Evaluation of Cell Membrane Expression of Annexin A2 on Monocytes by Flow Cytometry in Primary Antiphospholipid Syndrome
For patients and families
In plain language
An automatic summary of structured registry data. It is an orientation aid, not a substitute for the official protocol or a physician assessment.
- What is being studied
- The protocol lists: blood withdrawal.
- Who it may be relevant to
- Registry conditions: Antiphospholipid Syndrome. Basic parameters: from 18 years · All.
- What needs checking
- Age, condition and sex are only basic indicators. Prior treatment, laboratory values and other mandatory requirements appear in the eligibility criteria below.
- Where it takes place
- France
- Next step
- Save the trial, show it to the treating physician, and confirm current recruitment with the study center. Costs, documents and travel →
Unsure about the terms? Read our patient guide →
Overview
Annexin A2 (ANXA2), an endothelial cell receptor for plasminogen and tissue plasminogen activator, plays a pivotal role in regulation of fibrinolysis in vitro and in vivo and has been identified as a new autoantigen in antiphospholipid syndrome (APS). ANXA2 can exist as a monomer or a heterotetrameric complex with S100A10 protein. The aim of this study was to evaluate the cell membrane expression of ANXA2 on circulating monocytes in APS by flow cytometry. Several pathogenic mechanisms are involved in APS such as activation of endothelial cells, platelets and monocytes, inhibition of the natural anticoagulant protein C/protein S pathway, activation of the complement system and also impairment of fibrinolysis. Annexin A2 which hits binding partner S100A10, ANXA2 forms a cell surface complex that regulates generation of plasmin. ANXA2 is involved in the pathogenesis of APS-associated through several possible mechanisms. Human peripheral blood monocytes represent the major circulating ANXA2-expressing cell and ANXA2-mediated assembly of plasminogen and tissue activator of plasminogen (tPA) on monocyte/macrophages contributes to plasmin generation. Thus the investigators could suppose that decrease of cell membrane expression of ANXA2 on circulating monocytes represent a new pathogenic mechanism in APS.
Interventions
- Biological blood withdrawal
blood withdrawal
Primary outcome measures
- Cell membrane expression rate of ANXA2 on circulating monocytes in APS [Time frame: 1 hour]
Secondary outcome measures (2)
- Cellular expression of ANXA2 and S100A10 in APS patients [Time frame: 1 hour]
- cell membrane expression of ANXA2 and S100A10 in APS patients [Time frame: 1 hour]
Eligibility criteria
Inclusion criteria
- APS patients who fulfilled the revised criteria for APS
Exclusion criteria
- Patients less than 18 years old
- Solid and hematological malignancies
- Other autoimmune diseases
- Cirrhosis
Criteria are shown verbatim from the registry (in English). Final eligibility is always assessed by the study center.
Healthy volunteers: Yes
Study design
- Allocation
- Non-randomized
- Model
- Parallel assignment
- Masking
- Open label
- Primary purpose
- Diagnostic
Study locations
France · 1 center
- CHU Amiens — Amiens
Identifiers
NCT: NCT06373926 · PI2019_843_0010