The common exon 3 polymorphism of the growth hormone receptor gene and the effect of growth hormone therapy on growth in Korean patients with Turner syndrome
Identifieur interne : 001E69 ( Istex/Corpus ); précédent : 001E68; suivant : 001E70The common exon 3 polymorphism of the growth hormone receptor gene and the effect of growth hormone therapy on growth in Korean patients with Turner syndrome
Auteurs : Jung Min Ko ; Jae-Min Kim ; Chong-Kun Cheon ; Duk-Hee Kim ; Dae-Yeol Lee ; Woo Yeong Cheong ; Eun Young Kim ; Mi Jung Park ; Han-Wook YooSource :
- Clinical Endocrinology [ 0300-0664 ] ; 2010-02.
Abstract
Objective Recombinant human growth hormone (GH) can achieve final adult height gain in girls with Turner syndrome (TS), but its efficacy varies widely across individuals. The exon 3‐deleted polymorphism of growth hormone receptor (d3‐GHR) has been reported to be associated with responsiveness to GH therapy. The short‐term growth response of Turner patients to GH therapy was analysed according to their GHR‐exon 3 polymorphism genotype.
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DOI: 10.1111/j.1365-2265.2009.03681.x
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Cheon</name><affiliation><mods:affiliation>Department of Pediatrics, Pusan National University School of Medicine, Pusan</mods:affiliation></affiliation></author><author><name sortKey="Kim, Duk Ee" sort="Kim, Duk Ee" uniqKey="Kim D" first="Duk-Hee" last="Kim">Duk-Hee Kim</name><affiliation><mods:affiliation>Department of Pediatrics, Yonsei University College of Medicine, Seoul</mods:affiliation></affiliation></author><author><name sortKey="Lee, Dae Eol" sort="Lee, Dae Eol" uniqKey="Lee D" first="Dae-Yeol" last="Lee">Dae-Yeol Lee</name><affiliation><mods:affiliation>Department of Pediatrics, School of Medicine, Chonbuk National University, Jeonju</mods:affiliation></affiliation></author><author><name sortKey="Cheong, Woo Yeong" sort="Cheong, Woo Yeong" uniqKey="Cheong W" first="Woo Yeong" last="Cheong">Woo Yeong Cheong</name><affiliation><mods:affiliation>Department of Pediatrics, Pusan Paik Hospital, College of Medicine, Inje University, Busan</mods:affiliation></affiliation></author><author><name sortKey="Kim, Eun Young" sort="Kim, Eun Young" uniqKey="Kim E" first="Eun Young" last="Kim">Eun Young Kim</name><affiliation><mods:affiliation>Department of Pediatrics, Kwangju Christian Hospital, Gwangju</mods:affiliation></affiliation></author><author><name sortKey="Park, Mi Jung" sort="Park, Mi Jung" uniqKey="Park M" first="Mi Jung" last="Park">Mi Jung Park</name><affiliation><mods:affiliation>Department of Pediatrics, Inje University Colledge of Medicine, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Yoo, Han Ook" sort="Yoo, Han Ook" uniqKey="Yoo H" first="Han-Wook" last="Yoo">Han-Wook Yoo</name><affiliation><mods:affiliation>Genome Research Center for Birth Defects and Genetic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno 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sort="Kim, Jae In" uniqKey="Kim J" first="Jae-Min" last="Kim">Jae-Min Kim</name><affiliation><mods:affiliation>Genome Research Center for Birth Defects and Genetic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul</mods:affiliation></affiliation></author><author><name sortKey="Cheon, Chong Un" sort="Cheon, Chong Un" uniqKey="Cheon C" first="Chong-Kun" last="Cheon">Chong-Kun Cheon</name><affiliation><mods:affiliation>Department of Pediatrics, Pusan National University School of Medicine, Pusan</mods:affiliation></affiliation></author><author><name sortKey="Kim, Duk Ee" sort="Kim, Duk Ee" uniqKey="Kim D" first="Duk-Hee" last="Kim">Duk-Hee Kim</name><affiliation><mods:affiliation>Department of Pediatrics, Yonsei University College of Medicine, Seoul</mods:affiliation></affiliation></author><author><name sortKey="Lee, Dae Eol" sort="Lee, Dae Eol" uniqKey="Lee D" first="Dae-Yeol" last="Lee">Dae-Yeol Lee</name><affiliation><mods:affiliation>Department of Pediatrics, School of Medicine, Chonbuk National University, Jeonju</mods:affiliation></affiliation></author><author><name sortKey="Cheong, Woo Yeong" sort="Cheong, Woo Yeong" uniqKey="Cheong W" first="Woo Yeong" last="Cheong">Woo Yeong Cheong</name><affiliation><mods:affiliation>Department of Pediatrics, Pusan Paik Hospital, College of Medicine, Inje University, Busan</mods:affiliation></affiliation></author><author><name sortKey="Kim, Eun Young" sort="Kim, Eun Young" uniqKey="Kim E" first="Eun Young" last="Kim">Eun Young Kim</name><affiliation><mods:affiliation>Department of Pediatrics, Kwangju Christian Hospital, Gwangju</mods:affiliation></affiliation></author><author><name sortKey="Park, Mi Jung" sort="Park, Mi Jung" uniqKey="Park M" first="Mi Jung" last="Park">Mi Jung Park</name><affiliation><mods:affiliation>Department of Pediatrics, Inje University Colledge of Medicine, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Yoo, Han Ook" sort="Yoo, Han Ook" uniqKey="Yoo H" first="Han-Wook" last="Yoo">Han-Wook Yoo</name><affiliation><mods:affiliation>Genome Research Center for Birth Defects and Genetic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Clinical Endocrinology</title><title level="j" type="alt">CLINICAL ENDOCRINOLOGY</title><idno type="ISSN">0300-0664</idno><idno type="eISSN">1365-2265</idno><imprint><biblScope unit="vol">72</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="196">196</biblScope><biblScope unit="page" to="202">202</biblScope><biblScope unit="page-count">7</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2010-02">2010-02</date></imprint><idno type="ISSN">0300-0664</idno></series></biblStruct></sourceDesc><seriesStmt><idno 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The exon 3‐deleted polymorphism of growth hormone receptor (d3‐GHR) has been reported to be associated with responsiveness to GH therapy. The short‐term growth response of Turner patients to GH therapy was analysed according to their GHR‐exon 3 polymorphism genotype.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>genotype</json:string><json:string>endocrinology</json:string><json:string>polymorphism</json:string><json:string>clinical endocrinology</json:string><json:string>receptor</json:string><json:string>exon</json:string><json:string>growth response</json:string><json:string>chromosome</json:string><json:string>growth hormone</json:string><json:string>turner syndrome</json:string><json:string>karyotype</json:string><json:string>allele</json:string><json:string>pediatrics</json:string><json:string>blackwell publishing</json:string><json:string>short children</json:string><json:string>genotype frequency</json:string><json:string>growth hormone receptor</json:string><json:string>genotype groups</json:string><json:string>short 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Cheon</name><affiliations><json:string>Department of Pediatrics, Pusan National University School of Medicine, Pusan</json:string></affiliations></json:item><json:item><name>Duk‐Hee Kim</name><affiliations><json:string>Department of Pediatrics, Yonsei University College of Medicine, Seoul</json:string></affiliations></json:item><json:item><name>Dae‐Yeol Lee</name><affiliations><json:string>Department of Pediatrics, School of Medicine, Chonbuk National University, Jeonju</json:string></affiliations></json:item><json:item><name>Woo Yeong Cheong</name><affiliations><json:string>Department of Pediatrics, Pusan Paik Hospital, College of Medicine, Inje University, Busan</json:string></affiliations></json:item><json:item><name>Eun Young Kim</name><affiliations><json:string>Department of Pediatrics, Kwangju Christian Hospital, Gwangju</json:string></affiliations></json:item><json:item><name>Mi Jung Park</name><affiliations><json:string>Department of Pediatrics, Inje University Colledge of Medicine, Seoul, Korea</json:string></affiliations></json:item><json:item><name>Han‐Wook Yoo</name><affiliations><json:string>Genome Research Center for Birth Defects and Genetic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul</json:string></affiliations></json:item></author><articleId><json:string>CEN3681</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><qualityIndicators><score>5.757</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>439</abstractCharCount><pdfWordCount>4989</pdfWordCount><pdfCharCount>32045</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>64</abstractWordCount></qualityIndicators><title>The common exon 3 polymorphism of the growth hormone receptor gene and the effect of growth hormone therapy on growth in Korean patients with Turner 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syndrome</title></titleStmt><publicationStmt><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><licence>© 2010 Blackwell Publishing Ltd</licence></availability><date type="published" when="2010-02"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">The common exon 3 polymorphism of the growth hormone receptor gene and the effect of growth hormone therapy on growth in Korean patients with Turner syndrome</title><title level="a" type="short">GHR‐exon 3 polymorphism and growth hormone response</title><author xml:id="author-0000"><persName><forename type="first">Jung Min</forename><surname>Ko</surname></persName><affiliation>Departments of Medical Genetics, Ajou Medical Center, University of Ajou College of Medicine, Suwon</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Jae‐Min</forename><surname>Kim</surname></persName><affiliation>Genome Research Center for Birth Defects and Genetic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Chong‐Kun</forename><surname>Cheon</surname></persName><affiliation>Department of Pediatrics, Pusan National University School of Medicine, Pusan</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Duk‐Hee</forename><surname>Kim</surname></persName><affiliation>Department of Pediatrics, Yonsei University College of Medicine, Seoul</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Dae‐Yeol</forename><surname>Lee</surname></persName><affiliation>Department of Pediatrics, School of Medicine, Chonbuk National University, Jeonju</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Woo Yeong</forename><surname>Cheong</surname></persName><affiliation>Department of Pediatrics, Pusan Paik Hospital, College of Medicine, Inje University, Busan</affiliation></author><author xml:id="author-0006"><persName><forename type="first">Eun Young</forename><surname>Kim</surname></persName><affiliation>Department of Pediatrics, Kwangju Christian Hospital, Gwangju</affiliation></author><author xml:id="author-0007"><persName><forename type="first">Mi Jung</forename><surname>Park</surname></persName><affiliation>Department of Pediatrics, Inje University Colledge of Medicine, Seoul, Korea<address><country key="KR"></country></address></affiliation></author><author xml:id="author-0008"><persName><forename type="first">Han‐Wook</forename><surname>Yoo</surname></persName><affiliation>Genome Research Center for Birth Defects and Genetic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul</affiliation></author><idno type="istex">43003FCA458F52999433FD528968524207AA139D</idno><idno type="DOI">10.1111/j.1365-2265.2009.03681.x</idno><idno type="unit">CEN3681</idno><idno type="toTypesetVersion">file:CEN.CEN3681.pdf</idno></analytic><monogr><title level="j" type="main">Clinical Endocrinology</title><title level="j" type="alt">CLINICAL ENDOCRINOLOGY</title><idno type="pISSN">0300-0664</idno><idno type="eISSN">1365-2265</idno><idno type="book-DOI">10.1111/(ISSN)1365-2265</idno><idno type="book-part-DOI">10.1111/cen.2010.72.issue-2</idno><idno type="product">CEN</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">72</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="196">196</biblScope><biblScope unit="page" to="202">202</biblScope><biblScope unit="page-count">7</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2010-02"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><head>Summary</head><p><hi rend="bold">Objective </hi> Recombinant human growth hormone (GH) can achieve final adult height gain in girls with Turner syndrome (TS), but its efficacy varies widely across individuals. The exon 3‐deleted polymorphism of growth hormone receptor (<hi rend="italic">d3</hi>‐GHR) has been reported to be associated with responsiveness to GH therapy. The short‐term growth response of Turner patients to GH therapy was analysed according to their <hi rend="italic">GHR</hi>‐exon 3 polymorphism genotype.</p><p><hi rend="bold">Design and patients </hi> This was a retrospective study of 175 TS patients. Auxological and endocrine parameters were measured, and the <hi rend="italic">GHR</hi>‐exon 3 genotype was analysed. Allelic frequencies of <hi rend="italic">GHR</hi>‐exon 3 genotype were compared between patients with TS and control individuals. GH had been administered to 147 patients, 115 of which remained pre‐pubertal after the first follow‐up year. Changes in height standard deviation score (SDS), height velocity (HV), body mass index (BMI), IGF‐1 and IGF binding protein‐3 (IGFBP‐3) concentrations were compared between these patients, grouped according to genotype, after the first follow‐up year.</p><p><hi rend="bold">Results </hi> There was no difference in <hi rend="italic">GHR</hi>‐exon 3 genotype frequency between the TS and control groups of Koreans. According to the <hi rend="italic">GHR</hi>‐exon 3 genotype (<hi rend="italic">fl</hi>/<hi rend="italic">fl</hi> group <hi rend="italic">vs</hi>. <hi rend="italic">d3/fl</hi> and <hi rend="italic">d3/d3</hi> group), HV gain and height SDS gain did not differ significantly at the first year of GH therapy. Moreover, changes in IGF‐1, IGFBP‐3 concentration and BMI showed no significant difference between the groups with and without <hi rend="italic">d3</hi>‐GHR after 1 year of GH therapy.</p><p><hi rend="bold">Conclusion </hi> The distribution of the <hi rend="italic">GHR</hi>‐exon 3 genotype was similar in the TS and control groups in a Korean population. The growth promotion efficacy of GH therapy did not differ significantly between TS patients with and without the <hi rend="italic">d3</hi>‐GHR allele. These findings indicate that the <hi rend="italic">GHR</hi>‐exon 3 genotype may not be a major factor to affect the GH response in Korean Turner patients.</p></abstract><textClass><classCode scheme="tocHeading1">Original Articles</classCode><classCode scheme="tocHeading2">Paediatric Endocrinology</classCode></textClass><langUsage><language ident="EN"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/43003FCA458F52999433FD528968524207AA139D/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1365-2265</doi><issn type="print">0300-0664</issn><issn type="electronic">1365-2265</issn><idGroup><id type="product" value="CEN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="CLINICAL ENDOCRINOLOGY">Clinical Endocrinology</title></titleGroup></publicationMeta><publicationMeta level="part" position="02002"><doi origin="wiley">10.1111/cen.2010.72.issue-2</doi><numberingGroup><numbering type="journalVolume" number="72">72</numbering><numbering type="journalIssue" number="2">2</numbering></numberingGroup><coverDate startDate="2010-02">February 2010</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="9" status="forIssue"><doi origin="wiley">10.1111/j.1365-2265.2009.03681.x</doi><idGroup><id type="unit" value="CEN3681"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title><title type="tocHeading2">Paediatric Endocrinology</title></titleGroup><copyright>© 2010 Blackwell Publishing Ltd</copyright><eventGroup><event type="firstOnline" date="2009-08-04"></event><event type="publishedOnlineFinalForm" date="2010-01-19"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-06"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-09"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="196">196</numbering><numbering type="pageLast" number="202">202</numbering></numberingGroup><correspondenceTo>Han‐Wook Yoo, MD, PhD, Department of Pediatrics, Asan Medical Center, 388‐1, Pungnap‐2dong, Songpa‐gu, Seoul 138‐736, Korea. Tel.: +82‐2‐3010‐3386; Fax: +82‐2‐473‐3725; E‐mail: <email>hwyoo@amc.seoul.kr</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:CEN.CEN3681.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>(Received 23 March 2009; returned for revision 17 April 2009; finally revised 6 May 2009; accepted 23 July 2009)</unparsedEditorialHistory><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="4"></count></countGroup><titleGroup><title type="main">The common exon 3 polymorphism of the growth hormone receptor gene and the effect of growth hormone therapy on growth in Korean patients with Turner syndrome</title><title type="shortAuthors"><i>J. M. Ko</i> et al.</title><title type="short"><i>GHR‐exon 3 polymorphism and growth hormone response</i></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Jung Min</givenNames><familyName>Ko</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>Jae‐Min</givenNames><familyName>Kim</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a3"><personName><givenNames>Chong‐Kun</givenNames><familyName>Cheon</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a4"><personName><givenNames>Duk‐Hee</givenNames><familyName>Kim</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a5"><personName><givenNames>Dae‐Yeol</givenNames><familyName>Lee</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a6"><personName><givenNames>Woo Yeong</givenNames><familyName>Cheong</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a7"><personName><givenNames>Eun Young</givenNames><familyName>Kim</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a8"><personName><givenNames>Mi Jung</givenNames><familyName>Park</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a2"><personName><givenNames>Han‐Wook</givenNames><familyName>Yoo</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Departments of Medical Genetics, Ajou Medical Center, University of Ajou College of Medicine, Suwon</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>Genome Research Center for Birth Defects and Genetic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul</unparsedAffiliation></affiliation><affiliation xml:id="a3"><unparsedAffiliation>Department of Pediatrics, Pusan National University School of Medicine, Pusan</unparsedAffiliation></affiliation><affiliation xml:id="a4"><unparsedAffiliation>Department of Pediatrics, Yonsei University College of Medicine, Seoul</unparsedAffiliation></affiliation><affiliation xml:id="a5"><unparsedAffiliation>Department of Pediatrics, School of Medicine, Chonbuk National University, Jeonju</unparsedAffiliation></affiliation><affiliation xml:id="a6"><unparsedAffiliation>Department of Pediatrics, Pusan Paik Hospital, College of Medicine, Inje University, Busan</unparsedAffiliation></affiliation><affiliation xml:id="a7"><unparsedAffiliation>Department of Pediatrics, Kwangju Christian Hospital, Gwangju</unparsedAffiliation></affiliation><affiliation xml:id="a8" countryCode="KR"><unparsedAffiliation>Department of Pediatrics, Inje University Colledge of Medicine, Seoul, Korea</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Summary</title><p><b>Objective </b> Recombinant human growth hormone (GH) can achieve final adult height gain in girls with Turner syndrome (TS), but its efficacy varies widely across individuals. The exon 3‐deleted polymorphism of growth hormone receptor (<i>d3</i>‐GHR) has been reported to be associated with responsiveness to GH therapy. The short‐term growth response of Turner patients to GH therapy was analysed according to their <i>GHR</i>‐exon 3 polymorphism genotype.</p><p><b>Design and patients </b> This was a retrospective study of 175 TS patients. Auxological and endocrine parameters were measured, and the <i>GHR</i>‐exon 3 genotype was analysed. Allelic frequencies of <i>GHR</i>‐exon 3 genotype were compared between patients with TS and control individuals. GH had been administered to 147 patients, 115 of which remained pre‐pubertal after the first follow‐up year. Changes in height standard deviation score (SDS), height velocity (HV), body mass index (BMI), IGF‐1 and IGF binding protein‐3 (IGFBP‐3) concentrations were compared between these patients, grouped according to genotype, after the first follow‐up year.</p><p><b>Results </b> There was no difference in <i>GHR</i>‐exon 3 genotype frequency between the TS and control groups of Koreans. According to the <i>GHR</i>‐exon 3 genotype (<i>fl</i>/<i>fl</i> group <i>vs</i>. <i>d3/fl</i> and <i>d3/d3</i> group), HV gain and height SDS gain did not differ significantly at the first year of GH therapy. Moreover, changes in IGF‐1, IGFBP‐3 concentration and BMI showed no significant difference between the groups with and without <i>d3</i>‐GHR after 1 year of GH therapy.</p><p><b>Conclusion </b> The distribution of the <i>GHR</i>‐exon 3 genotype was similar in the TS and control groups in a Korean population. The growth promotion efficacy of GH therapy did not differ significantly between TS patients with and without the <i>d3</i>‐GHR allele. These findings indicate that the <i>GHR</i>‐exon 3 genotype may not be a major factor to affect the GH response in Korean Turner patients.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The common exon 3 polymorphism of the growth hormone receptor gene and the effect of growth hormone therapy on growth in Korean patients with Turner syndrome</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>GHR‐exon 3 polymorphism and growth hormone response</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The common exon 3 polymorphism of the growth hormone receptor gene and the effect of growth hormone therapy on growth in Korean patients with Turner syndrome</title></titleInfo><name type="personal"><namePart type="given">Jung Min</namePart><namePart type="family">Ko</namePart><affiliation>Departments of Medical Genetics, Ajou Medical Center, University of Ajou College of Medicine, Suwon</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jae‐Min</namePart><namePart type="family">Kim</namePart><affiliation>Genome Research Center for Birth Defects and Genetic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chong‐Kun</namePart><namePart type="family">Cheon</namePart><affiliation>Department of Pediatrics, Pusan National University School of Medicine, Pusan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Duk‐Hee</namePart><namePart type="family">Kim</namePart><affiliation>Department of Pediatrics, Yonsei University College of Medicine, Seoul</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dae‐Yeol</namePart><namePart type="family">Lee</namePart><affiliation>Department of Pediatrics, School of Medicine, Chonbuk National University, Jeonju</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Woo Yeong</namePart><namePart type="family">Cheong</namePart><affiliation>Department of Pediatrics, Pusan Paik Hospital, College of Medicine, Inje University, Busan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eun Young</namePart><namePart type="family">Kim</namePart><affiliation>Department of Pediatrics, Kwangju Christian Hospital, Gwangju</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mi Jung</namePart><namePart type="family">Park</namePart><affiliation>Department of Pediatrics, Inje University Colledge of Medicine, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Han‐Wook</namePart><namePart type="family">Yoo</namePart><affiliation>Genome Research Center for Birth Defects and Genetic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2010-02</dateIssued><edition>(Received 23 March 2009; returned for revision 17 April 2009; finally revised 6 May 2009; accepted 23 July 2009)</edition><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="tables">4</extent></physicalDescription><abstract>Objective Recombinant human growth hormone (GH) can achieve final adult height gain in girls with Turner syndrome (TS), but its efficacy varies widely across individuals. The exon 3‐deleted polymorphism of growth hormone receptor (d3‐GHR) has been reported to be associated with responsiveness to GH therapy. The short‐term growth response of Turner patients to GH therapy was analysed according to their GHR‐exon 3 polymorphism genotype.</abstract><abstract>Design and patients This was a retrospective study of 175 TS patients. Auxological and endocrine parameters were measured, and the GHR‐exon 3 genotype was analysed. Allelic frequencies of GHR‐exon 3 genotype were compared between patients with TS and control individuals. GH had been administered to 147 patients, 115 of which remained pre‐pubertal after the first follow‐up year. Changes in height standard deviation score (SDS), height velocity (HV), body mass index (BMI), IGF‐1 and IGF binding protein‐3 (IGFBP‐3) concentrations were compared between these patients, grouped according to genotype, after the first follow‐up year.</abstract><abstract>Results There was no difference in GHR‐exon 3 genotype frequency between the TS and control groups of Koreans. According to the GHR‐exon 3 genotype (fl/fl group vs. d3/fl and d3/d3 group), HV gain and height SDS gain did not differ significantly at the first year of GH therapy. Moreover, changes in IGF‐1, IGFBP‐3 concentration and BMI showed no significant difference between the groups with and without d3‐GHR after 1 year of GH therapy.</abstract><abstract>Conclusion The distribution of the GHR‐exon 3 genotype was similar in the TS and control groups in a Korean population. The growth promotion efficacy of GH therapy did not differ significantly between TS patients with and without the d3‐GHR allele. These findings indicate that the GHR‐exon 3 genotype may not be a major factor to affect the GH response in Korean Turner patients.</abstract><relatedItem type="host"><titleInfo><title>Clinical Endocrinology</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0300-0664</identifier><identifier type="eISSN">1365-2265</identifier><identifier type="DOI">10.1111/(ISSN)1365-2265</identifier><identifier type="PublisherID">CEN</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>72</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>196</start><end>202</end><total>7</total></extent></part></relatedItem><identifier type="istex">43003FCA458F52999433FD528968524207AA139D</identifier><identifier type="DOI">10.1111/j.1365-2265.2009.03681.x</identifier><identifier type="ArticleID">CEN3681</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2010 Blackwell Publishing Ltd</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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