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Growth hormone effects on cortical bone dimensions in young adults with childhood-onset growth hormone deficiency

Identifieur interne : 000C62 ( Pmc/Curation ); précédent : 000C61; suivant : 000C63

Growth hormone effects on cortical bone dimensions in young adults with childhood-onset growth hormone deficiency

Auteurs : L. Hyldstrup [Danemark] ; G. S. Conway [Royaume-Uni] ; K. Racz [Hongrie] ; A. Keller [Allemagne] ; P. Chanson [France] ; M. Zacharin ; A. L. Lysgaard [Danemark] ; A. H. Andreasen [Danemark] ; A.-M. Kappelgaard [Danemark]

Source :

RBID : PMC:3406313

Abstract

Summary

Growth hormone (GH) treatment in young adults with childhood-onset GH deficiency has beneficial effects on bone mass. The present study shows that cortical bone dimensions also benefit from GH treatment, with endosteal expansion and increased cortical thickness leading to improved bone strength.

Introduction

In young adults with childhood-onset growth hormone deficiency (CO GHD), GH treatment after final height is reached has been shown to have beneficial effects on spine and hip bone mineral density. The objective of the study was to evaluate the influence of GH on cortical bone dimensions.

Methods

Patients (n = 160; mean age, 21.2 years; 63% males) with CO GHD were randomised 2:1 to GH or no treatment for 24 months. Cortical bone dimensions were evaluated by digital x-ray radiogrammetry of the metacarpal bones every 6 months.

Results

After 24 months, cortical thickness was increased compared with the controls (6.43%, CI 3.34 to 9.61%; p = 0.0001) and metacarpal index (MCI) (6.14%, CI 3.95 to 8.38%; p < 0.0001), while the endosteal diameter decreased (−4.64%, CI −7.15 to −2.05; p < 0.001). Total bone width did not change significantly (0.68%, CI −1.17 to 2.57%; not significant (NS)). A gender effect was seen on bone width (p < 0.0001), endosteal diameter (p < 0.01) and cortical thickness (p < 0.01), but not with MCI (NS).

Conclusions

Cortical bone reacts promptly to reinstitution of GH beyond the attainment of final height by increasing the cortical thickness through endosteal bone growth. This leads to a higher peak bone mass and may reduce the risk of cortical bone fragility later in life.


Url:
DOI: 10.1007/s00198-011-1854-0
PubMed: 22124576
PubMed Central: 3406313

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M. Zacharin
<affiliation>
<nlm:aff id="Aff6">Department of Endocrinology and Diabetes, Royal Children’s Hospital, Parkville, VIC Australia</nlm:aff>
<wicri:noCountry code="subfield">VIC Australia</wicri:noCountry>
</affiliation>

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<title>Summary</title>
<p>Growth hormone (GH) treatment in young adults with childhood-onset GH deficiency has beneficial effects on bone mass. The present study shows that cortical bone dimensions also benefit from GH treatment, with endosteal expansion and increased cortical thickness leading to improved bone strength.</p>
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<sec>
<title>Introduction</title>
<p>In young adults with childhood-onset growth hormone deficiency (CO GHD), GH treatment after final height is reached has been shown to have beneficial effects on spine and hip bone mineral density. The objective of the study was to evaluate the influence of GH on cortical bone dimensions.</p>
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<p>Patients (
<italic>n</italic>
 = 160; mean age, 21.2 years; 63% males) with CO GHD were randomised 2:1 to GH or no treatment for 24 months. Cortical bone dimensions were evaluated by digital x-ray radiogrammetry of the metacarpal bones every 6 months.</p>
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<sec>
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<p>After 24 months, cortical thickness was increased compared with the controls (6.43%, CI 3.34 to 9.61%;
<italic>p</italic>
 = 0.0001) and metacarpal index (MCI) (6.14%, CI 3.95 to 8.38%;
<italic>p</italic>
 < 0.0001), while the endosteal diameter decreased (−4.64%, CI −7.15 to −2.05;
<italic>p</italic>
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<italic>p</italic>
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<p>Cortical bone reacts promptly to reinstitution of GH beyond the attainment of final height by increasing the cortical thickness through endosteal bone growth. This leads to a higher peak bone mass and may reduce the risk of cortical bone fragility later in life.</p>
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</TEI>
<pmc article-type="research-article">
<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">Osteoporos Int</journal-id>
<journal-id journal-id-type="iso-abbrev">Osteoporos Int</journal-id>
<journal-title-group>
<journal-title>Osteoporosis International</journal-title>
</journal-title-group>
<issn pub-type="ppub">0937-941X</issn>
<issn pub-type="epub">1433-2965</issn>
<publisher>
<publisher-name>Springer-Verlag</publisher-name>
<publisher-loc>London</publisher-loc>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">22124576</article-id>
<article-id pub-id-type="pmc">3406313</article-id>
<article-id pub-id-type="publisher-id">1854</article-id>
<article-id pub-id-type="doi">10.1007/s00198-011-1854-0</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Original Article</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Growth hormone effects on cortical bone dimensions in young adults with childhood-onset growth hormone deficiency</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author" corresp="yes">
<name>
<surname>Hyldstrup</surname>
<given-names>L.</given-names>
</name>
<address>
<phone>+45-3862-2290</phone>
<fax>+45-3862-3640</fax>
<email>hyld@dadlnet.dk</email>
</address>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Conway</surname>
<given-names>G. S.</given-names>
</name>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Racz</surname>
<given-names>K.</given-names>
</name>
<xref ref-type="aff" rid="Aff3">3</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Keller</surname>
<given-names>A.</given-names>
</name>
<xref ref-type="aff" rid="Aff4">4</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Chanson</surname>
<given-names>P.</given-names>
</name>
<xref ref-type="aff" rid="Aff5">5</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Zacharin</surname>
<given-names>M.</given-names>
</name>
<xref ref-type="aff" rid="Aff6">6</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Lysgaard</surname>
<given-names>A. L.</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Andreasen</surname>
<given-names>A. H.</given-names>
</name>
<xref ref-type="aff" rid="Aff7">7</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Kappelgaard</surname>
<given-names>A.-M.</given-names>
</name>
<xref ref-type="aff" rid="Aff7">7</xref>
</contrib>
<aff id="Aff1">
<label>1</label>
Department of Endocrinology (541), Hvidovre University Hospital, DK-2650 Hvidovre, Denmark</aff>
<aff id="Aff2">
<label>2</label>
Department of Endocrinology and Diabetes, University College London Hospitals, London, UK</aff>
<aff id="Aff3">
<label>3</label>
2nd Department of Medicine, Semmelweis University, Budapest, Hungary</aff>
<aff id="Aff4">
<label>4</label>
Children’s Hospital, University of Leipzig, Leipzig, Germany</aff>
<aff id="Aff5">
<label>5</label>
Service d’Endocrinologie et des Maladies de la Reproduction, and Centre de Référence des Maladies Endocriniennes Rares de la Croissance, Assistance-Publique Hôpitaux de Paris, Hôpital de Bicêtre, University Paris-Sud, Le Kremlin-Bicêtre, France</aff>
<aff id="Aff6">
<label>6</label>
Department of Endocrinology and Diabetes, Royal Children’s Hospital, Parkville, VIC Australia</aff>
<aff id="Aff7">
<label>7</label>
GHT Medical Affairs, Global Marketing, Novo Nordisk, Bagsvaerd, Denmark</aff>
</contrib-group>
<pub-date pub-type="epub">
<day>29</day>
<month>11</month>
<year>2011</year>
</pub-date>
<pub-date pub-type="pmc-release">
<day>29</day>
<month>11</month>
<year>2011</year>
</pub-date>
<pub-date pub-type="ppub">
<month>8</month>
<year>2012</year>
</pub-date>
<volume>23</volume>
<issue>8</issue>
<fpage>2219</fpage>
<lpage>2226</lpage>
<history>
<date date-type="received">
<day>11</day>
<month>8</month>
<year>2011</year>
</date>
<date date-type="accepted">
<day>26</day>
<month>10</month>
<year>2011</year>
</date>
</history>
<permissions>
<copyright-statement>© The Author(s) 2011</copyright-statement>
</permissions>
<abstract id="Abs1">
<sec>
<title>Summary</title>
<p>Growth hormone (GH) treatment in young adults with childhood-onset GH deficiency has beneficial effects on bone mass. The present study shows that cortical bone dimensions also benefit from GH treatment, with endosteal expansion and increased cortical thickness leading to improved bone strength.</p>
</sec>
<sec>
<title>Introduction</title>
<p>In young adults with childhood-onset growth hormone deficiency (CO GHD), GH treatment after final height is reached has been shown to have beneficial effects on spine and hip bone mineral density. The objective of the study was to evaluate the influence of GH on cortical bone dimensions.</p>
</sec>
<sec>
<title>Methods</title>
<p>Patients (
<italic>n</italic>
 = 160; mean age, 21.2 years; 63% males) with CO GHD were randomised 2:1 to GH or no treatment for 24 months. Cortical bone dimensions were evaluated by digital x-ray radiogrammetry of the metacarpal bones every 6 months.</p>
</sec>
<sec>
<title>Results</title>
<p>After 24 months, cortical thickness was increased compared with the controls (6.43%, CI 3.34 to 9.61%;
<italic>p</italic>
 = 0.0001) and metacarpal index (MCI) (6.14%, CI 3.95 to 8.38%;
<italic>p</italic>
 < 0.0001), while the endosteal diameter decreased (−4.64%, CI −7.15 to −2.05;
<italic>p</italic>
 < 0.001). Total bone width did not change significantly (0.68%, CI −1.17 to 2.57%; not significant (NS)). A gender effect was seen on bone width (
<italic>p</italic>
 < 0.0001), endosteal diameter (
<italic>p</italic>
 < 0.01) and cortical thickness (
<italic>p</italic>
 < 0.01), but not with MCI (NS).</p>
</sec>
<sec>
<title>Conclusions</title>
<p>Cortical bone reacts promptly to reinstitution of GH beyond the attainment of final height by increasing the cortical thickness through endosteal bone growth. This leads to a higher peak bone mass and may reduce the risk of cortical bone fragility later in life.</p>
</sec>
</abstract>
<kwd-group xml:lang="en">
<title>Keywords</title>
<kwd>Bone strength</kwd>
<kwd>Cortical bone</kwd>
<kwd>Growth hormone deficiency</kwd>
<kwd>Growth hormone treatment</kwd>
<kwd>Metacarpal index</kwd>
</kwd-group>
<custom-meta-group>
<custom-meta>
<meta-name>issue-copyright-statement</meta-name>
<meta-value>© International Osteoporosis Foundation and National Osteoporosis Foundation 2012</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
</record>

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