subject>Dosage and administration</subject><subject>Drug metabolism</subject><subject>Gene Expression</subject><subject>Genetic aspects</subject><subject>Genetic variation</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Identification and classification</subject><subject>Methylphenidate</subject><subject>Methylphenidate - therapeutic use</subject><subject>Methylphenidate hydrochloride</subject><subject>Oncology</subject><subject>Original</subject><subject>original-article</subject><subject>Pervasive developmental disorders</subject><subject>Pharmacotherapy</subject><subject>Psychopharmacology</subject><issn>1470-269X</issn><issn>1473-1150</issn><issn>1473-1150</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkk2LFDEQhhtR3HX15F0CXgSdMV-d7r4Iy-IXLOhBwVvIJJXpDN1Jm6RH-j_4o80467ore5AcklQ99Sb1UlX1lOA1wax9nafdmmLC1pTdq04Jb9iKkBrf_33GKyq6byfVo5R2GBNBmvZhdUJZW4u25qfVz88huez2gMBa0DmhYNEIuV-GqQfvjMqAgkf9MkFUupAuL0hFQGMwJZLBoM1SLj6o0XmIW6fRFjygvYpO-SLoPNK9G0wEj3643CM1Z5dGlKbyXpxHZFwKsYilx9UDq4YET672s-rru7dfLj6sLj-9_3hxfrnSNRd51bXQCAGU05qSjSYMBHDOG2pLC7Wua21sbSw3RG-o3lhDOKbQaKyIxZZ07Kx6c9Sd5s0IRoPPUQ1yim5UcZFBOXk7410vt2EvOWa8eFsEXlwJxPB9hpTl6JKGYVAewpxkQXhLRCvof6C0ZawRNS_o83_QXZijL04cKNHhrqPdX2qrBpDO21C-qA-i8pw1uG0bwUmh1ndQZRkYnQ4erCvxWwUvjwU6hpQi2Gs7CJaHOZNlzuRhziRlhX5208Fr9s9gFeDVEUgl5bcQb_Ryh94vhqzgJg</recordid><startdate>20140601</startdate><enddate>20140601</enddate><creator>McCracken, J T</creator><creator>Badashova, K K</creator><creator>Posey, D J</creator><creator>Aman, M G</creator><creator>Scahill, L</creator><creator>Tierney, E</creator><creator>Arnold, L E</creator><creator>Vitiello, B</creator><creator>Whelan, F</creator><creator>Chuang, S Z</creator><creator>Davies, M</creator><creator>Shah, B</creator><creator>McDougle, C J</creator><creator>Nurmi, E L</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><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><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140601</creationdate><title>Positive effects of methylphenidate on hyperactivity are moderated by monoaminergic gene variants in children with autism spectrum disorders</title><author>McCracken, J T ; Badashova, K K ; Posey, D J ; Aman, M G ; Scahill, L ; Tierney, E ; Arnold, L E ; Vitiello, B ; Whelan, F ; Chuang, S Z ; Davies, M ; Shah, B ; McDougle, C J ; Nurmi, E L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c546t-98e766e242521bc13e6e44472fffe5c55cdf5df4d1cb2cbfd1402e7c0a1f0f193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>631/154/436/108</topic><topic>631/154/436/434</topic><topic>631/208/726/649</topic><topic>692/699/476/1312</topic><topic>Attention Deficit Disorder with Hyperactivity - complications</topic><topic>Attention Deficit Disorder with Hyperactivity - drug therapy</topic><topic>Attention Deficit Disorder with Hyperactivity - genetics</topic><topic>Biogenic Monoamines - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Care and treatment</topic><topic>Central Nervous System Stimulants - therapeutic use</topic><topic>Child</topic><topic>Child Development Disorders, Pervasive - complications</topic><topic>Child Development Disorders, Pervasive - genetics</topic><topic>Dosage and administration</topic><topic>Drug metabolism</topic><topic>Gene Expression</topic><topic>Genetic aspects</topic><topic>Genetic variation</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Identification and classification</topic><topic>Methylphenidate</topic><topic>Methylphenidate - therapeutic use</topic><topic>Methylphenidate hydrochloride</topic><topic>Oncology</topic><topic>Original</topic><topic>original-article</topic><topic>Pervasive developmental disorders</topic><topic>Pharmacotherapy</topic><topic>Psychopharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McCracken, J T</creatorcontrib><creatorcontrib>Badashova, K K</creatorcontrib><creatorcontrib>Posey, D J</creatorcontrib><creatorcontrib>Aman, M G</creatorcontrib><creatorcontrib>Scahill, L</creatorcontrib><creatorcontrib>Tierney, E</creatorcontrib><creatorcontrib>Arnold, L E</creatorcontrib><creatorcontrib>Vitiello, B</creatorcontrib><creatorcontrib>Whelan, F</creatorcontrib><creatorcontrib>Chuang, S Z</creatorcontrib><creatorcontrib>Davies, M</creatorcontrib><creatorcontrib>Shah, B</creatorcontrib><creatorcontrib>McDougle, C J</creatorcontrib><creatorcontrib>Nurmi, E L</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><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><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The pharmacogenomics journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McCracken, J T</au><au>Badashova, K K</au><au>Posey, D J</au><au>Aman, M G</au><au>Scahill, L</au><au>Tierney, E</au><au>Arnold, L E</au><au>Vitiello, B</au><au>Whelan, F</au><au>Chuang, S Z</au><au>Davies, M</au><au>Shah, B</au><au>McDougle, C J</au><au>Nurmi, E L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Positive effects of methylphenidate on hyperactivity are moderated by monoaminergic gene variants in children with autism spectrum disorders</atitle><jtitle>The pharmacogenomics journal</jtitle><stitle>Pharmacogenomics J</stitle><addtitle>Pharmacogenomics J</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>14</volume><issue>3</issue><spage>295</spage><epage>302</epage><pages>295-302</pages><issn>1470-269X</issn><issn>1473-1150</issn><eissn>1473-1150</eissn><abstract><![CDATA[Methylphenidate (MPH) reduces hyperactive-impulsive symptoms common in children with autism spectrum disorders (ASDs), however, response and tolerability varies widely. We hypothesized monoaminergic gene variants may moderate MPH effects in ASD, as in typically developing children with attention-deficit/hyperactivity disorder. Genotype data were available for 64 children with ASD and hyperactivity who were exposed to MPH during a 1-week safety/tolerability lead-in phase and 58 who went on to be randomized to placebo and three doses of MPH during a 4-week blinded, crossover study. Outcome measures included the Clinical Global Impression-Improvement (CGI-I) scale and the Aberrant Behavior Checklist (ABC-hyperactivity index). A total of 14 subjects discontinued the study because of MPH side effects. Subjects were genotyped for variants in
DRD1–DRD5
,
ADRA2A
,
SLC6A3
,
SLC6A4
,
MAOA
and
MAOB
, and
COMT
. Forty-nine percent of the sample met positive responder criteria. In this modest but relatively homogeneous sample, significant differences by
DRD1
(
P
=0.006),
ADRA2A
(
P
<0.02),
COMT
(
P
<0.04),
DRD3
(
P
<0.05)
, DRD4
(
P
<0.05)
, SLC6A3
(
P
<0.05) and
SLC6A4
(
P
<0.05) genotypes were found for responders versus non-responders. Variants in
DRD2
(
P
<0.001) and
DRD3
(
P
<0.04) were associated with tolerability in the 14 subjects who discontinued the trial. For this first MPH pharmacogenetic study in children with ASD, multiple monoaminergic gene variants may help explain individual differences in MPH’s efficacy and tolerability.]]></abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>23856854</pmid><doi>10.1038/tpj.2013.23</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1470-269X |
| ispartof | The pharmacogenomics journal, 2014-06, Vol.14 (3), p.295-302 |
| issn | 1470-269X 1473-1150 1473-1150 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4034115 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | 631/154/436/108 631/154/436/434 631/208/726/649 692/699/476/1312 Attention Deficit Disorder with Hyperactivity - complications Attention Deficit Disorder with Hyperactivity - drug therapy Attention Deficit Disorder with Hyperactivity - genetics Biogenic Monoamines - metabolism Biomedical and Life Sciences Biomedicine Care and treatment Central Nervous System Stimulants - therapeutic use Child Child Development Disorders, Pervasive - complications Child Development Disorders, Pervasive - genetics Dosage and administration Drug metabolism Gene Expression Genetic aspects Genetic variation Human Genetics Humans Identification and classification Methylphenidate Methylphenidate - therapeutic use Methylphenidate hydrochloride Oncology Original original-article Pervasive developmental disorders Pharmacotherapy Psychopharmacology |
| title | Positive effects of methylphenidate on hyperactivity are moderated by monoaminergic gene variants in children with autism spectrum disorders |
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