<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT03229395</url>
  </required_header>
  <id_info>
    <org_study_id>UCL-MYOSECRET 2014-1</org_study_id>
    <nct_id>NCT03229395</nct_id>
  </id_info>
  <brief_title>Alterations of Muscle Secretome Associated With Muscle Atrophy Caused by Glucocorticoids</brief_title>
  <acronym>MYOSECRET</acronym>
  <official_title>Alterations of Muscle Secretome Associated With Muscle Atrophy Caused by Glucocorticoids</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Cliniques universitaires Saint-Luc- Université Catholique de Louvain</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Cliniques universitaires Saint-Luc- Université Catholique de Louvain</source>
  <oversight_info>
    <has_dmc>No</has_dmc>
  </oversight_info>
  <brief_summary>
    <textblock>
      Several studies have shown that lean mass, in particular muscle mass, is an excellent&#xD;
      predictive survival factor in many diseases. A better knowledge of the mechanisms responsible&#xD;
      for muscle atrophy and the identification of atrophic process markers are deeply needed for&#xD;
      the development of new anti-atrophic therapies. Either as drugs used to treat several medical&#xD;
      conditions or as endocrine hormones released in response to many stress situations (e.g.,&#xD;
      sepsis, cancer, insulinopenia…), glucocorticoids (GC) are recognized to play a major role in&#xD;
      skeletal muscle atrophy. Indeed, the inhibition of GC action by a receptor antagonist (RU486)&#xD;
      or by muscle-specific invalidation of the GC receptor inhibits the muscle atrophy in these&#xD;
      stress situations. Therefore, all these data clearly indicate that GC play a major role in&#xD;
      skeletal muscle atrophy observed in several conditions. Emerging evidence has revealed that&#xD;
      the skeletal muscle has a secretory function. Human skeletal muscle secretome was first&#xD;
      estimated at about 300 proteins by computational analysis and proteomic analysis have&#xD;
      recently confirmed these results. Some of these secreted proteins, conceptualized as&#xD;
      myokines, can act locally on muscle cells through autocrine/paracrine loops and on&#xD;
      surrounding tissues such as muscle blood vessels or can be released into the blood stream to&#xD;
      produce systemic effects. One prominent example is interleukin (IL)-6 which is released into&#xD;
      circulation by contracting skeletal muscle and can regulate metabolic and inflammatory&#xD;
      processes. As IL-6, several other potential myokines have been identified including IL-8,&#xD;
      IL-15, insulin-growth factor I (IGF-I), follistatin-like 1 (FSTL1) or fibroblast-growth&#xD;
      factor (FGF)-21. Moreover, secreted proteins may also reflected metabolic changes which take&#xD;
      place in muscle cells. Indeed, myoblast differentiation is accompanied by dramatic changes in&#xD;
      the secreted proteins profile as increased expression of Semaphorins, IGF-I, matrix&#xD;
      metalloproteinase (MMP)-2 or Collagens. Thereby, the investigators hypothesized that skeletal&#xD;
      muscle atrophy induced by GC is associated with specific alterations of the muscle secretome.&#xD;
      The aim of this project is to identify the GC-induced changes in the secretome of human&#xD;
      skeletal muscle cells in culture (in vitro approach) and to determine how these changes&#xD;
      translate into the circulation of subjects exposed to high concentrations of GC (Cushing's&#xD;
      syndrome) (in vivo approach). Characterization of these changes in human subjects should&#xD;
      allow to better understand the cellular mechanisms involved in muscle atrophy and might lead&#xD;
      to identify circulating biomarkers associated with skeletal muscle atrophy, as telopeptides&#xD;
      are for bone tissue.&#xD;
    </textblock>
  </brief_summary>
  <overall_status>Completed</overall_status>
  <start_date type="Actual">January 2, 2014</start_date>
  <completion_date type="Actual">July 18, 2017</completion_date>
  <primary_completion_date type="Actual">July 13, 2017</primary_completion_date>
  <study_type>Observational</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <observational_model>Other</observational_model>
    <time_perspective>Prospective</time_perspective>
  </study_design_info>
  <primary_outcome>
    <measure>Measurement of BMI in kg/m^2</measure>
    <time_frame>1 day (one assessment at diagnosis)</time_frame>
    <description>Measurement of weight in kilograms and height in meters to determine BMI as BMI=weight/height^2</description>
  </primary_outcome>
  <primary_outcome>
    <measure>Evaluation of quality of life of Cushing's patients</measure>
    <time_frame>1 day (one assessment at diagnosis)</time_frame>
    <description>The CushingQoL questionnaire was used to evaluate quality of life of Cushing's patients</description>
  </primary_outcome>
  <primary_outcome>
    <measure>Measure of body lean mass of Cushing's and control patients</measure>
    <time_frame>1 day (one assessment at diagnosis)</time_frame>
    <description>Bioelectrical Impedance Vector Analysis (BIA) was used for evaluation of lean and fat mass.</description>
  </primary_outcome>
  <primary_outcome>
    <measure>Muscle strenght measurement of Cushing's and control patients</measure>
    <time_frame>1 day (one assessment at diagnosis)</time_frame>
    <description>Evalutation by dynamometer &quot;Jamar type&quot;</description>
  </primary_outcome>
  <primary_outcome>
    <measure>Measurement of Mid-arm muscle circumference (MAMC, cm)</measure>
    <time_frame>1 day (one assessment at diagnosis)</time_frame>
    <description>Measurement of triceps skinfold thickness (TSF, in cm), and midarm circumference (MAC, in cm) to determine the MAMC according to the following formula: MAMC= MAC - (Pi x TSF).&#xD;
MAMC is a bedside anthropometric measurement that estimates somatic protein reserve, an early indicator of nutritional depletion.</description>
  </primary_outcome>
  <primary_outcome>
    <measure>Evaluation of daily energy expenditure (DEE) of Cushing's and control patients</measure>
    <time_frame>1 day (one assessment at diagnosis)</time_frame>
    <description>Evaluation of DEE by completing the QAPSE questionnaire.</description>
  </primary_outcome>
  <number_of_groups>2</number_of_groups>
  <enrollment type="Actual">35</enrollment>
  <condition>Cushing Syndrome</condition>
  <arm_group>
    <arm_group_label>patients with Cushing's syndrome</arm_group_label>
    <description>Patients were selected by the PI at the diagnosis.</description>
  </arm_group>
  <arm_group>
    <arm_group_label>control patients</arm_group_label>
    <description>Selected patients are matched for age and sex.</description>
  </arm_group>
  <biospec_retention>Samples With DNA</biospec_retention>
  <biospec_descr>
    <textblock>
      blood&#xD;
    </textblock>
  </biospec_descr>
  <eligibility>
    <study_pop>
      <textblock>
        Patients with Cushing's syndrome are caracterised by elevated circulating glucocorticoid&#xD;
        levels generally due to a pitiutary or adrenal adenoma. These patients were compared to&#xD;
        heathly control patients who are matched for age and sex.&#xD;
      </textblock>
    </study_pop>
    <sampling_method>Probability Sample</sampling_method>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  Pituitary or adrenal endogenous Cushing's syndrome formally demonstrated by the&#xD;
             standard endocrinological assessment&#xD;
&#xD;
          -  New diagnosis or recurrence or persistent Cushing's syndrome after pituitary surgery&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  Pseudo Cushing's syndrome&#xD;
&#xD;
          -  Paraneoplasic Cushing's syndrome&#xD;
&#xD;
          -  Cyclic Cushing's syndrome&#xD;
&#xD;
          -  Adrenocortical carcinoma&#xD;
&#xD;
          -  Pituitary irradiation during the last six months&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>18 Years</minimum_age>
    <maximum_age>N/A</maximum_age>
    <healthy_volunteers>Accepts Healthy Volunteers</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>Marie De Barsy, Nurse</last_name>
    <role>Study Chair</role>
    <affiliation>Cliniques Universitaires St Luc</affiliation>
  </overall_official>
  <location>
    <facility>
      <name>De Barsy Marie</name>
      <address>
        <city>Brussels</city>
        <zip>1200</zip>
        <country>Belgium</country>
      </address>
    </facility>
  </location>
  <location_countries>
    <country>Belgium</country>
  </location_countries>
  <reference>
    <citation>Pedersen BK. Muscle as a secretory organ. Compr Physiol. 2013 Jul;3(3):1337-62. doi: 10.1002/cphy.c120033.</citation>
    <PMID>23897689</PMID>
  </reference>
  <reference>
    <citation>Schakman O, Kalista S, Barbe C, Loumaye A, Thissen JP. Glucocorticoid-induced skeletal muscle atrophy. Int J Biochem Cell Biol. 2013 Oct;45(10):2163-72. doi: 10.1016/j.biocel.2013.05.036. Epub 2013 Jun 24.</citation>
    <PMID>23806868</PMID>
  </reference>
  <reference>
    <citation>Stastna M, Van Eyk JE. Secreted proteins as a fundamental source for biomarker discovery. Proteomics. 2012 Feb;12(4-5):722-35. doi: 10.1002/pmic.201100346. Epub 2012 Jan 19.</citation>
    <PMID>22247067</PMID>
  </reference>
  <results_reference>
    <citation>Baracos VE, Reiman T, Mourtzakis M, Gioulbasanis I, Antoun S. Body composition in patients with non-small cell lung cancer: a contemporary view of cancer cachexia with the use of computed tomography image analysis. Am J Clin Nutr. 2010 Apr;91(4):1133S-1137S. doi: 10.3945/ajcn.2010.28608C. Epub 2010 Feb 17.</citation>
    <PMID>20164322</PMID>
  </results_reference>
  <results_reference>
    <citation>Bortoluzzi S, Scannapieco P, Cestaro A, Danieli GA, Schiaffino S. Computational reconstruction of the human skeletal muscle secretome. Proteins. 2006 Mar 15;62(3):776-92. doi: 10.1002/prot.20803.</citation>
    <PMID>16342272</PMID>
  </results_reference>
  <results_reference>
    <citation>Braun TP, Grossberg AJ, Krasnow SM, Levasseur PR, Szumowski M, Zhu XX, Maxson JE, Knoll JG, Barnes AP, Marks DL. Cancer- and endotoxin-induced cachexia require intact glucocorticoid signaling in skeletal muscle. FASEB J. 2013 Sep;27(9):3572-82. doi: 10.1096/fj.13-230375. Epub 2013 Jun 3.</citation>
    <PMID>23733748</PMID>
  </results_reference>
  <results_reference>
    <citation>Gueugneau M, Coudy-Gandilhon C, Theron L, Meunier B, Barboiron C, Combaret L, Taillandier D, Polge C, Attaix D, Picard B, Verney J, Roche F, Feasson L, Barthelemy JC, Bechet D. Skeletal muscle lipid content and oxidative activity in relation to muscle fiber type in aging and metabolic syndrome. J Gerontol A Biol Sci Med Sci. 2015 May;70(5):566-76. doi: 10.1093/gerona/glu086. Epub 2014 Jun 17.</citation>
    <PMID>24939997</PMID>
  </results_reference>
  <results_reference>
    <citation>Henningsen J, Rigbolt KT, Blagoev B, Pedersen BK, Kratchmarova I. Dynamics of the skeletal muscle secretome during myoblast differentiation. Mol Cell Proteomics. 2010 Nov;9(11):2482-96. doi: 10.1074/mcp.M110.002113. Epub 2010 Jul 14.</citation>
    <PMID>20631206</PMID>
  </results_reference>
  <results_reference>
    <citation>Hu Z, Wang H, Lee IH, Du J, Mitch WE. Endogenous glucocorticoids and impaired insulin signaling are both required to stimulate muscle wasting under pathophysiological conditions in mice. J Clin Invest. 2009 Oct;119(10):3059-69. doi: 10.1172/JCI38770. Epub 2009 Sep 14.</citation>
    <PMID>19759515</PMID>
  </results_reference>
  <results_reference>
    <citation>Le Bihan MC, Bigot A, Jensen SS, Dennis JL, Rogowska-Wrzesinska A, Laine J, Gache V, Furling D, Jensen ON, Voit T, Mouly V, Coulton GR, Butler-Browne G. In-depth analysis of the secretome identifies three major independent secretory pathways in differentiating human myoblasts. J Proteomics. 2012 Dec 21;77:344-56. doi: 10.1016/j.jprot.2012.09.008. Epub 2012 Sep 20.</citation>
    <PMID>23000592</PMID>
  </results_reference>
  <results_reference>
    <citation>Mourtzakis M, Prado CM, Lieffers JR, Reiman T, McCargar LJ, Baracos VE. A practical and precise approach to quantification of body composition in cancer patients using computed tomography images acquired during routine care. Appl Physiol Nutr Metab. 2008 Oct;33(5):997-1006. doi: 10.1139/H08-075.</citation>
    <PMID>18923576</PMID>
  </results_reference>
  <results_reference>
    <citation>Neves M Jr, Barreto G, Boobis L, Harris R, Roschel H, Tricoli V, Ugrinowitsch C, Negrao C, Gualano B. Incidence of adverse events associated with percutaneous muscular biopsy among healthy and diseased subjects. Scand J Med Sci Sports. 2012 Apr;22(2):175-8. doi: 10.1111/j.1600-0838.2010.01264.x. Epub 2011 Mar 10.</citation>
    <PMID>21392121</PMID>
  </results_reference>
  <results_reference>
    <citation>Piccoli A. Patterns of bioelectrical impedance vector analysis: learning from electrocardiography and forgetting electric circuit models. Nutrition. 2002 Jun;18(6):520-1. doi: 10.1016/s0899-9007(02)00771-2. No abstract available.</citation>
    <PMID>12044826</PMID>
  </results_reference>
  <results_reference>
    <citation>Schakman O, Dehoux M, Bouchuari S, Delaere S, Lause P, Decroly N, Shoelson SE, Thissen JP. Role of IGF-I and the TNFalpha/NF-kappaB pathway in the induction of muscle atrogenes by acute inflammation. Am J Physiol Endocrinol Metab. 2012 Sep 15;303(6):E729-39. doi: 10.1152/ajpendo.00060.2012. Epub 2012 Jun 26.</citation>
    <PMID>22739109</PMID>
  </results_reference>
  <results_reference>
    <citation>Webb SM, Badia X, Barahona MJ, Colao A, Strasburger CJ, Tabarin A, van Aken MO, Pivonello R, Stalla G, Lamberts SW, Glusman JE. Evaluation of health-related quality of life in patients with Cushing's syndrome with a new questionnaire. Eur J Endocrinol. 2008 May;158(5):623-30. doi: 10.1530/EJE-07-0762.</citation>
    <PMID>18426820</PMID>
  </results_reference>
  <verification_date>December 2016</verification_date>
  <study_first_submitted>December 21, 2016</study_first_submitted>
  <study_first_submitted_qc>July 24, 2017</study_first_submitted_qc>
  <study_first_posted type="Actual">July 25, 2017</study_first_posted>
  <last_update_submitted>July 24, 2017</last_update_submitted>
  <last_update_submitted_qc>July 24, 2017</last_update_submitted_qc>
  <last_update_posted type="Actual">July 25, 2017</last_update_posted>
  <responsible_party>
    <responsible_party_type>Sponsor</responsible_party_type>
  </responsible_party>
  <keyword>skeletal muscle</keyword>
  <keyword>muscle mass</keyword>
  <keyword>glucocorticoids</keyword>
  <keyword>biomarkers</keyword>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Muscular Atrophy</mesh_term>
    <mesh_term>Cushing Syndrome</mesh_term>
    <mesh_term>Atrophy</mesh_term>
  </condition_browse>
  <patient_data>
    <sharing_ipd>No</sharing_ipd>
  </patient_data>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT03229395
org study id: UCL-MYOSECRET 2014-1
nct id: NCT03229395
lead sponsor: 
has dmc: No
Several studies have shown that lean mass, in particular muscle mass, is an excellent
      predictive survival factor in many diseases. A better knowledge of the mechanisms responsible
      for muscle atrophy and the identification of atrophic process markers are deeply needed for
      the development of new anti-atrophic therapies. Either as drugs used to treat several medical
      conditions or as endocrine hormones released in response to many stress situations (e.g.,
      sepsis, cancer, insulinopenia…), glucocorticoids (GC) are recognized to play a major role in
      skeletal muscle atrophy. Indeed, the inhibition of GC action by a receptor antagonist (RU486)
      or by muscle-specific invalidation of the GC receptor inhibits the muscle atrophy in these
      stress situations. Therefore, all these data clearly indicate that GC play a major role in
      skeletal muscle atrophy observed in several conditions. Emerging evidence has revealed that
      the skeletal muscle has a secretory function. Human skeletal muscle secretome was first
      estimated at about 300 proteins by computational analysis and proteomic analysis have
      recently confirmed these results. Some of these secreted proteins, conceptualized as
      myokines, can act locally on muscle cells through autocrine/paracrine loops and on
      surrounding tissues such as muscle blood vessels or can be released into the blood stream to
      produce systemic effects. One prominent example is interleukin (IL)-6 which is released into
      circulation by contracting skeletal muscle and can regulate metabolic and inflammatory
      processes. As IL-6, several other potential myokines have been identified including IL-8,
      IL-15, insulin-growth factor I (IGF-I), follistatin-like 1 (FSTL1) or fibroblast-growth
      factor (FGF)-21. Moreover, secreted proteins may also reflected metabolic changes which take
      place in muscle cells. Indeed, myoblast differentiation is accompanied by dramatic changes in
      the secreted proteins profile as increased expression of Semaphorins, IGF-I, matrix
      metalloproteinase (MMP)-2 or Collagens. Thereby, the investigators hypothesized that skeletal
      muscle atrophy induced by GC is associated with specific alterations of the muscle secretome.
      The aim of this project is to identify the GC-induced changes in the secretome of human
      skeletal muscle cells in culture (in vitro approach) and to determine how these changes
      translate into the circulation of subjects exposed to high concentrations of GC (Cushing's
      syndrome) (in vivo approach). Characterization of these changes in human subjects should
      allow to better understand the cellular mechanisms involved in muscle atrophy and might lead
      to identify circulating biomarkers associated with skeletal muscle atrophy, as telopeptides
      are for bone tissue.
observational model: Other
time perspective: Prospective
measure: Measurement of BMI in kg/m^2
time frame: 1 day (one assessment at diagnosis)
description: Measurement of weight in kilograms and height in meters to determine BMI as BMI=weight/height^2
measure: Evaluation of quality of life of Cushing's patients
time frame: 1 day (one assessment at diagnosis)
description: The CushingQoL questionnaire was used to evaluate quality of life of Cushing's patients
measure: Measure of body lean mass of Cushing's and control patients
time frame: 1 day (one assessment at diagnosis)
description: Bioelectrical Impedance Vector Analysis (BIA) was used for evaluation of lean and fat mass.
measure: Muscle strenght measurement of Cushing's and control patients
time frame: 1 day (one assessment at diagnosis)
description: Evalutation by dynamometer "Jamar type"
measure: Measurement of Mid-arm muscle circumference (MAMC, cm)
time frame: 1 day (one assessment at diagnosis)
description: Measurement of triceps skinfold thickness (TSF, in cm), and midarm circumference (MAC, in cm) to determine the MAMC according to the following formula: MAMC= MAC - (Pi x TSF).
MAMC is a bedside anthropometric measurement that estimates somatic protein reserve, an early indicator of nutritional depletion.
measure: Evaluation of daily energy expenditure (DEE) of Cushing's and control patients
time frame: 1 day (one assessment at diagnosis)
description: Evaluation of DEE by completing the QAPSE questionnaire.
arm group label: patients with Cushing's syndrome
description: Patients were selected by the PI at the diagnosis.
arm group label: control patients
description: Selected patients are matched for age and sex.
blood
study pop: 
sampling method: Probability Sample
criteria: 
gender: All
minimum age: 18 Years
maximum age: N/A
healthy volunteers: Accepts Healthy Volunteers
last name: Marie De Barsy, Nurse
role: Study Chair
affiliation: Cliniques Universitaires St Luc
facility: 
country: Belgium
citation: Pedersen BK. Muscle as a secretory organ. Compr Physiol. 2013 Jul;3(3):1337-62. doi: 10.1002/cphy.c120033.
PMID: 23897689
citation: Schakman O, Kalista S, Barbe C, Loumaye A, Thissen JP. Glucocorticoid-induced skeletal muscle atrophy. Int J Biochem Cell Biol. 2013 Oct;45(10):2163-72. doi: 10.1016/j.biocel.2013.05.036. Epub 2013 Jun 24.
PMID: 23806868
citation: Stastna M, Van Eyk JE. Secreted proteins as a fundamental source for biomarker discovery. Proteomics. 2012 Feb;12(4-5):722-35. doi: 10.1002/pmic.201100346. Epub 2012 Jan 19.
PMID: 22247067
citation: Baracos VE, Reiman T, Mourtzakis M, Gioulbasanis I, Antoun S. Body composition in patients with non-small cell lung cancer: a contemporary view of cancer cachexia with the use of computed tomography image analysis. Am J Clin Nutr. 2010 Apr;91(4):1133S-1137S. doi: 10.3945/ajcn.2010.28608C. Epub 2010 Feb 17.
PMID: 20164322
citation: Bortoluzzi S, Scannapieco P, Cestaro A, Danieli GA, Schiaffino S. Computational reconstruction of the human skeletal muscle secretome. Proteins. 2006 Mar 15;62(3):776-92. doi: 10.1002/prot.20803.
PMID: 16342272
citation: Braun TP, Grossberg AJ, Krasnow SM, Levasseur PR, Szumowski M, Zhu XX, Maxson JE, Knoll JG, Barnes AP, Marks DL. Cancer- and endotoxin-induced cachexia require intact glucocorticoid signaling in skeletal muscle. FASEB J. 2013 Sep;27(9):3572-82. doi: 10.1096/fj.13-230375. Epub 2013 Jun 3.
PMID: 23733748
citation: Gueugneau M, Coudy-Gandilhon C, Theron L, Meunier B, Barboiron C, Combaret L, Taillandier D, Polge C, Attaix D, Picard B, Verney J, Roche F, Feasson L, Barthelemy JC, Bechet D. Skeletal muscle lipid content and oxidative activity in relation to muscle fiber type in aging and metabolic syndrome. J Gerontol A Biol Sci Med Sci. 2015 May;70(5):566-76. doi: 10.1093/gerona/glu086. Epub 2014 Jun 17.
PMID: 24939997
citation: Henningsen J, Rigbolt KT, Blagoev B, Pedersen BK, Kratchmarova I. Dynamics of the skeletal muscle secretome during myoblast differentiation. Mol Cell Proteomics. 2010 Nov;9(11):2482-96. doi: 10.1074/mcp.M110.002113. Epub 2010 Jul 14.
PMID: 20631206
citation: Hu Z, Wang H, Lee IH, Du J, Mitch WE. Endogenous glucocorticoids and impaired insulin signaling are both required to stimulate muscle wasting under pathophysiological conditions in mice. J Clin Invest. 2009 Oct;119(10):3059-69. doi: 10.1172/JCI38770. Epub 2009 Sep 14.
PMID: 19759515
citation: Le Bihan MC, Bigot A, Jensen SS, Dennis JL, Rogowska-Wrzesinska A, Laine J, Gache V, Furling D, Jensen ON, Voit T, Mouly V, Coulton GR, Butler-Browne G. In-depth analysis of the secretome identifies three major independent secretory pathways in differentiating human myoblasts. J Proteomics. 2012 Dec 21;77:344-56. doi: 10.1016/j.jprot.2012.09.008. Epub 2012 Sep 20.
PMID: 23000592
citation: Mourtzakis M, Prado CM, Lieffers JR, Reiman T, McCargar LJ, Baracos VE. A practical and precise approach to quantification of body composition in cancer patients using computed tomography images acquired during routine care. Appl Physiol Nutr Metab. 2008 Oct;33(5):997-1006. doi: 10.1139/H08-075.
PMID: 18923576
citation: Neves M Jr, Barreto G, Boobis L, Harris R, Roschel H, Tricoli V, Ugrinowitsch C, Negrao C, Gualano B. Incidence of adverse events associated with percutaneous muscular biopsy among healthy and diseased subjects. Scand J Med Sci Sports. 2012 Apr;22(2):175-8. doi: 10.1111/j.1600-0838.2010.01264.x. Epub 2011 Mar 10.
PMID: 21392121
citation: Piccoli A. Patterns of bioelectrical impedance vector analysis: learning from electrocardiography and forgetting electric circuit models. Nutrition. 2002 Jun;18(6):520-1. doi: 10.1016/s0899-9007(02)00771-2. No abstract available.
PMID: 12044826
citation: Schakman O, Dehoux M, Bouchuari S, Delaere S, Lause P, Decroly N, Shoelson SE, Thissen JP. Role of IGF-I and the TNFalpha/NF-kappaB pathway in the induction of muscle atrogenes by acute inflammation. Am J Physiol Endocrinol Metab. 2012 Sep 15;303(6):E729-39. doi: 10.1152/ajpendo.00060.2012. Epub 2012 Jun 26.
PMID: 22739109
citation: Webb SM, Badia X, Barahona MJ, Colao A, Strasburger CJ, Tabarin A, van Aken MO, Pivonello R, Stalla G, Lamberts SW, Glusman JE. Evaluation of health-related quality of life in patients with Cushing's syndrome with a new questionnaire. Eur J Endocrinol. 2008 May;158(5):623-30. doi: 10.1530/EJE-07-0762.
PMID: 18426820
responsible party type: Sponsor
mesh term: Muscular Atrophy
mesh term: Cushing Syndrome
mesh term: Atrophy
sharing ipd: No