Distrubance of growth hormone-insulin-like growth factor axis in uraemia
Identifieur interne : 000A47 ( Main/Corpus ); précédent : 000A46; suivant : 000A48Distrubance of growth hormone-insulin-like growth factor axis in uraemia
Auteurs : B. Tönshoff ; F. Schaefer ; O. MehlsSource :
- Pediatric Nephrology [ 0931-041X ] ; 1990-11-01.
Abstract
Abstract: The growth hormone/insulin-like growth factor (IGF) axis is disturbed in uraemia. Elevated plasma growth hormone (GH) levels despite diminished growth suggest GH resistance, which may be due in part to a decreased expression of the growth hormone receptor at the cell membrane. The hepatic production of IGFs under the control of GH is impaired. Furthermore, there is an excess of IGF-binding protein over total IGF as a consequence of reduced renal clearance of low-molecular-weight subunits of the IGF-binding protein (IGF-BP). This results in an absolute (diminished production) and a relative (low bioavailability) deficiency of IGF. Recombinant human growth hormone (rhGH) in doses of 4 IU/m2 per day is able to induce catch-up growth in children with preterminal and terminal renal failure. The growth stimulation of exogenous GH is attributed to its potency to increase the ratio of IGF-I to IGF-BP, followed by a normalization of IGF bioactivity. In renal transplanted children growth is not only disturbed by decreased renal function but also by steroid treatment. Corticosteroids, are responsible for catabolism, for suppression of pituitary GH secretion and for inhibition of local production of IGFs. Exogenous rhGH is able to counteract these growth-inhibiting effects. However, it remains to be seen whether long-term GH treatment definitely improves final adult height.
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DOI: 10.1007/BF00858645
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Distrubance of growth hormone-insulin-like growth factor axis in uraemia</title><author><name sortKey="Tonshoff, B" sort="Tonshoff, B" uniqKey="Tonshoff B" first="B." last="Tönshoff">B. Tönshoff</name><affiliation><mods:affiliation>Division of Paediatric Nephrology, University Children's Hospital, Im Neuenheimer Feld 150, D-6900, Heidelberg, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Schaefer, F" sort="Schaefer, F" uniqKey="Schaefer F" first="F." last="Schaefer">F. Schaefer</name><affiliation><mods:affiliation>Division of Paediatric Nephrology, University Children's Hospital, Im Neuenheimer Feld 150, D-6900, Heidelberg, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Mehls, O" sort="Mehls, O" uniqKey="Mehls O" first="O." last="Mehls">O. Mehls</name><affiliation><mods:affiliation>Division of Paediatric Nephrology, University Children's Hospital, Im Neuenheimer Feld 150, D-6900, Heidelberg, Federal Republic of Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:F429FF95D9939F5170958E1DA433CE81EAACCEFF</idno><date when="1990" year="1990">1990</date><idno type="doi">10.1007/BF00858645</idno><idno type="url">https://api.istex.fr/document/F429FF95D9939F5170958E1DA433CE81EAACCEFF/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000A47</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Distrubance of growth hormone-insulin-like growth factor axis in uraemia</title><author><name sortKey="Tonshoff, B" sort="Tonshoff, B" uniqKey="Tonshoff B" first="B." last="Tönshoff">B. Tönshoff</name><affiliation><mods:affiliation>Division of Paediatric Nephrology, University Children's Hospital, Im Neuenheimer Feld 150, D-6900, Heidelberg, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Schaefer, F" sort="Schaefer, F" uniqKey="Schaefer F" first="F." last="Schaefer">F. Schaefer</name><affiliation><mods:affiliation>Division of Paediatric Nephrology, University Children's Hospital, Im Neuenheimer Feld 150, D-6900, Heidelberg, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Mehls, O" sort="Mehls, O" uniqKey="Mehls O" first="O." last="Mehls">O. Mehls</name><affiliation><mods:affiliation>Division of Paediatric Nephrology, University Children's Hospital, Im Neuenheimer Feld 150, D-6900, Heidelberg, Federal Republic of Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Pediatric Nephrology</title><title level="j" type="sub">Journal of the International Pediatric Nephrology Association</title><title level="j" type="abbrev">Pediatr Nephrol</title><idno type="ISSN">0931-041X</idno><idno type="eISSN">1432-198X</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1990-11-01">1990-11-01</date><biblScope unit="volume">4</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="654">654</biblScope><biblScope unit="page" to="662">662</biblScope></imprint><idno type="ISSN">0931-041X</idno></series><idno type="istex">F429FF95D9939F5170958E1DA433CE81EAACCEFF</idno><idno type="DOI">10.1007/BF00858645</idno><idno type="ArticleID">Art21</idno><idno type="ArticleID">BF00858645</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0931-041X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The growth hormone/insulin-like growth factor (IGF) axis is disturbed in uraemia. Elevated plasma growth hormone (GH) levels despite diminished growth suggest GH resistance, which may be due in part to a decreased expression of the growth hormone receptor at the cell membrane. The hepatic production of IGFs under the control of GH is impaired. Furthermore, there is an excess of IGF-binding protein over total IGF as a consequence of reduced renal clearance of low-molecular-weight subunits of the IGF-binding protein (IGF-BP). This results in an absolute (diminished production) and a relative (low bioavailability) deficiency of IGF. Recombinant human growth hormone (rhGH) in doses of 4 IU/m2 per day is able to induce catch-up growth in children with preterminal and terminal renal failure. The growth stimulation of exogenous GH is attributed to its potency to increase the ratio of IGF-I to IGF-BP, followed by a normalization of IGF bioactivity. In renal transplanted children growth is not only disturbed by decreased renal function but also by steroid treatment. Corticosteroids, are responsible for catabolism, for suppression of pituitary GH secretion and for inhibition of local production of IGFs. Exogenous rhGH is able to counteract these growth-inhibiting effects. However, it remains to be seen whether long-term GH treatment definitely improves final adult height.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>B. Tönshoff</name><affiliations><json:string>Division of Paediatric Nephrology, University Children's Hospital, Im Neuenheimer Feld 150, D-6900, Heidelberg, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>F. Schaefer</name><affiliations><json:string>Division of Paediatric Nephrology, University Children's Hospital, Im Neuenheimer Feld 150, D-6900, Heidelberg, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>O. Mehls</name><affiliations><json:string>Division of Paediatric Nephrology, University Children's Hospital, Im Neuenheimer Feld 150, D-6900, Heidelberg, Federal Republic of Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Growth hormone</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Insulin-like growth factors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>IGF-binding proteins</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Growth hormone binding activity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Chronic renal failure</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Recombinant human growth hormone</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Abstract: The growth hormone/insulin-like growth factor (IGF) axis is disturbed in uraemia. Elevated plasma growth hormone (GH) levels despite diminished growth suggest GH resistance, which may be due in part to a decreased expression of the growth hormone receptor at the cell membrane. The hepatic production of IGFs under the control of GH is impaired. Furthermore, there is an excess of IGF-binding protein over total IGF as a consequence of reduced renal clearance of low-molecular-weight subunits of the IGF-binding protein (IGF-BP). This results in an absolute (diminished production) and a relative (low bioavailability) deficiency of IGF. Recombinant human growth hormone (rhGH) in doses of 4 IU/m2 per day is able to induce catch-up growth in children with preterminal and terminal renal failure. The growth stimulation of exogenous GH is attributed to its potency to increase the ratio of IGF-I to IGF-BP, followed by a normalization of IGF bioactivity. In renal transplanted children growth is not only disturbed by decreased renal function but also by steroid treatment. Corticosteroids, are responsible for catabolism, for suppression of pituitary GH secretion and for inhibition of local production of IGFs. Exogenous rhGH is able to counteract these growth-inhibiting effects. 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Elevated plasma growth hormone (GH) levels despite diminished growth suggest GH resistance, which may be due in part to a decreased expression of the growth hormone receptor at the cell membrane. The hepatic production of IGFs under the control of GH is impaired. Furthermore, there is an excess of IGF-binding protein over total IGF as a consequence of reduced renal clearance of low-molecular-weight subunits of the IGF-binding protein (IGF-BP). This results in an absolute (diminished production) and a relative (low bioavailability) deficiency of IGF. Recombinant human growth hormone (rhGH) in doses of 4 IU/m2 per day is able to induce catch-up growth in children with preterminal and terminal renal failure. The growth stimulation of exogenous GH is attributed to its potency to increase the ratio of IGF-I to IGF-BP, followed by a normalization of IGF bioactivity. In renal transplanted children growth is not only disturbed by decreased renal function but also by steroid treatment. Corticosteroids, are responsible for catabolism, for suppression of pituitary GH secretion and for inhibition of local production of IGFs. Exogenous rhGH is able to counteract these growth-inhibiting effects. 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Elevated plasma growth hormone (GH) levels despite diminished growth suggest GH resistance, which may be due in part to a decreased expression of the growth hormone receptor at the cell membrane. The hepatic production of IGFs under the control of GH is impaired. Furthermore, there is an excess of IGF-binding protein over total IGF as a consequence of reduced renal clearance of low-molecular-weight subunits of the IGF-binding protein (IGF-BP). This results in an absolute (diminished production) and a relative (low bioavailability) deficiency of IGF. Recombinant human growth hormone (rhGH) in doses of 4 IU/m<Superscript>2</Superscript> per day is able to induce catch-up growth in children with preterminal and terminal renal failure. The growth stimulation of exogenous GH is attributed to its potency to increase the ratio of IGF-I to IGF-BP, followed by a normalization of IGF bioactivity. In renal transplanted children growth is not only disturbed by decreased renal function but also by steroid treatment. Corticosteroids, are responsible for catabolism, for suppression of pituitary GH secretion and for inhibition of local production of IGFs. Exogenous rhGH is able to counteract these growth-inhibiting effects. However, it remains to be seen whether long-term GH treatment definitely improves final adult height.</Para></Abstract><KeywordGroup Language="En"><Heading>Key words</Heading><Keyword>Growth hormone</Keyword><Keyword>Insulin-like growth factors</Keyword><Keyword>IGF-binding proteins</Keyword><Keyword>Growth hormone binding activity</Keyword><Keyword>Chronic renal failure</Keyword><Keyword>Recombinant human growth hormone</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Distrubance of growth hormone-insulin-like growth factor axis in uraemia</title><subTitle>Implications for recombinant human growth hormone treatment</subTitle></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Distrubance of growth hormone-insulin-like growth factor axis in uraemia</title><subTitle>Implications for recombinant human growth hormone treatment</subTitle></titleInfo><name type="personal"><namePart type="given">B.</namePart><namePart type="family">Tönshoff</namePart><affiliation>Division of Paediatric Nephrology, University Children's Hospital, Im Neuenheimer Feld 150, D-6900, Heidelberg, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F.</namePart><namePart type="family">Schaefer</namePart><affiliation>Division of Paediatric Nephrology, University Children's Hospital, Im Neuenheimer Feld 150, D-6900, Heidelberg, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">O.</namePart><namePart type="family">Mehls</namePart><affiliation>Division of Paediatric Nephrology, University Children's Hospital, Im Neuenheimer Feld 150, D-6900, Heidelberg, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="ReviewPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Berlin/Heidelberg</placeTerm></place><dateCreated encoding="w3cdtf">1990-07-18</dateCreated><dateIssued encoding="w3cdtf">1990-11-01</dateIssued><copyrightDate encoding="w3cdtf">1990</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Abstract: The growth hormone/insulin-like growth factor (IGF) axis is disturbed in uraemia. Elevated plasma growth hormone (GH) levels despite diminished growth suggest GH resistance, which may be due in part to a decreased expression of the growth hormone receptor at the cell membrane. The hepatic production of IGFs under the control of GH is impaired. Furthermore, there is an excess of IGF-binding protein over total IGF as a consequence of reduced renal clearance of low-molecular-weight subunits of the IGF-binding protein (IGF-BP). This results in an absolute (diminished production) and a relative (low bioavailability) deficiency of IGF. Recombinant human growth hormone (rhGH) in doses of 4 IU/m2 per day is able to induce catch-up growth in children with preterminal and terminal renal failure. The growth stimulation of exogenous GH is attributed to its potency to increase the ratio of IGF-I to IGF-BP, followed by a normalization of IGF bioactivity. In renal transplanted children growth is not only disturbed by decreased renal function but also by steroid treatment. Corticosteroids, are responsible for catabolism, for suppression of pituitary GH secretion and for inhibition of local production of IGFs. Exogenous rhGH is able to counteract these growth-inhibiting effects. However, it remains to be seen whether long-term GH treatment definitely improves final adult height.</abstract><note>Invited Review</note><relatedItem type="host"><titleInfo><title>Pediatric Nephrology</title><subTitle>Journal of the International Pediatric Nephrology Association</subTitle></titleInfo><titleInfo type="abbreviated"><title>Pediatr Nephrol</title></titleInfo><genre type="Journal" displayLabel="Archive Journal"></genre><originInfo><dateIssued encoding="w3cdtf">1990-11-01</dateIssued><copyrightDate encoding="w3cdtf">1990</copyrightDate></originInfo><subject><genre>Medicine & Public Health</genre><topic>Pediatrics</topic></subject><identifier type="ISSN">0931-041X</identifier><identifier type="eISSN">1432-198X</identifier><identifier type="JournalID">467</identifier><identifier type="IssueArticleCount">29</identifier><identifier type="VolumeIssueCount">6</identifier><part><date>1990</date><detail type="volume"><number>4</number><caption>vol.</caption></detail><detail type="issue"><number>6</number><caption>no.</caption></detail><extent unit="pages"><start>654</start><end>662</end></extent></part><recordInfo><recordOrigin>IPNA, 1990</recordOrigin></recordInfo></relatedItem><identifier type="istex">F429FF95D9939F5170958E1DA433CE81EAACCEFF</identifier><identifier type="DOI">10.1007/BF00858645</identifier><identifier type="ArticleID">Art21</identifier><identifier type="ArticleID">BF00858645</identifier><accessCondition type="use and reproduction" contentType="copyright">IPNA</accessCondition><recordInfo><recordContentSource>SPRINGER</recordContentSource><recordOrigin>IPNA, 1990</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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