Defining Immune Tolerance in ANCA-associated Vasculitis (AAV)
The goal of the study is to find biological markers (certain proteins or cellular markers found in a blood test) that will inform doctors which AAV patients are most likely to be able to stop their medications suppressing their immune systems and remain in remission.
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
- Tolerance Biomarker Identification [ Time Frame: Difference from baseline to week 26 ] [ Designated as safety issue: No ]Identification of biomarkers associated with clinical tolerance in patients with ANCA-associated vasculitis by comparative immunophenotyping of individual leukocyte subsets from tolerant and non-tolerant patients with AAV.
- Tolerance Signature Stability [ Time Frame: Baseline to Week 26 ] [ Designated as safety issue: No ]Measurement of the stability of a tolerance immune signature in patients with AAV over time.
- Tolerance Signature vs. Clinical Status [ Time Frame: Baseline to Week 26 ] [ Designated as safety issue: No ]Correlation of possible changes in the tolerance signature with changes in clinical status.
- Immunosuppression Associated Signature [ Time Frame: Baseline to 8 Weeks Post-Immunosuppression Withdrawal ] [ Designated as safety issue: No ]Definition of an immune signature associated with maintenance immunosuppression.
|Study Start Date:||December 2013|
|Estimated Study Completion Date:||September 2016|
|Estimated Primary Completion Date:||September 2016 (Final data collection date for primary outcome measure)|
Non-Tolerant participants with AAV
|Healthy Control Participants|
Tolerant participants with AAV
Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV) are small vessel vasculitides that typically follow a chronic course and are associated with death and serious illness. Three clinical conditions are recognized: microscopic polyangiitis (MPA), granulomatosis with polyangiitis (Wegener's, GPA) and eosinophilic granulomatosis with polyangiitis (EPA, formerly Churg Strauss Syndrome). These have different clinical features but can have some overlapping immunological characteristics.
The precise cause of AAV is not understood, but there are clear genetic associations which, in the context of predisposing environmental factors, such as infections, may lead to development of disease. There are no diagnostic criteria for AAV, but there are validated classification criteria and disease definitions. There is a need to find biological markers that define immunological tolerance so that immunotherapy medicines may be correctly changed and safely withdrawn in some people.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01934504
|Contact: Alan Salama, MD||a.salama@.ucl.ac.uk|
|School of Immunity and Infection, Centre for Translational Inflammation Research, University of Birmingham Research Laboratories, Queen Elizabeth Hospital Birmingham||Not yet recruiting|
|Birmingham, England, United Kingdom|
|Principal Investigator: Lorraine Harper, MD|
|Cambridge, England, United Kingdom, CB2 0QQ|
|Principal Investigator: David Jayne, MD|
|London, England, United Kingdom, W12 0HS|
|Principal Investigator: Charles Pusey, MD|
|University College London, Centre for Nephrology||Recruiting|
|London, England, United Kingdom, NW32PF|
|Contact: Cindy Bhagwandin 44 2077940500 ext 34914 firstname.lastname@example.org|
|Principal Investigator: Alan Salama, MD|
|Study Chair:||Alan Salama, MD||University College London, Centre for Nephrology|