<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/NCT01660308</url>
  </required_header>
  <id_info>
    <org_study_id>201105045RC</org_study_id>
    <nct_id>NCT01660308</nct_id>
  </id_info>
  <brief_title>Observing the Changes of Fibroblast Growth Factor 23 in Patients of Tumor Induced Osteomalacia</brief_title>
  <official_title>Observing the Changes of Fibroblast Growth Factor 23 in Patients of Tumor Induced Osteomalacia</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>National Taiwan University Hospital</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>National Taiwan University Hospital</source>
  <oversight_info>
    <has_dmc>No</has_dmc>
  </oversight_info>
  <brief_summary>
    <textblock>
      Fibroblast froth factors (FGFs) are humoral factors identified by their ability to stimulate&#xD;
      cell proliferation1. They play different roles in the regulation of cell proliferation,&#xD;
      differentiation and function. Most FGF family members act as paracrine factors. But&#xD;
      FGF19(FGF19) subfamily members, including FGF19, 21, and 23, work as endocrine factors to&#xD;
      regulate bile acid, carbohydrate and phosphate metabolism2. Of these, FGF23 plays an&#xD;
      important role in phosphate and bone metabolism3. FGF23 gene encodes 251 amino acids,&#xD;
      including a 24-amino acid signal peptide4. The secreted FGF23 is a protein consisted of 227&#xD;
      amino acids. It works by binding to a Klotho-FGF receptor 1c (FGF1c) complex5. FGF suppresses&#xD;
      the expression of type 2a and 2c sodium-phosphate cotransporters, which mediate phosphate&#xD;
      reabsorption in proximal tubules.6 FGF23 decreases 25-hydroxyvitamin D-1α-hydroxylase&#xD;
      expression and enhances 25-hydroxyvitamin D-24-hydroxylase expression6. Therefore, FGF23&#xD;
      reduces serum 1,25-dihydroxyvitamin D〔1,25(OH)2D〕, which stimulates intestinal calcium and&#xD;
      phosphate absorption. FGF23 decreases serum phosphate through the above mechanisms FGF23&#xD;
      over-expression might result in hypophosphatemic rickets and osteomalacia.&#xD;
&#xD;
      Tumor induced osteomalacia (TIO) is a paraneoplastic syndrome usually caused by benign&#xD;
      phosphaturic mesenchymal tumors. Symptoms are nonspecific, such as general weakness, fatigue,&#xD;
      and bone pain. Sometimes fracture may occurs. The responsible tumors are sometimes small and&#xD;
      difficult to detect. Tumors secrete FGF23. FGF23 reduced phosphate reabsorption in the&#xD;
      proximal tubules and decrease 1,25(OH)2D levels, which result in hypophosphatemia and then&#xD;
      osteomalacia.&#xD;
&#xD;
      The investigators would like to observe the changes of FGF23 in patients who receive&#xD;
      operation or medical treatment and hope this will benefit future treatment.&#xD;
    </textblock>
  </brief_summary>
  <overall_status>Unknown status</overall_status>
  <last_known_status>Recruiting</last_known_status>
  <start_date>June 2011</start_date>
  <completion_date type="Anticipated">August 2016</completion_date>
  <primary_completion_date type="Anticipated">August 2016</primary_completion_date>
  <study_type>Observational</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <observational_model>Case-Control</observational_model>
    <time_perspective>Prospective</time_perspective>
  </study_design_info>
  <primary_outcome>
    <measure>FGF23, P</measure>
    <time_frame>at the time TIO is diagnosed</time_frame>
  </primary_outcome>
  <number_of_groups>1</number_of_groups>
  <enrollment type="Anticipated">40</enrollment>
  <condition>Hypophosphatemia</condition>
  <arm_group>
    <arm_group_label>Tumor induced osteomalcia</arm_group_label>
  </arm_group>
  <eligibility>
    <study_pop>
      <textblock>
        Patients with tumor induced osteomalacia and people without osteomalacia&#xD;
      </textblock>
    </study_pop>
    <sampling_method>Non-Probability Sample</sampling_method>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  patients with tumor induced osteomalacia.&#xD;
&#xD;
          -  people without osteomalacia such as healthy people,&#xD;
&#xD;
          -  people under dialysis,&#xD;
&#xD;
          -  people with poor nutrition.&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  people younger than 20 years old or older than 85 years old.&#xD;
&#xD;
          -  people who are pregnant.&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>20 Years</minimum_age>
    <maximum_age>85 Years</maximum_age>
    <healthy_volunteers>Accepts Healthy Volunteers</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>Shyang-Rong Shih, PhD</last_name>
    <role>Principal Investigator</role>
    <affiliation>National Taiwan University Hospital</affiliation>
  </overall_official>
  <overall_contact>
    <last_name>Shyang-Rong Shih, PhD</last_name>
    <email>srshih@ntu.edu.tw</email>
  </overall_contact>
  <location>
    <facility>
      <name>National Taiwan University Hospital</name>
      <address>
        <city>Taipei</city>
        <country>Taiwan</country>
      </address>
    </facility>
    <status>Recruiting</status>
    <contact>
      <last_name>Shyang-Rong Shih, PhD</last_name>
      <phone>886-972653337</phone>
      <email>srshih@ntu.edu.tw</email>
    </contact>
    <investigator>
      <last_name>Shyang-Rong Shih, PhD</last_name>
      <role>Principal Investigator</role>
    </investigator>
  </location>
  <location_countries>
    <country>Taiwan</country>
  </location_countries>
  <verification_date>July 2016</verification_date>
  <study_first_submitted>August 5, 2012</study_first_submitted>
  <study_first_submitted_qc>August 7, 2012</study_first_submitted_qc>
  <study_first_posted type="Estimate">August 8, 2012</study_first_posted>
  <last_update_submitted>July 4, 2016</last_update_submitted>
  <last_update_submitted_qc>July 4, 2016</last_update_submitted_qc>
  <last_update_posted type="Estimate">July 6, 2016</last_update_posted>
  <responsible_party>
    <responsible_party_type>Sponsor</responsible_party_type>
  </responsible_party>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Osteomalacia</mesh_term>
    <mesh_term>Hypophosphatemia</mesh_term>
  </condition_browse>
  <!-- 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/NCT01660308
org study id: 201105045RC
nct id: NCT01660308
lead sponsor: 
has dmc: No
Fibroblast froth factors (FGFs) are humoral factors identified by their ability to stimulate
      cell proliferation1. They play different roles in the regulation of cell proliferation,
      differentiation and function. Most FGF family members act as paracrine factors. But
      FGF19(FGF19) subfamily members, including FGF19, 21, and 23, work as endocrine factors to
      regulate bile acid, carbohydrate and phosphate metabolism2. Of these, FGF23 plays an
      important role in phosphate and bone metabolism3. FGF23 gene encodes 251 amino acids,
      including a 24-amino acid signal peptide4. The secreted FGF23 is a protein consisted of 227
      amino acids. It works by binding to a Klotho-FGF receptor 1c (FGF1c) complex5. FGF suppresses
      the expression of type 2a and 2c sodium-phosphate cotransporters, which mediate phosphate
      reabsorption in proximal tubules.6 FGF23 decreases 25-hydroxyvitamin D-1α-hydroxylase
      expression and enhances 25-hydroxyvitamin D-24-hydroxylase expression6. Therefore, FGF23
      reduces serum 1,25-dihydroxyvitamin D〔1,25(OH)2D〕, which stimulates intestinal calcium and
      phosphate absorption. FGF23 decreases serum phosphate through the above mechanisms FGF23
      over-expression might result in hypophosphatemic rickets and osteomalacia.

      Tumor induced osteomalacia (TIO) is a paraneoplastic syndrome usually caused by benign
      phosphaturic mesenchymal tumors. Symptoms are nonspecific, such as general weakness, fatigue,
      and bone pain. Sometimes fracture may occurs. The responsible tumors are sometimes small and
      difficult to detect. Tumors secrete FGF23. FGF23 reduced phosphate reabsorption in the
      proximal tubules and decrease 1,25(OH)2D levels, which result in hypophosphatemia and then
      osteomalacia.

      The investigators would like to observe the changes of FGF23 in patients who receive
      operation or medical treatment and hope this will benefit future treatment.
observational model: Case-Control
time perspective: Prospective
measure: FGF23, P
time frame: at the time TIO is diagnosed
arm group label: Tumor induced osteomalcia
study pop: 
sampling method: Non-Probability Sample
criteria: 
gender: All
minimum age: 20 Years
maximum age: 85 Years
healthy volunteers: Accepts Healthy Volunteers
last name: Shyang-Rong Shih, PhD
role: Principal Investigator
affiliation: National Taiwan University Hospital
last name: Shyang-Rong Shih, PhD
email: srshih@ntu.edu.tw
facility: 
status: Recruiting
contact: 
investigator: 
country: Taiwan
responsible party type: Sponsor
mesh term: Osteomalacia
mesh term: Hypophosphatemia