Serotonin Receptor 2A Gene Polymorphism (–1438A/G) and Short-Term Treatment Response to Citalopram
The 5-HTR2A gene is a candidate gene for influencing the clinical response to antidepressant treatment. The purpose of this study was to determine the relationship between the –1438A/G polymorphism in the 5-HTR2A gene and the response to citalopram in a Korean population with major depressive disord...
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| Veröffentlicht in: | Neuropsychobiology 2005-01, Vol.52 (3), p.155-162 |
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| creator | Choi, Myoung-Jin Kang, Rhee-Hun Ham, Byung-Joo Jeong, Han-Yong Lee, Min-Soo |
| description | The 5-HTR2A gene is a candidate gene for influencing the clinical response to antidepressant treatment. The purpose of this study was to determine the relationship between the –1438A/G polymorphism in the 5-HTR2A gene and the response to citalopram in a Korean population with major depressive disorder (MDD). Citalopram was administered for 4 weeks to the 71 patients who completed this study. We found significant differences in genotype, allele, and carrier distribution between the normal group and MDD patients (genotypes: χ 2 = 6.473, d.f. = 2, p = 0.039; alleles: χ 2 = 5.589, d.f. = 1, p = 0.018; OR = 0.618, 95% CI = 0.414–0.922; allele carriers: χ 2 = 5.383, d.f. = 1, p = 0.020; OR = 0.473, 95% CI = 0.249–0.879). The frequency of the –1438G allele was much higher in MDD patients than in the normal group (allele carriers: χ 2 = 5.383, d.f. = 1, p = 0.020; OR = 0.473, 95% CI = 0.249–0.879). There were also significant differences in response to citalopram according to the –1438A/G variation of 5-HTR2A in MDD patients. The group of remitters carried a higher frequency of the GG allele than of the AA and AG alleles. More of nonremitters carried the A allele than were without it (genotype: χ 2 = 8.016, p = 0.018; allele carrier: χ 2 = 4.512, p = 0.034; OR = 0.324, 95% CI = 0.112–0.936). The response to citalopram differed with the –1438A/G polymorphism genotype and allele carriers. The –1438G/–1438G genotype appeared to be associated with a better response to citalopram, with especially the G allele being related to core depressive symptoms and psychic anxiety improvement (p |
| doi_str_mv | 10.1159/000087847 |
| format | Article |
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The purpose of this study was to determine the relationship between the –1438A/G polymorphism in the 5-HTR2A gene and the response to citalopram in a Korean population with major depressive disorder (MDD). Citalopram was administered for 4 weeks to the 71 patients who completed this study. We found significant differences in genotype, allele, and carrier distribution between the normal group and MDD patients (genotypes: χ 2 = 6.473, d.f. = 2, p = 0.039; alleles: χ 2 = 5.589, d.f. = 1, p = 0.018; OR = 0.618, 95% CI = 0.414–0.922; allele carriers: χ 2 = 5.383, d.f. = 1, p = 0.020; OR = 0.473, 95% CI = 0.249–0.879). The frequency of the –1438G allele was much higher in MDD patients than in the normal group (allele carriers: χ 2 = 5.383, d.f. = 1, p = 0.020; OR = 0.473, 95% CI = 0.249–0.879). There were also significant differences in response to citalopram according to the –1438A/G variation of 5-HTR2A in MDD patients. The group of remitters carried a higher frequency of the GG allele than of the AA and AG alleles. More of nonremitters carried the A allele than were without it (genotype: χ 2 = 8.016, p = 0.018; allele carrier: χ 2 = 4.512, p = 0.034; OR = 0.324, 95% CI = 0.112–0.936). The response to citalopram differed with the –1438A/G polymorphism genotype and allele carriers. The –1438G/–1438G genotype appeared to be associated with a better response to citalopram, with especially the G allele being related to core depressive symptoms and psychic anxiety improvement (p<0.05). These results suggest that the G allele of the –1438A/G polymorphism in the 5-HTR2A gene is associated with MDD, and that patients with –1438G/–1438G have a better response to citalopram treatment than patients with –1438A/–1438A or –1438A/–1438G.</description><identifier>ISSN: 0302-282X</identifier><identifier>EISSN: 1423-0224</identifier><identifier>DOI: 10.1159/000087847</identifier><identifier>PMID: 16127283</identifier><identifier>CODEN: NPBYAL</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Adult and adolescent clinical studies ; Alleles ; Antidepressive Agents - therapeutic use ; Biological and medical sciences ; Citalopram - therapeutic use ; Depression ; Depressive Disorder, Major - drug therapy ; Depressive Disorder, Major - genetics ; Depressive Disorder, Major - psychology ; DNA - genetics ; Female ; Heterozygote ; Humans ; Korea ; Male ; Medical sciences ; Middle Aged ; Mood disorders ; Neuropharmacology ; Original Paper ; Pharmacology. Drug treatments ; Polymorphism, Genetic - genetics ; Psychiatric Status Rating Scales ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Psychopharmacology ; Receptor, Serotonin, 5-HT2A - genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Serotonin Uptake Inhibitors - therapeutic use</subject><ispartof>Neuropsychobiology, 2005-01, Vol.52 (3), p.155-162</ispartof><rights>2005 S. Karger AG, Basel</rights><rights>2005 INIST-CNRS</rights><rights>Copyright (c) 2005 S. Karger AG, Basel.</rights><rights>Copyright (c) 2005 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-21ff5e6fb95ef06a037eac03b60b9d35dd93aacfe8c61b10d1fc398caa10b4153</citedby><cites>FETCH-LOGICAL-c391t-21ff5e6fb95ef06a037eac03b60b9d35dd93aacfe8c61b10d1fc398caa10b4153</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2423,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17097869$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16127283$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Choi, Myoung-Jin</creatorcontrib><creatorcontrib>Kang, Rhee-Hun</creatorcontrib><creatorcontrib>Ham, Byung-Joo</creatorcontrib><creatorcontrib>Jeong, Han-Yong</creatorcontrib><creatorcontrib>Lee, Min-Soo</creatorcontrib><title>Serotonin Receptor 2A Gene Polymorphism (–1438A/G) and Short-Term Treatment Response to Citalopram</title><title>Neuropsychobiology</title><addtitle>Neuropsychobiology</addtitle><description>The 5-HTR2A gene is a candidate gene for influencing the clinical response to antidepressant treatment. The purpose of this study was to determine the relationship between the –1438A/G polymorphism in the 5-HTR2A gene and the response to citalopram in a Korean population with major depressive disorder (MDD). Citalopram was administered for 4 weeks to the 71 patients who completed this study. We found significant differences in genotype, allele, and carrier distribution between the normal group and MDD patients (genotypes: χ 2 = 6.473, d.f. = 2, p = 0.039; alleles: χ 2 = 5.589, d.f. = 1, p = 0.018; OR = 0.618, 95% CI = 0.414–0.922; allele carriers: χ 2 = 5.383, d.f. = 1, p = 0.020; OR = 0.473, 95% CI = 0.249–0.879). The frequency of the –1438G allele was much higher in MDD patients than in the normal group (allele carriers: χ 2 = 5.383, d.f. = 1, p = 0.020; OR = 0.473, 95% CI = 0.249–0.879). There were also significant differences in response to citalopram according to the –1438A/G variation of 5-HTR2A in MDD patients. The group of remitters carried a higher frequency of the GG allele than of the AA and AG alleles. More of nonremitters carried the A allele than were without it (genotype: χ 2 = 8.016, p = 0.018; allele carrier: χ 2 = 4.512, p = 0.034; OR = 0.324, 95% CI = 0.112–0.936). The response to citalopram differed with the –1438A/G polymorphism genotype and allele carriers. The –1438G/–1438G genotype appeared to be associated with a better response to citalopram, with especially the G allele being related to core depressive symptoms and psychic anxiety improvement (p<0.05). These results suggest that the G allele of the –1438A/G polymorphism in the 5-HTR2A gene is associated with MDD, and that patients with –1438G/–1438G have a better response to citalopram treatment than patients with –1438A/–1438A or –1438A/–1438G.</description><subject>Adult and adolescent clinical studies</subject><subject>Alleles</subject><subject>Antidepressive Agents - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Citalopram - therapeutic use</subject><subject>Depression</subject><subject>Depressive Disorder, Major - drug therapy</subject><subject>Depressive Disorder, Major - genetics</subject><subject>Depressive Disorder, Major - psychology</subject><subject>DNA - genetics</subject><subject>Female</subject><subject>Heterozygote</subject><subject>Humans</subject><subject>Korea</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mood disorders</subject><subject>Neuropharmacology</subject><subject>Original Paper</subject><subject>Pharmacology. 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Psychiatry</subject><subject>Psychopharmacology</subject><subject>Receptor, Serotonin, 5-HT2A - genetics</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Serotonin Uptake Inhibitors - therapeutic use</subject><issn>0302-282X</issn><issn>1423-0224</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqF0U9LHDEYBvAgLbq1HnoulCAoepiaPzOT5LgsdRWElroFb0Mm86aOnUnGJHvw1u_gN-wnMbKLQi_mkssvz5uXB6FPlHyltFJnJB8pZCl20IyWjBeEsfIdmhFOWMEku9lDH2K8I4SWSqhdtEdrygSTfIa6awg-edc7_BMMTMkHzOZ4CQ7wDz88jD5Mt30c8cm_v4-05HJ-tjzF2nX4-taHVKwgjHgVQKcRXMoZcfIuAk4eL_qkBz8FPX5E760eIhxs73306_zbanFRXH1fXi7mV4XhiqaCUWsrqG2rKrCk1oQL0Ibwtiat6njVdYprbSxIU9OWko7a_FAarSlpS1rxfXS8yZ2Cv19DTM3YRwPDoB34dWxqWSmqavImZESxkiiR4eF_8M6vg8tLNIzzshJCPo893SATfIwBbDOFftThoaGkeS6oeSko2y_bwHU7Qvcqt41kcLQFOho92KCd6eOrE_lbslbZfd64Pzr8hvACNmOeAIWun-s</recordid><startdate>20050101</startdate><enddate>20050101</enddate><creator>Choi, Myoung-Jin</creator><creator>Kang, Rhee-Hun</creator><creator>Ham, Byung-Joo</creator><creator>Jeong, Han-Yong</creator><creator>Lee, Min-Soo</creator><general>Karger</general><general>S. 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Drug treatments</topic><topic>Polymorphism, Genetic - genetics</topic><topic>Psychiatric Status Rating Scales</topic><topic>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Psychopharmacology</topic><topic>Receptor, Serotonin, 5-HT2A - genetics</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Serotonin Uptake Inhibitors - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Choi, Myoung-Jin</creatorcontrib><creatorcontrib>Kang, Rhee-Hun</creatorcontrib><creatorcontrib>Ham, Byung-Joo</creatorcontrib><creatorcontrib>Jeong, Han-Yong</creatorcontrib><creatorcontrib>Lee, Min-Soo</creatorcontrib><collection>Pascal-Francis</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>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</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>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>ProQuest Psychology</collection><collection>Science Database</collection><collection>Biological Science Database</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>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuropsychobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Choi, Myoung-Jin</au><au>Kang, Rhee-Hun</au><au>Ham, Byung-Joo</au><au>Jeong, Han-Yong</au><au>Lee, Min-Soo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Serotonin Receptor 2A Gene Polymorphism (–1438A/G) and Short-Term Treatment Response to Citalopram</atitle><jtitle>Neuropsychobiology</jtitle><addtitle>Neuropsychobiology</addtitle><date>2005-01-01</date><risdate>2005</risdate><volume>52</volume><issue>3</issue><spage>155</spage><epage>162</epage><pages>155-162</pages><issn>0302-282X</issn><eissn>1423-0224</eissn><coden>NPBYAL</coden><abstract>The 5-HTR2A gene is a candidate gene for influencing the clinical response to antidepressant treatment. The purpose of this study was to determine the relationship between the –1438A/G polymorphism in the 5-HTR2A gene and the response to citalopram in a Korean population with major depressive disorder (MDD). Citalopram was administered for 4 weeks to the 71 patients who completed this study. We found significant differences in genotype, allele, and carrier distribution between the normal group and MDD patients (genotypes: χ 2 = 6.473, d.f. = 2, p = 0.039; alleles: χ 2 = 5.589, d.f. = 1, p = 0.018; OR = 0.618, 95% CI = 0.414–0.922; allele carriers: χ 2 = 5.383, d.f. = 1, p = 0.020; OR = 0.473, 95% CI = 0.249–0.879). The frequency of the –1438G allele was much higher in MDD patients than in the normal group (allele carriers: χ 2 = 5.383, d.f. = 1, p = 0.020; OR = 0.473, 95% CI = 0.249–0.879). There were also significant differences in response to citalopram according to the –1438A/G variation of 5-HTR2A in MDD patients. The group of remitters carried a higher frequency of the GG allele than of the AA and AG alleles. More of nonremitters carried the A allele than were without it (genotype: χ 2 = 8.016, p = 0.018; allele carrier: χ 2 = 4.512, p = 0.034; OR = 0.324, 95% CI = 0.112–0.936). The response to citalopram differed with the –1438A/G polymorphism genotype and allele carriers. The –1438G/–1438G genotype appeared to be associated with a better response to citalopram, with especially the G allele being related to core depressive symptoms and psychic anxiety improvement (p<0.05). These results suggest that the G allele of the –1438A/G polymorphism in the 5-HTR2A gene is associated with MDD, and that patients with –1438G/–1438G have a better response to citalopram treatment than patients with –1438A/–1438A or –1438A/–1438G.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>16127283</pmid><doi>10.1159/000087847</doi><tpages>8</tpages></addata></record> |
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| ispartof | Neuropsychobiology, 2005-01, Vol.52 (3), p.155-162 |
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| subjects | Adult and adolescent clinical studies Alleles Antidepressive Agents - therapeutic use Biological and medical sciences Citalopram - therapeutic use Depression Depressive Disorder, Major - drug therapy Depressive Disorder, Major - genetics Depressive Disorder, Major - psychology DNA - genetics Female Heterozygote Humans Korea Male Medical sciences Middle Aged Mood disorders Neuropharmacology Original Paper Pharmacology. Drug treatments Polymorphism, Genetic - genetics Psychiatric Status Rating Scales Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychopharmacology Receptor, Serotonin, 5-HT2A - genetics Reverse Transcriptase Polymerase Chain Reaction Serotonin Uptake Inhibitors - therapeutic use |
| title | Serotonin Receptor 2A Gene Polymorphism (–1438A/G) and Short-Term Treatment Response to Citalopram |
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