Giant Cell ArteritisCH-GCANCT06244069
Clonal Hematopoiesis in Giant Cell Arteritis
An observational study of Giant Cell Arteritis and Temporal Arteritis, run by ASST Fatebenefratelli Sacco.
Trial summary
The goal of this clinical trial is to verify whether CHIP is correlated with the clinical, instrumental, and histological characteristics of GCA, and to characterize the pathogenetic effects of clonal hemopoiesis on vasculitis. Read more about this study
- Who is it for?
- Ages 18 years and olderHealthy volunteers can take part
- Conditions the study is for
- Giant Cell Arteritis, Temporal Arteritis, Clonal Hematopoiesis of Indeterminate Potential
- What is being tested?
- Temporal arterial biopsy, Whole exome sequencing and Single cell transcriptomics
- Type of treatment
- Injection or infusion
- How many people
- 326 participants
- Where
- No sites listed yet
- Study dates
- Mar 2024to Mar 2031
- Phase
- Observational
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Study population: The study will rely on the patients with GCA enrolled in referral centers for vasculitis, All centers have a fast-track for suspected GCA, mainly from their Emergency Departments. This allows clinical evaluation of patients with multi-dimensional disease characterization, comprising ultrasonography of the temporal, axillary and carotid arteries, temporal artery biopsies, and screening for large vessels involvement with a combination of ultrasonography and Position Emission Tomography/Computed Tomography within five days from clinical evaluation. Temporal artery biopsy will be performed in all patients with cranial symptoms for GCA or in the case of diagnostic uncertainty.
Who may be able to join
- Patients with suspected active GCA entering into a fast-track work-up and healthy matched controls.
- Capability of providing valid consent to study enrollment.
- Possibility of performing temporal artery biopsy within three hours from enrollment.
Who cannot join
- Active concurrent viral, fungal or bacterial infections (including active/latent tuberculosis treated for less than 4 weeks, HIV and Hepatitis B/C virus (HBV/HCV) infections.
- Concurrent systemic inflammation not attributable to GCA (inflammatory diseases in treatment-free remission are accepted).
- Use of other immunosuppressive agents in the last 3 months.
- Use of systemic steroids (any dose in the last week, > 15 mg/die of prednisone equivalent in the last month).
- Solid or hematologic malignancies (active or with less than 6 months free of disease or antiblastic chemotherapy (hormone therapy is allowed).
- Previous solid or hematopoietic stem cell transplantation (corneal transplants are allowed).
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- Any systemic immunosuppressive or steroidal therapy.
- Chronic renal failure with Glomerular Filtration Rate (GFR) < 45 ml/min *1.73 m2.
- Moderate-severe liver failure (Child-Pugh B or C), hepatitis in stages of activity.
- Diabetes mellitus.
- Heart failure with New York Heart Association score (NYHA) >=2.
- Severe hypoproteinemia/malnutrition.
- Chronic respiratory failure requiring O2 therapy or ventilation therapy at home.
- Any other condition judged by the local investigator as a contra-indication to eligibility.
Trial locations and contacts
No sites are listed yet. Contact the study team or a site near you to ask about taking part.
About this study
The goal of this clinical trial is to verify whether CHIP is correlated with the clinical, instrumental, and histological characteristics of GCA, and to characterize the pathogenetic effects of clonal hemopoiesis on vasculitis. The main objective of this study is to verify if clonal hematopoiesis of indeterminate potential (CHIP) affects GCA manifestations, course/response to therapies, and pathogenesis.
Patients who are going to be diagnosed with GCA and for which a fast track is available for a rapid diagnostic work-up including pre-treatment temporal artery biopsy. Patients with CHIP will be identified and characterized by using whole exome sequencing from the peripheral blood samples. The presence and characteristics of CHIP will be correlated with baseline clinical, instrumental, and histologic GCA features.
Read the detailed description
GCA is the most frequent idiopathic vasculitis in the elderly, characterized by significant morbidity, with possible formation of aneurysms and arterial dissections and with possible evolution into ischemic tissue events, such as irreversible blindness or stroke. Arterial inflammation is maintained by a leukocyte infiltrate infiltrating the vessel wall through vasa vasorum, composed primarily of macrophages (sometimes structured into granulomas with multinucleated giant cells) and Cluster of Differentiation (CD) 4+ T cells, but also from Cluster of Differentiation (CD) 8+ and dendritic cells. However, there are heterogeneous clinical pictures, in correlation to the spatial distribution of arterial lesions, to the finding of arterial ischemia, aneurysms or any relapses. Even today, there is a need to understand the pathogenetic mechanisms underlying clinical and prognostic differences in GCA and to identify patients with different clinical outcomes and response to therapies in advance.
Clonal hemopoiesis is instead characterized by the presence in the bloodstream of a hematopoietic clone with a selective advantage following somatic mutations, in the absence of other obvious hematological conditions: in fact, it cannot be detected by standard diagnostic tools, but requires a genetic assessment of blood mosaicism or the presence of known relevant mutations. Mutated leukocytes have a more intense inflammatory and atherogenic response with inflammatory stimuli, both infectious and non-infectious, favoring a proinflammatory microenvironment in elderly patients, underlying the concept of "age-related inflammation". One study identified CHIP in 33% of patients with GCA. The investigators hypothesize that specific mutations responsible for the hematopoietic clone could favor a proinflammatory dysregulation of leukocytes within vasculitic lesions, affecting the activity of arterial injury. The purpose of this study is to verify whether CHIP is correlated with the clinical, instrumental and histological characteristics of GCA, and to characterize the pathophysiologic effects of clonal hemopoiesis on vasculitis.
- Conditions
- Giant Cell Arteritis, Temporal Arteritis, Clonal Hematopoiesis of Indeterminate Potential, Horton Disease, Systemic Vasculitis Primary
- Being tested
- Temporal arterial biopsy, Whole exome sequencing, Single cell transcriptomics
- Keywords
- Temporal artery biopsy, Giant cell arteritis, Clonal Hematopoiesis of Indeterminate Potential, Single cell transcriptomics, Large vessels vasculitis, Horton disease, Whole Exome Sequencing
- Medical subject headings
- Giant Cell Arteritis
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Temporal arterial biopsyDiagnostic test
Collection of 30 ml of peripheral blood in ethylenediaminetetraacetic acid (EDTA) tubes performed at baseline, 6 months, 12 months and in case of flare before month 12. In addition, the temporal artery specimen (at least 5 mm in length) exceeding that used for clinical activity (at least 10 mm in length in accordance with current clinical recommendations) will be digested to use for research purposes (about protocols for collecting, processing, storing and sending biopsy, refer to Standard Operating Procedures, SOP).
Whole exome sequencingDiagnostic test
Also called Genetic analysis for CHIP
Patients with CHIP will be identified and characterized by using whole exome sequencing from the peripheral blood samples. M-CHIP will be further characterized by:
- clone dimension as defined by Variant Allele Fraction (VAF); ii) mutations in specific genes such as DNMT3A, Tet methylcytosine dioxygenase 2 (TET2), Additional Sex combs (ASXL1), or Janus kinase 2 (JAK2); iii) multiple mutations.
L-CHIP will be further characterized by:
- clone dimension as defined by the VAF; ii) mutations in specific genes such as Dual Specificity Phosphatase 22 (DUSP22), FAT atypical cadherin 1 (FAT1), (Histone-lysine N-methyltransferase 2D (KMT2D); iii) multiple mutations; iv) co-occurrence of mutations heralding M- and L-CHIP.
Single cell transcriptomicsDiagnostic test
The investigators will identify actively inflamed arterial biopsies from three treatment-naïve patients without CHIP, and three treatment-naïve patients with CHIP driven by the most relevant gene mutation. Arterial wall Cluster of Differentiation (CD) 45+ leukocytes will be isolated after digestion of arterial tissue and characterized by single cell transcriptomics, with a specific focus on wall infiltrating T cells and macrophages and their subsets (eg: Vascular dendritic cells, Th1, Th2, Th17, Treg, M1- and M2-like,…). Frequencies of these subsets and their genetic expression will be compared between wall-infiltrating leukocytes from GCA patients with or without CH, focusing on histological events supposed to be pathogenic in GCA, or known to be dysfunctional in CHIP.
| Study group | Role | What they receive |
|---|---|---|
| GCA patients | Patients who are going to be diagnosed with GCA and for which a fast track is available for a rapid diagnostic work-up including pre-treatment temporal artery biopsy. The main biopsy specimen will be sent for histopathology for clinical diagnosis or final validation, while the remaining specimen (at least 5 mm in length) will be digested to use for research purposes. In the fast-track, patients should rapidly receive a multi-dimensional diagnostic assessment including ultrasonography of the temporal and axillary arteries. Screening for large vessels involvement should be performed according to the local practice by a combination of ultrasonography, Position Emission Tomography (PET) and Magnetic Resonance (MR). Ideally, this assessment should be performed within five days from clinical evaluation. Receives: Diagnostic Test: Temporal arterial biopsy; Diagnostic Test: Whole exome sequencing; Diagnostic Test: Single cell transcriptomics | |
| Healthy subjects | Healthy controls matched with GCA patients for age, sex, smoking status, previous cardiovascular events, BMI, history of cancer and cytotoxic chemo/radiotherapy. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Correlation of GCA with M-CHIP-driven by DNMT3A mutations
Patients with M-CHIP will be identified by whole exome sequencing from the peripheral blood. The prevalence of DNMT3A-driven M-CHIP will be compared in the GCA patients vs matched controls by Chi-squared test or Fisher test.
Measured: From beginning of study for 11 months
Secondary outcomes (12)
Correlation of GCA with M-CHIP-driven by TET2, ASXL1 and JAK2 mutations
Patients with M-CHIP will be identified by whole exome sequencing from the peripheral blood. The prevalence of TET2, ASXL1 or JAK2-driven M-CHIP will be compared in the GCA patients vs matched controls by Chi-squared test or Fisher test.
Measured: From beginning of study for 11 months
Correlation of GCA with L-CHIP-driven by DUSP22, FAT1 and KMT2D mutations
Patients with L-CHIP will be identified by whole exome sequencing from the peripheral blood. The prevalence of DUSP22, FAT1 or KMT2D-driven L-CHIP will be compared in the GCA patients vs matched controls by Chi-squared test or Fisher test.
Measured: From beginning of study for 11 months
Correlation of GCA with M-CHIP and L-CHIP clone dimension
Patients with M-CHIP or L-CHIP will be characterized for the dimension of the mutated clone in the peripheral blood by assessing the Variant Allele Fraction (VAF) at whole exome sequencing. The VAF will be compared between the GCA group and the matched controls by an unmatched non-parametric test (Mann-Whitney U test).
Measured: From beginning of study for 11 months
Correlation of GCA with M-CHIP and L-CHIP multiple mutations
The prevalence of M-CHIP and L-CHIP driven by multiple mutations as assessed by whole exome sequencing will be compared between the GCA group and the matched controls by Chi-squared test or Fisher test.
Measured: From beginning of study for 11 months
Correlation of ischemic features in GCA with specific CHIP mutations
The prevalence of specific CHIP mutations (assessed and defined as above) will be compared between GCA patients with vs without ischemic features (claudicatio mandibularis, soft tissue necrosis, ischemic optic neuropathy) by Chi-squared test or Fisher test.
Measured: From beginning of study for 11 months
Correlation of ischemic features in GCA with CHIP clone dimension
The clone dimension as assessed by VAF (see above) will be compared between GCA patients with vs without ischemic features by the Mann-Whitney U test.
Measured: From beginning of study for 11 months
Correlation of rate of complications with specific CHIP mutations
GCA patients will be followed prospectively; the prevalence of specific CHIP mutations (assessed and defined as above) will be compared between GCA patients with vs without complications at 12 months (disease relapse, venous thromboembolism, acute coronary syndromes/strokes, infection) by Chi-squared test or Fisher test.
Measured: From patients' enrollment for 12 months
Correlation of rate of complications with CHIP clone dimension
GCA patients will be followed prospectively; the clone dimension as assessed by VAF (see above) will be compared between GCA patients with vs without complications at 12 months (disease relapse, venous thromboembolism, acute coronary syndromes/strokes, infection) by the Mann-Whitney U test.
Measured: From patients' enrollment for 12 months
Correlation of vascular quantitative score in GCA with specific CHIP mutations
The prevalence of specific CHIP mutations (assessed and defined as above) will be compared between GCA patients with vs without incidence of large vessel involvement and burden of arterial stenosis and dilatation using quantitative activity scores such as Birmingham Vasculitis Activity Score (BVAS) and Vasculitis Damage Index (VDI), using the Mann-Whitney U test.
Measured: From beginning of study for 11 months
Correlation of vascular quantitative score in GCA with CHIP clone dimension
The clone dimension as assessed by VAF (see above) will be compared between GCA patients with incidence of large vessel involvement and burden of arterial stenosis and dilatation using quantitative activity scores such as Birmingham Vasculitis Activity Score (BVAS) and Vasculitis Damage Index (VDI), using Spearman's rank correlation coefficient.
Measured: From beginning of study for 11 months
Correlation of histologic features in GCA with specific CHIP mutations
The prevalence of specific CHIP mutations (assessed and defined as above) will be compared between GCA patients with histologic features such as intimal hyperplasia, fragmentation of internal elastic membrane, transmural inflammation, vasa-vasorum neoangiogenesis, and presence of giant cells by Chi-squared test or Fisher test.
Measured: From beginning of study for 11 months
Correlation of histologic features in GCA with CHIP clone dimension
The clone dimension as assessed by VAF (see above) will be compared between GCA patients with histologic features such as intimal hyperplasia, fragmentation of internal elastic membrane, transmural inflammation, vasa-vasorum neoangiogenesis, and presence of giant cells, by the Mann-Whitney U test.
Measured: From beginning of study for 11 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted6 Feb 2024
- Study startMar 2024 (estimated)
- Primary completionMar 2028 (estimated)
- Study completionMar 2031 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for Giant Cell ArteritisStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 326 participants (estimated)
Sponsor and investigators
- Lead sponsor
- ASST Fatebenefratelli Sacco
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Enrico Tombetti, ASST Fatebenefratelli Sacco
- Investigators
- Enrico Tombetti, Dr., Principal investigator, ASST Fatebenefratelli Sacco
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06244069
- Sponsor's protocol ID
- The CH-GCA Trial
- Acronym
- CH-GCA
- Status last verified
- Feb 2024
- First submitted
- 23 Jan 2024
- Last updated
- 6 Feb 2024
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided
Study at a glance
From the registry record, last updated by the sponsor on 6 Feb 2024. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Clonal Hematopoiesis in Giant Cell Arteritis
- ClinicalTrials.gov ID
- NCT06244069
- Acronym / sponsor ID
- CH-GCA / The CH-GCA Trial
- Conditions
- Giant Cell Arteritis, Temporal Arteritis, Clonal Hematopoiesis of Indeterminate Potential, Horton Disease, Systemic Vasculitis Primary
- Keywords
- Temporal artery biopsy, Giant cell arteritis, Clonal Hematopoiesis of Indeterminate Potential, Single cell transcriptomics, Large vessels vasculitis, Horton disease, Whole Exome Sequencing
- Study type
- Observational
- Recruitment status
- Not yet recruiting
- Enrolment
- 326 participants (estimated)
- Lead sponsor
- ASST Fatebenefratelli SaccoUniversity, hospital or other
- Study start
- Mar 2024 (estimated)
- Primary completion
- Mar 2028 (estimated)
- Study completion
- Mar 2031 (estimated)
- First posted
- 6 Feb 2024 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The goal of this clinical trial is to verify whether CHIP is correlated with the clinical, instrumental, and histological characteristics of GCA, and to characterize the pathogenetic effects of clonal hemopoiesis on vasculitis. The main objective of this study is to verify if clonal hematopoiesis of indeterminate potential (CHIP) affects GCA manifestations, course/response to therapies, and pathogenesis.
Patients who are going to be diagnosed with GCA and for which a fast track is available for a rapid diagnostic work-up including pre-treatment temporal artery biopsy. Patients with CHIP will be identified and characterized by using whole exome sequencing from the peripheral blood samples. The presence and characteristics of CHIP will be correlated with baseline clinical, instrumental, and histologic GCA features.
Detailed description
GCA is the most frequent idiopathic vasculitis in the elderly, characterized by significant morbidity, with possible formation of aneurysms and arterial dissections and with possible evolution into ischemic tissue events, such as irreversible blindness or stroke. Arterial inflammation is maintained by a leukocyte infiltrate infiltrating the vessel wall through vasa vasorum, composed primarily of macrophages (sometimes structured into granulomas with multinucleated giant cells) and Cluster of Differentiation (CD) 4+ T cells, but also from Cluster of Differentiation (CD) 8+ and dendritic cells. However, there are heterogeneous clinical pictures, in correlation to the spatial distribution of arterial lesions, to the finding of arterial ischemia, aneurysms or any relapses. Even today, there is a need to understand the pathogenetic mechanisms underlying clinical and prognostic differences in GCA and to identify patients with different clinical outcomes and response to therapies in advance.
Clonal hemopoiesis is instead characterized by the presence in the bloodstream of a hematopoietic clone with a selective advantage following somatic mutations, in the absence of other obvious hematological conditions: in fact, it cannot be detected by standard diagnostic tools, but requires a genetic assessment of blood mosaicism or the presence of known relevant mutations. Mutated leukocytes have a more intense inflammatory and atherogenic response with inflammatory stimuli, both infectious and non-infectious, favoring a proinflammatory microenvironment in elderly patients, underlying the concept of "age-related inflammation". One study identified CHIP in 33% of patients with GCA. The investigators hypothesize that specific mutations responsible for the hematopoietic clone could favor a proinflammatory dysregulation of leukocytes within vasculitic lesions, affecting the activity of arterial injury. The purpose of this study is to verify whether CHIP is correlated with the clinical, instrumental and histological characteristics of GCA, and to characterize the pathophysiologic effects of clonal hemopoiesis on vasculitis.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| GCA patients | – | Diagnostic Test: Temporal arterial biopsy, Diagnostic Test: Whole exome sequencing, Diagnostic Test: Single cell transcriptomicsPatients who are going to be diagnosed with GCA and for which a fast track is available for a rapid diagnostic work-up including pre-treatment temporal artery biopsy. The main biopsy specimen will be sent for histopathology for clinical diagnosis or final validation, while the remaining specimen (at least 5 mm in length) will be digested to use for research purposes. In the fast-track, patients should rapidly receive a multi-dimensional diagnostic assessment including ultrasonography of the temporal and axillary arteries. Screening for large vessels involvement should be performed according to the local practice by a combination of ultrasonography, Position Emission Tomography (PET) and Magnetic Resonance (MR). Ideally, this assessment should be performed within five days from clinical evaluation. |
| Healthy subjects | – | –Healthy controls matched with GCA patients for age, sex, smoking status, previous cardiovascular events, BMI, history of cancer and cytotoxic chemo/radiotherapy. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- The study will rely on the patients with GCA enrolled in referral centers for vasculitis, All centers have a fast-track for suspected GCA, mainly from their Emergency Departments. This allows clinical evaluation of patients with multi-dimensional disease characterization, comprising ultrasonography of the temporal, axillary and carotid arteries, temporal artery biopsies, and screening for large vessels involvement with a combination of ultrasonography and Position Emission Tomography/Computed Tomography within five days from clinical evaluation. Temporal artery biopsy will be performed in all patients with cranial symptoms for GCA or in the case of diagnostic uncertainty.
Key inclusion criteria (3 listed)
- Patients with suspected active GCA entering into a fast-track work-up and healthy matched controls.
- Capability of providing valid consent to study enrollment.
- Possibility of performing temporal artery biopsy within three hours from enrollment.
Key exclusion criteria (14 listed)
- Active concurrent viral, fungal or bacterial infections (including active/latent tuberculosis treated for less than 4 weeks, HIV and Hepatitis B/C virus (HBV/HCV) infections.
- Concurrent systemic inflammation not attributable to GCA (inflammatory diseases in treatment-free remission are accepted).
- Use of other immunosuppressive agents in the last 3 months.
- Use of systemic steroids (any dose in the last week, > 15 mg/die of prednisone equivalent in the last month).
- Solid or hematologic malignancies (active or with less than 6 months free of disease or antiblastic chemotherapy (hormone therapy is allowed).
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Temporal arterial biopsyCollection of 30 ml of peripheral blood in ethylenediaminetetraacetic acid (EDTA) tubes performed at baseline, 6 months, 12 months and in case of flare before month 12. In addition, the temporal artery specimen (at least 5 mm in length) exceeding that used for clinical activity (at least 10 mm in length in accordance with current clinical recommendations) will be digested to use for research purposes (about protocols for collecting, processing, storing and sending biopsy, refer to Standard Operating Procedures, SOP). | Diagnostic test | GCA patients |
| Whole exome sequencingAlso: Genetic analysis for CHIPPatients with CHIP will be identified and characterized by using whole exome sequencing from the peripheral blood samples. M-CHIP will be further characterized by: i) clone dimension as defined by Variant Allele Fraction (VAF); ii) mutations in specific genes such as DNMT3A, Tet methylcytosine dioxygenase 2 (TET2), Additional Sex combs (ASXL1), or Janus kinase 2 (JAK2); iii) multiple mutations. L-CHIP will be further characterized by: i) clone dimension as defined by the VAF; ii) mutations in specific genes such as Dual Specificity Phosphatase 22 (DUSP22), FAT atypical cadherin 1 (FAT1), (Histone-lysine N-methyltransferase 2D (KMT2D); iii) multiple mutations; iv) co-occurrence of mutations heralding M- and L-CHIP. | Diagnostic test | GCA patients |
| Single cell transcriptomicsThe investigators will identify actively inflamed arterial biopsies from three treatment-naïve patients without CHIP, and three treatment-naïve patients with CHIP driven by the most relevant gene mutation. Arterial wall Cluster of Differentiation (CD) 45+ leukocytes will be isolated after digestion of arterial tissue and characterized by single cell transcriptomics, with a specific focus on wall infiltrating T cells and macrophages and their subsets (eg: Vascular dendritic cells, Th1, Th2, Th17, Treg, M1- and M2-like,…). Frequencies of these subsets and their genetic expression will be compared between wall-infiltrating leukocytes from GCA patients with or without CH, focusing on histological events supposed to be pathogenic in GCA, or known to be dysfunctional in CHIP. | Diagnostic test | GCA patients |
Primary outcome
Correlation of GCA with M-CHIP-driven by DNMT3A mutations
Time frame: From beginning of study for 11 months
Patients with M-CHIP will be identified by whole exome sequencing from the peripheral blood. The prevalence of DNMT3A-driven M-CHIP will be compared in the GCA patients vs matched controls by Chi-squared test or Fisher test.
12 secondary outcomes
Correlation of GCA with M-CHIP-driven by TET2, ASXL1 and JAK2 mutations
Time frame: From beginning of study for 11 months
Correlation of GCA with L-CHIP-driven by DUSP22, FAT1 and KMT2D mutations
Time frame: From beginning of study for 11 months
Correlation of GCA with M-CHIP and L-CHIP clone dimension
Time frame: From beginning of study for 11 months
Correlation of GCA with M-CHIP and L-CHIP multiple mutations
Time frame: From beginning of study for 11 months
Correlation of ischemic features in GCA with specific CHIP mutations
Time frame: From beginning of study for 11 months
Correlation of ischemic features in GCA with CHIP clone dimension
Time frame: From beginning of study for 11 months
Correlation of rate of complications with specific CHIP mutations
Time frame: From patients' enrollment for 12 months
Correlation of rate of complications with CHIP clone dimension
Time frame: From patients' enrollment for 12 months
Correlation of vascular quantitative score in GCA with specific CHIP mutations
Time frame: From beginning of study for 11 months
Correlation of vascular quantitative score in GCA with CHIP clone dimension
Time frame: From beginning of study for 11 months
Correlation of histologic features in GCA with specific CHIP mutations
Time frame: From beginning of study for 11 months
Correlation of histologic features in GCA with CHIP clone dimension
Time frame: From beginning of study for 11 months
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 6 Feb 2024.
- Individual participant dataSharing planned: Undecided
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part.
Enrico Tombetti, Dr. principal investigator
ASST Fatebenefratelli Sacco
Questions about this trial
What is this clinical trial studying?
An observational study of Giant Cell Arteritis and Temporal Arteritis, run by ASST Fatebenefratelli Sacco.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 3 inclusion and 14 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: opening soon, as of the sponsor's last update on 6 Feb 2024. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Enrico Tombetti, Dr. (+393289098793, enrico.tombetti@asst-fbf-sacco.it), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Correlation of GCA with M-CHIP-driven by DNMT3A mutations (time frame: From beginning of study for 11 months). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 6 Feb 2024.