Effect of recombinant hGH (rhGH) replacement on gonadal function in male patients with organic adult‐onset GH deficiency
Identifieur interne : 000937 ( Main/Corpus ); précédent : 000936; suivant : 000938Effect of recombinant hGH (rhGH) replacement on gonadal function in male patients with organic adult‐onset GH deficiency
Auteurs : Claudia Giavoli ; Emanuele Ferrante ; Federica Ermetici ; Silvia Bergamaschi ; Cristina L. Ronchi ; Andrea G. Lania ; Bruno Ambrosi ; Anna Spada ; Paolo Beck EccozSource :
- Clinical Endocrinology [ 0300-0664 ] ; 2006-12.
Abstract
Objective Previous evidence indicated that, in adults with organic hypopituitarism, GH deficiency (GHD) may mask the presence of other pituitary deficits, in particular central hypothyroidism and hypoadrenalism. Little and conflicting information is available about the relationship between GHD, rhGH therapy and gonadal function in males. The aim of the present study was to investigate the hypothalamic–pituitary–gonadal axis (HPG) in male adults with organic GHD and normal HPG axis. Patients Twelve male adults (mean age 48 ± 7 years) with organic GHD and normal HPG axis. Measurements Serum levels of testosterone, LH and FSH (basal and after GnRH stimulation test), SHBG and IGF‐I and percentage body fat (BF%) were evaluated before and during rhGH (mean dose 0·24 ± 0·02 mg/day for 13 ± 1 months) treatment. Results Serum IGF‐I levels normalized during rhGH treatment and BF% significantly decreased. Serum testosterone levels significantly decreased (from 18·1 ± 1·7 to 14·2 ± 1·6 nmol/l, P = 0·01), with a parallel and significant decrease of serum SHBG (from 31·1 ± 3·6 to 24·3 ± 2·3 nmol/l, P < 0·05). Thus, calculated free testosterone (cFT) did not change (from 0·39 ± 0·17 to 0·33 ± 0·14 nmol/l, P = ns). Finally, no difference was found in basal and GnRH stimulated gonadotrophins levels. Conclusions In conclusion, the condition of GHD does not seem to mask central hypogonadism, in contrast to what is observed for central hypothyroidism and hypoadrenalism. However, the significant decrease in serum testosterone levels, strictly related to SHBG decrease, suggests that evaluation of the HPG axis during rhGH treatment cannot be based on the measurement of total testosterone levels, but should mainly rely on calculation of cFT and a careful clinical evaluation, in order to avoid unnecessary replacement therapy.
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DOI: 10.1111/j.1365-2265.2006.02655.x
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Ronchi</name><affiliation><mods:affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</mods:affiliation></affiliation></author><author><name sortKey="Lania, Andrea G" sort="Lania, Andrea G" uniqKey="Lania A" first="Andrea G." last="Lania">Andrea G. Lania</name><affiliation><mods:affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</mods:affiliation></affiliation></author><author><name sortKey="Ambrosi, Bruno" sort="Ambrosi, Bruno" uniqKey="Ambrosi B" first="Bruno" last="Ambrosi">Bruno Ambrosi</name><affiliation><mods:affiliation>Endocrinology Unit, Policlinico San Donato, University of Milan, Milan, Italy</mods:affiliation></affiliation></author><author><name sortKey="Spada, Anna" sort="Spada, Anna" uniqKey="Spada A" first="Anna" last="Spada">Anna Spada</name><affiliation><mods:affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</mods:affiliation></affiliation></author><author><name sortKey="Beck Eccoz, Paolo" sort="Beck Eccoz, Paolo" uniqKey="Beck Eccoz P" first="Paolo" last="Beck Eccoz">Paolo Beck Eccoz</name><affiliation><mods:affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Clinical Endocrinology</title><idno type="ISSN">0300-0664</idno><idno type="eISSN">1365-2265</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2006-12">2006-12</date><biblScope unit="volume">65</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="717">717</biblScope><biblScope unit="page" to="721">721</biblScope></imprint><idno type="ISSN">0300-0664</idno></series><idno type="istex">D92F6DBA05FCADB8DB4C7322820B42B35CBA907E</idno><idno type="DOI">10.1111/j.1365-2265.2006.02655.x</idno><idno type="ArticleID">CEN2655</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0300-0664</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objective Previous evidence indicated that, in adults with organic hypopituitarism, GH deficiency (GHD) may mask the presence of other pituitary deficits, in particular central hypothyroidism and hypoadrenalism. Little and conflicting information is available about the relationship between GHD, rhGH therapy and gonadal function in males. The aim of the present study was to investigate the hypothalamic–pituitary–gonadal axis (HPG) in male adults with organic GHD and normal HPG axis. Patients Twelve male adults (mean age 48 ± 7 years) with organic GHD and normal HPG axis. Measurements Serum levels of testosterone, LH and FSH (basal and after GnRH stimulation test), SHBG and IGF‐I and percentage body fat (BF%) were evaluated before and during rhGH (mean dose 0·24 ± 0·02 mg/day for 13 ± 1 months) treatment. Results Serum IGF‐I levels normalized during rhGH treatment and BF% significantly decreased. Serum testosterone levels significantly decreased (from 18·1 ± 1·7 to 14·2 ± 1·6 nmol/l, P = 0·01), with a parallel and significant decrease of serum SHBG (from 31·1 ± 3·6 to 24·3 ± 2·3 nmol/l, P < 0·05). Thus, calculated free testosterone (cFT) did not change (from 0·39 ± 0·17 to 0·33 ± 0·14 nmol/l, P = ns). Finally, no difference was found in basal and GnRH stimulated gonadotrophins levels. Conclusions In conclusion, the condition of GHD does not seem to mask central hypogonadism, in contrast to what is observed for central hypothyroidism and hypoadrenalism. However, the significant decrease in serum testosterone levels, strictly related to SHBG decrease, suggests that evaluation of the HPG axis during rhGH treatment cannot be based on the measurement of total testosterone levels, but should mainly rely on calculation of cFT and a careful clinical evaluation, in order to avoid unnecessary replacement therapy.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Claudia Giavoli</name><affiliations><json:string>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</json:string></affiliations></json:item><json:item><name>Emanuele Ferrante</name><affiliations><json:string>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</json:string></affiliations></json:item><json:item><name>Federica Ermetici</name><affiliations><json:string>Endocrinology Unit, Policlinico San Donato, University of Milan, Milan, Italy</json:string></affiliations></json:item><json:item><name>Silvia Bergamaschi</name><affiliations><json:string>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</json:string></affiliations></json:item><json:item><name>Cristina L. Ronchi</name><affiliations><json:string>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</json:string></affiliations></json:item><json:item><name>Andrea G. Lania</name><affiliations><json:string>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</json:string></affiliations></json:item><json:item><name>Bruno Ambrosi</name><affiliations><json:string>Endocrinology Unit, Policlinico San Donato, University of Milan, Milan, Italy</json:string></affiliations></json:item><json:item><name>Anna Spada</name><affiliations><json:string>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</json:string></affiliations></json:item><json:item><name>Paolo Beck‐Peccoz</name><affiliations><json:string>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</json:string></affiliations></json:item></author><language><json:string>eng</json:string></language><abstract>Objective Previous evidence indicated that, in adults with organic hypopituitarism, GH deficiency (GHD) may mask the presence of other pituitary deficits, in particular central hypothyroidism and hypoadrenalism. Little and conflicting information is available about the relationship between GHD, rhGH therapy and gonadal function in males. The aim of the present study was to investigate the hypothalamic–pituitary–gonadal axis (HPG) in male adults with organic GHD and normal HPG axis. Patients Twelve male adults (mean age 48 ± 7 years) with organic GHD and normal HPG axis. Measurements Serum levels of testosterone, LH and FSH (basal and after GnRH stimulation test), SHBG and IGF‐I and percentage body fat (BF%) were evaluated before and during rhGH (mean dose 0·24 ± 0·02 mg/day for 13 ± 1 months) treatment. Results Serum IGF‐I levels normalized during rhGH treatment and BF% significantly decreased. Serum testosterone levels significantly decreased (from 18·1 ± 1·7 to 14·2 ± 1·6 nmol/l, P = 0·01), with a parallel and significant decrease of serum SHBG (from 31·1 ± 3·6 to 24·3 ± 2·3 nmol/l, P > 0·05). Thus, calculated free testosterone (cFT) did not change (from 0·39 ± 0·17 to 0·33 ± 0·14 nmol/l, P = ns). Finally, no difference was found in basal and GnRH stimulated gonadotrophins levels. Conclusions In conclusion, the condition of GHD does not seem to mask central hypogonadism, in contrast to what is observed for central hypothyroidism and hypoadrenalism. However, the significant decrease in serum testosterone levels, strictly related to SHBG decrease, suggests that evaluation of the HPG axis during rhGH treatment cannot be based on the measurement of total testosterone levels, but should mainly rely on calculation of cFT and a careful clinical evaluation, in order to avoid unnecessary replacement therapy.</abstract><qualityIndicators><score>6.371</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595 x 782 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1837</abstractCharCount><pdfWordCount>3371</pdfWordCount><pdfCharCount>21248</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>255</abstractWordCount></qualityIndicators><title>Effect of recombinant hGH (rhGH) replacement on gonadal function in male patients with organic adult‐onset GH 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deficiency</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2006</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Effect of recombinant hGH (rhGH) replacement on gonadal function in male patients with organic adult‐onset GH deficiency</title><author><persName><forename type="first">Claudia</forename><surname>Giavoli</surname></persName><affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</affiliation></author><author><persName><forename type="first">Emanuele</forename><surname>Ferrante</surname></persName><affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</affiliation></author><author><persName><forename type="first">Federica</forename><surname>Ermetici</surname></persName><affiliation>Endocrinology Unit, Policlinico San Donato, University of Milan, Milan, Italy</affiliation></author><author><persName><forename type="first">Silvia</forename><surname>Bergamaschi</surname></persName><affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</affiliation></author><author><persName><forename type="first">Cristina L.</forename><surname>Ronchi</surname></persName><affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</affiliation></author><author><persName><forename type="first">Andrea G.</forename><surname>Lania</surname></persName><affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</affiliation></author><author><persName><forename type="first">Bruno</forename><surname>Ambrosi</surname></persName><affiliation>Endocrinology Unit, Policlinico San Donato, University of Milan, Milan, Italy</affiliation></author><author><persName><forename type="first">Anna</forename><surname>Spada</surname></persName><affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</affiliation></author><author><persName><forename type="first">Paolo</forename><surname>Beck‐Peccoz</surname></persName><affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</affiliation></author></analytic><monogr><title level="j">Clinical Endocrinology</title><idno type="pISSN">0300-0664</idno><idno type="eISSN">1365-2265</idno><idno type="DOI">10.1111/(ISSN)1365-2265</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2006-12"></date><biblScope unit="volume">65</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="717">717</biblScope><biblScope unit="page" to="721">721</biblScope></imprint></monogr><idno type="istex">D92F6DBA05FCADB8DB4C7322820B42B35CBA907E</idno><idno type="DOI">10.1111/j.1365-2265.2006.02655.x</idno><idno type="ArticleID">CEN2655</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2006</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Objective Previous evidence indicated that, in adults with organic hypopituitarism, GH deficiency (GHD) may mask the presence of other pituitary deficits, in particular central hypothyroidism and hypoadrenalism. Little and conflicting information is available about the relationship between GHD, rhGH therapy and gonadal function in males. The aim of the present study was to investigate the hypothalamic–pituitary–gonadal axis (HPG) in male adults with organic GHD and normal HPG axis. Patients Twelve male adults (mean age 48 ± 7 years) with organic GHD and normal HPG axis. Measurements Serum levels of testosterone, LH and FSH (basal and after GnRH stimulation test), SHBG and IGF‐I and percentage body fat (BF%) were evaluated before and during rhGH (mean dose 0·24 ± 0·02 mg/day for 13 ± 1 months) treatment. Results Serum IGF‐I levels normalized during rhGH treatment and BF% significantly decreased. Serum testosterone levels significantly decreased (from 18·1 ± 1·7 to 14·2 ± 1·6 nmol/l, P = 0·01), with a parallel and significant decrease of serum SHBG (from 31·1 ± 3·6 to 24·3 ± 2·3 nmol/l, P < 0·05). Thus, calculated free testosterone (cFT) did not change (from 0·39 ± 0·17 to 0·33 ± 0·14 nmol/l, P = ns). Finally, no difference was found in basal and GnRH stimulated gonadotrophins levels. Conclusions In conclusion, the condition of GHD does not seem to mask central hypogonadism, in contrast to what is observed for central hypothyroidism and hypoadrenalism. However, the significant decrease in serum testosterone levels, strictly related to SHBG decrease, suggests that evaluation of the HPG axis during rhGH treatment cannot be based on the measurement of total testosterone levels, but should mainly rely on calculation of cFT and a careful clinical evaluation, in order to avoid unnecessary replacement therapy.</p></abstract></profileDesc><revisionDesc><change when="2006-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/D92F6DBA05FCADB8DB4C7322820B42B35CBA907E/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="12006"><doi origin="wiley">10.1111/cen.2006.65.issue-6</doi><numberingGroup><numbering type="journalVolume" number="65">65</numbering><numbering type="journalIssue" number="6">6</numbering></numberingGroup><coverDate startDate="2006-12">December 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="4" status="forIssue"><doi origin="wiley">10.1111/j.1365-2265.2006.02655.x</doi><idGroup><id type="unit" value="CEN2655"></id></idGroup><countGroup><count type="pageTotal" number="5"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title></titleGroup><eventGroup><event type="firstOnline" date="2006-09-05"></event><event type="publishedOnlineFinalForm" date="2006-10-20"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-09"></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="717">717</numbering><numbering type="pageLast" number="721">721</numbering></numberingGroup><correspondenceTo> Paolo Beck‐Peccoz, Institute of Endocrine Sciences, Ospedale Maggiore IRCCS, Pad. Granelli, Via F. Sforza, 35, 20122‐Milano, Italy. Tel.: +39 02 50320607; Fax: +39 02 50320605; E‐mail: <email>paolo.beckpeccoz@unimi.it</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:CEN.CEN2655.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>(Received 4 May 2006; accepted 28 May 2006)</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="2"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="27"></count><count type="wordTotal" number="3886"></count></countGroup><titleGroup><title type="main">Effect of recombinant hGH (rhGH) replacement on gonadal function in male patients with organic adult‐onset GH deficiency</title><title type="shortAuthors"><i>C. Giavoli </i>et al.</title><title type="short"><i>Gonadal function during rhGH therapy</i></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Claudia</givenNames><familyName>Giavoli</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Emanuele</givenNames><familyName>Ferrante</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>Federica</givenNames><familyName>Ermetici</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>Silvia</givenNames><familyName>Bergamaschi</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>Cristina L.</givenNames><familyName>Ronchi</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>Andrea G.</givenNames><familyName>Lania</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a2"><personName><givenNames>Bruno</givenNames><familyName>Ambrosi</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a1"><personName><givenNames>Anna</givenNames><familyName>Spada</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a1"><personName><givenNames>Paolo</givenNames><familyName>Beck‐Peccoz</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="IT"><unparsedAffiliation>Endocrinology Unit, Policlinico San Donato, University of Milan, Milan, Italy</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Summary</title><p><b>Objective </b> Previous evidence indicated that, in adults with organic hypopituitarism, GH deficiency (GHD) may mask the presence of other pituitary deficits, in particular central hypothyroidism and hypoadrenalism. Little and conflicting information is available about the relationship between GHD, rhGH therapy and gonadal function in males. The aim of the present study was to investigate the hypothalamic–pituitary–gonadal axis (HPG) in male adults with organic GHD and normal HPG axis.</p><p><b>Patients </b> Twelve male adults (mean age 48 ± 7 years) with organic GHD and normal HPG axis.</p><p><b>Measurements </b> Serum levels of testosterone, LH and FSH (basal and after GnRH stimulation test), SHBG and IGF‐I and percentage body fat (BF%) were evaluated before and during rhGH (mean dose 0·24 ± 0·02 mg/day for 13 ± 1 months) treatment.</p><p><b>Results </b> Serum IGF‐I levels normalized during rhGH treatment and BF% significantly decreased. Serum testosterone levels significantly decreased (from 18·1 ± 1·7 to 14·2 ± 1·6 nmol/l, <i>P</i> = 0·01), with a parallel and significant decrease of serum SHBG (from 31·1 ± 3·6 to 24·3 ± 2·3 nmol/l, <i>P</i> < 0·05). Thus, calculated free testosterone (cFT) did not change (from 0·39 ± 0·17 to 0·33 ± 0·14 nmol/l, <i>P</i> = ns). Finally, no difference was found in basal and GnRH stimulated gonadotrophins levels.</p><p><b>Conclusions </b> In conclusion, the condition of GHD does not seem to mask central hypogonadism, in contrast to what is observed for central hypothyroidism and hypoadrenalism. However, the significant decrease in serum testosterone levels, strictly related to SHBG decrease, suggests that evaluation of the HPG axis during rhGH treatment cannot be based on the measurement of total testosterone levels, but should mainly rely on calculation of cFT and a careful clinical evaluation, in order to avoid unnecessary replacement therapy.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Effect of recombinant hGH (rhGH) replacement on gonadal function in male patients with organic adult‐onset GH deficiency</title></titleInfo><titleInfo type="abbreviated"><title>Gonadal function during rhGH therapy</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Effect of recombinant hGH (rhGH) replacement on gonadal function in male patients with organic adult‐onset GH deficiency</title></titleInfo><name type="personal"><namePart type="given">Claudia</namePart><namePart type="family">Giavoli</namePart><affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Emanuele</namePart><namePart type="family">Ferrante</namePart><affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Federica</namePart><namePart type="family">Ermetici</namePart><affiliation>Endocrinology Unit, Policlinico San Donato, University of Milan, Milan, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Silvia</namePart><namePart type="family">Bergamaschi</namePart><affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Cristina L.</namePart><namePart type="family">Ronchi</namePart><affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrea G.</namePart><namePart type="family">Lania</namePart><affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bruno</namePart><namePart type="family">Ambrosi</namePart><affiliation>Endocrinology Unit, Policlinico San Donato, University of Milan, Milan, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anna</namePart><namePart type="family">Spada</namePart><affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paolo</namePart><namePart type="family">Beck‐Peccoz</namePart><affiliation>Endocrine Unit, Department of Medical Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena and</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">2006-12</dateIssued><edition>(Received 4 May 2006; accepted 28 May 2006)</edition><copyrightDate encoding="w3cdtf">2006</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="figures">1</extent><extent unit="tables">2</extent><extent unit="references">27</extent><extent unit="words">3886</extent></physicalDescription><abstract lang="en">Objective Previous evidence indicated that, in adults with organic hypopituitarism, GH deficiency (GHD) may mask the presence of other pituitary deficits, in particular central hypothyroidism and hypoadrenalism. Little and conflicting information is available about the relationship between GHD, rhGH therapy and gonadal function in males. The aim of the present study was to investigate the hypothalamic–pituitary–gonadal axis (HPG) in male adults with organic GHD and normal HPG axis. Patients Twelve male adults (mean age 48 ± 7 years) with organic GHD and normal HPG axis. Measurements Serum levels of testosterone, LH and FSH (basal and after GnRH stimulation test), SHBG and IGF‐I and percentage body fat (BF%) were evaluated before and during rhGH (mean dose 0·24 ± 0·02 mg/day for 13 ± 1 months) treatment. Results Serum IGF‐I levels normalized during rhGH treatment and BF% significantly decreased. Serum testosterone levels significantly decreased (from 18·1 ± 1·7 to 14·2 ± 1·6 nmol/l, P = 0·01), with a parallel and significant decrease of serum SHBG (from 31·1 ± 3·6 to 24·3 ± 2·3 nmol/l, P < 0·05). Thus, calculated free testosterone (cFT) did not change (from 0·39 ± 0·17 to 0·33 ± 0·14 nmol/l, P = ns). Finally, no difference was found in basal and GnRH stimulated gonadotrophins levels. Conclusions In conclusion, the condition of GHD does not seem to mask central hypogonadism, in contrast to what is observed for central hypothyroidism and hypoadrenalism. However, the significant decrease in serum testosterone levels, strictly related to SHBG decrease, suggests that evaluation of the HPG axis during rhGH treatment cannot be based on the measurement of total testosterone levels, but should mainly rely on calculation of cFT and a careful clinical evaluation, in order to avoid unnecessary replacement therapy.</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>2006</date><detail type="volume"><caption>vol.</caption><number>65</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>717</start><end>721</end><total>5</total></extent></part></relatedItem><identifier type="istex">D92F6DBA05FCADB8DB4C7322820B42B35CBA907E</identifier><identifier type="DOI">10.1111/j.1365-2265.2006.02655.x</identifier><identifier type="ArticleID">CEN2655</identifier><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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