<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/NCT03031925</url>
  </required_header>
  <id_info>
    <org_study_id>PI2017_843_0001</org_study_id>
    <nct_id>NCT03031925</nct_id>
  </id_info>
  <brief_title>Detection of Annexin A2 in Systemic Lupus Erythematosus</brief_title>
  <acronym>ANLUP</acronym>
  <official_title>Detection of Annexin A2 in Systemic Lupus Erythematosus</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Centre Hospitalier Universitaire, Amiens</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Centre Hospitalier Universitaire, Amiens</source>
  <oversight_info>
    <is_fda_regulated_drug>No</is_fda_regulated_drug>
    <is_fda_regulated_device>No</is_fda_regulated_device>
  </oversight_info>
  <brief_summary>
    <textblock>
      There is substantial clinical and biological intra and inter-patient variability in SLE.&#xD;
      Vascular, renal and neurologic deficiency can be organ-threatening or even life-threatening,&#xD;
      leading to increased morbidity and mortality.&#xD;
&#xD;
      Thus, biomarkers of disease activity and prognosis are required for regular follow-up of SLE&#xD;
      patients.&#xD;
&#xD;
      Implication of Toll-like Receptors (TLRs) in SLE has been extensively studied in mice models&#xD;
      and humans. Self nuclear antigens bind to TLRs which are located on the surface of dendritic&#xD;
      cells, B-cells, and endothelial cells, leading to production of pro-inflammatory cytokines&#xD;
      and pathologic autoantibodies involved in organ dysfunction of SLE patients. Moreover, TLR&#xD;
      expression in SLE is significantly higher and significantly correlated with disease activity.&#xD;
&#xD;
      Annexin A2 (ANXA2) is a member of the annexins superfamily which exists as a monomer or&#xD;
      heterotetramer and is implicated in several biological processes. Most notably, it binds to&#xD;
      ẞ2GP1/anti-ẞ2GP1 antibodies and mediates endothelial cell activation via a TLR4 signaling&#xD;
      pathway, highlighting its key role in Antiphospholipid Syndrome (APS) frequently associated&#xD;
      with SLE.&#xD;
&#xD;
      ANXA2 is also involved in the physiopathology of SLE. Anti-DNA autoantibodies can bind with&#xD;
      ANXA2 expressed on mesangial cells in lupus nephritis. Besides, a french study carried out in&#xD;
      Amiens' University Hospital showed that vascular lesions in lupus nephritis were associated&#xD;
      with a significant increase in vascular expression of ANXA2.&#xD;
    </textblock>
  </brief_summary>
  <overall_status>Completed</overall_status>
  <start_date type="Actual">May 9, 2017</start_date>
  <completion_date type="Actual">November 9, 2018</completion_date>
  <primary_completion_date type="Actual">November 9, 2018</primary_completion_date>
  <phase>N/A</phase>
  <study_type>Interventional</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <allocation>Non-Randomized</allocation>
    <intervention_model>Parallel Assignment</intervention_model>
    <primary_purpose>Basic Science</primary_purpose>
    <masking>None (Open Label)</masking>
  </study_design_info>
  <primary_outcome>
    <measure>serum concentration of ANXA2</measure>
    <time_frame>Day 0</time_frame>
  </primary_outcome>
  <primary_outcome>
    <measure>urinary concentration of ANXA2</measure>
    <time_frame>Day 0</time_frame>
  </primary_outcome>
  <number_of_arms>2</number_of_arms>
  <enrollment type="Actual">120</enrollment>
  <condition>Systemic Lupus Erythematosus (SLE)</condition>
  <condition>Lupus Nephritis</condition>
  <arm_group>
    <arm_group_label>SLE patients</arm_group_label>
    <arm_group_type>Experimental</arm_group_type>
    <description>Systemic Lupus Erythematosus</description>
  </arm_group>
  <arm_group>
    <arm_group_label>control subjects</arm_group_label>
    <arm_group_type>Active Comparator</arm_group_type>
    <description>age- and sex-matched control subjects</description>
  </arm_group>
  <intervention>
    <intervention_type>Other</intervention_type>
    <intervention_name>ANXA2</intervention_name>
    <description>serum and urinary concentration</description>
    <arm_group_label>SLE patients</arm_group_label>
    <arm_group_label>control subjects</arm_group_label>
  </intervention>
  <eligibility>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
        Inclusion criteria for patients :&#xD;
&#xD;
          -  Age ≥ 18 years old&#xD;
&#xD;
          -  All SLE patients fulfilling the 1997 ACR criteria, followed at the Departments of&#xD;
             Internal Medicine and Nephrology at CHU Amiens-Picardie, regardless of clinical&#xD;
             status, treatment, and disease activity.&#xD;
&#xD;
          -  Written informed consent&#xD;
&#xD;
        Inclusion criteria for control subjects :&#xD;
&#xD;
          -  Age ≥ 18 years old&#xD;
&#xD;
          -  Written informed consent&#xD;
&#xD;
        The patients will be compared with age- and sex-matched control subjects.&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  drug-induced lupus erythematosus&#xD;
&#xD;
          -  refusal or incapacity to provide a written informed consent&#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>Valéry SALLE, MD</last_name>
    <role>Principal Investigator</role>
    <affiliation>CHU Amiens</affiliation>
  </overall_official>
  <location>
    <facility>
      <name>CHU Amiens</name>
      <address>
        <city>Amiens</city>
        <zip>80054</zip>
        <country>France</country>
      </address>
    </facility>
  </location>
  <location_countries>
    <country>France</country>
  </location_countries>
  <verification_date>July 2020</verification_date>
  <study_first_submitted>January 20, 2017</study_first_submitted>
  <study_first_submitted_qc>January 24, 2017</study_first_submitted_qc>
  <study_first_posted type="Estimate">January 26, 2017</study_first_posted>
  <last_update_submitted>July 17, 2020</last_update_submitted>
  <last_update_submitted_qc>July 17, 2020</last_update_submitted_qc>
  <last_update_posted type="Actual">July 20, 2020</last_update_posted>
  <responsible_party>
    <responsible_party_type>Sponsor</responsible_party_type>
  </responsible_party>
  <keyword>Annexin A2</keyword>
  <keyword>biomarker</keyword>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Nephritis</mesh_term>
    <mesh_term>Lupus Nephritis</mesh_term>
    <mesh_term>Lupus Erythematosus, Systemic</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/NCT03031925
org study id: PI2017_843_0001
nct id: NCT03031925
lead sponsor: 
is fda regulated drug: No
is fda regulated device: No
There is substantial clinical and biological intra and inter-patient variability in SLE.
      Vascular, renal and neurologic deficiency can be organ-threatening or even life-threatening,
      leading to increased morbidity and mortality.

      Thus, biomarkers of disease activity and prognosis are required for regular follow-up of SLE
      patients.

      Implication of Toll-like Receptors (TLRs) in SLE has been extensively studied in mice models
      and humans. Self nuclear antigens bind to TLRs which are located on the surface of dendritic
      cells, B-cells, and endothelial cells, leading to production of pro-inflammatory cytokines
      and pathologic autoantibodies involved in organ dysfunction of SLE patients. Moreover, TLR
      expression in SLE is significantly higher and significantly correlated with disease activity.

      Annexin A2 (ANXA2) is a member of the annexins superfamily which exists as a monomer or
      heterotetramer and is implicated in several biological processes. Most notably, it binds to
      ẞ2GP1/anti-ẞ2GP1 antibodies and mediates endothelial cell activation via a TLR4 signaling
      pathway, highlighting its key role in Antiphospholipid Syndrome (APS) frequently associated
      with SLE.

      ANXA2 is also involved in the physiopathology of SLE. Anti-DNA autoantibodies can bind with
      ANXA2 expressed on mesangial cells in lupus nephritis. Besides, a french study carried out in
      Amiens' University Hospital showed that vascular lesions in lupus nephritis were associated
      with a significant increase in vascular expression of ANXA2.
allocation: Non-Randomized
intervention model: Parallel Assignment
primary purpose: Basic Science
masking: None (Open Label)
measure: serum concentration of ANXA2
time frame: Day 0
measure: urinary concentration of ANXA2
time frame: Day 0
arm group label: SLE patients
arm group type: Experimental
description: Systemic Lupus Erythematosus
arm group label: control subjects
arm group type: Active Comparator
description: age- and sex-matched control subjects
intervention type: Other
intervention name: ANXA2
description: serum and urinary concentration
arm group label: SLE patients
arm group label: control subjects
criteria: 
gender: All
minimum age: 18 Years
maximum age: N/A
healthy volunteers: Accepts Healthy Volunteers
last name: Valéry SALLE, MD
role: Principal Investigator
affiliation: CHU Amiens
facility: 
country: France
responsible party type: Sponsor
mesh term: Nephritis
mesh term: Lupus Nephritis
mesh term: Lupus Erythematosus, Systemic