Clinical and Imaging Cohort of Neuroinflammation Diseases in China (CLUE)

NCT ID: NCT04106830

Last Updated: 2024-12-24

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

RECRUITING

Total Enrollment

1000 participants

Study Classification

OBSERVATIONAL

Study Start Date

2019-01-01

Study Completion Date

2028-12-31

Brief Summary

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CLUE is a prospective study to determine structural and functional changes of brain and spinal cord, as well as the inflammatory environment in patients with neuroinflammatory and demyelination disease. Participants will receive new magnetic resonance (MR) technics including double inversion recovery (DIR) imaging diffusion kurtosis imaging (DKI), quantitative susceptibility mapping (QSM) and resting-state functional imaging and follow up for one year using 3T MRI. In addition, participants will receive T1WI, T2WI, FLAIR and SWI sequences on 7T MRI.

Detailed Description

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The study is an observational study of multi-model imaging to determine structural and functional changes of the brain, spinal cord and optic nervethe and inflammatory environment in patients with neuroinflammatory and demyelination disease. Brain, spinal cord and optic nerve involvement are common in neuroinflammatory and demyelination disease including clinical isolated syndrome (CIS), multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSDs), myelin oligodendrocyte glycoprotein antibody - associated disorders (MOGAD). The pathophysiology in neuroinflammatory disease involves the intensive autoimmune inflammatory response, resulting in demyelination and neuroaxonal injury and loss. Some cerebrospinal fluid (CSF) biomarkers have been reported to indicate the pathology and reflect disease activity, especially during the acute stage. However, they couldn't directly reflect the macroscopic and microscopic neuroaxonal change in the brain and spinal cord, which seem to be important determinants of long-term severe disability in chronic neuroinflammatory disease.

Finally, new MRI techniques are the most reliable and non-invasive method to assess the structure and function of brain and spinal cord, plus to monitor disease activity in clinical practice. Double inversion recovery (DIR) imaging allows better detection of cortical and white matter lesion, which has highlighted the role in MS. Diffusion kurtosis imaging (DKI) which has been proposed to characterize the deviation of water diffusion in neural tissues from Gaussian diffusion, is promising to provide information of demyelination and subsequent inflammatory processes in brain or spinal cord. Quantitative susceptibility mapping (QSM) has enabled MRI of tissue magnetic susceptibility to advance from simple qualitative detection of hypointense blooming artifacts to precise quantitative measurement of spatial biodistributions. QSM better depicts spatial susceptibility patterns in MS lesions compared to phase-based imaging. Besides, resting-state functional imaging has the potential to map the intrinsic functional brain networks and to detect early functional brain changes in neuroinflammatory disease.

This study will be a prospective cohort study of patients with neuroinflammatory and demyelination disease. Subjects will undertake MR scans at the acute stage and required follow-up visits after 1 month, 6 months, and 1 year. The MR scans are necessary at each visit.

This study does not limit treatment methods. Patients commonly use high-dose intravenous steroid therapy (HD-S) during the acute stage. The HD-S treatment course referred to intravenous administration of 1 g of glucocorticoid daily for 3 consecutive days and continuous dose 240 mg reduction for 60mg oral administration. Immunomodulatory therapies are necessary for the remission stage. The treatment methods include: Azathioprine (start at 50 mg per day, add 50 mg per week to 2 mg/kg\*d); Mycophenolate Mofetil (The initial dose was 0.25g bid, add 0.5g per week to 0.75g bid); and Rituximab (500 mg on the 1st day, the 15th day, then 500mg per half year).

Conditions

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NMO Spectrum Disorder MRI Multiple Sclerosis MOGAD

Study Design

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Observational Model Type

COHORT

Study Time Perspective

PROSPECTIVE

Study Groups

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NMOSD

Patients with neuromyelitis optica spectrum disorders

Intravenous steroid

Intervention Type DRUG

This study does not limit treatment methods.patients commonly use high-dose intravenous steroid therapy (HD-S) during acute stage. The HD-S treatment course referred to intravenous administration of 1 g of glucocorticoid daily for 3 consecutive days and continuous dose 240 mg reduction for 60mg oral administration. Immunomodulatory therapies are necessary for the remission stage. The treatment methods include: Azathioprine (start at 50 mg per day, add 50 mg per week to 2 mg/kg.d); Mycophenolate Mofetil (The initial dose was 0.25g bid, add 0.5g per week to 0.75g bid); and Rituximab (500 mg on the 1st day, the 15th day, then 500mg per half year).

Multiple sclerosis(MS)

Patients with multiple sclerosis

Intravenous steroid

Intervention Type DRUG

This study does not limit treatment methods.patients commonly use high-dose intravenous steroid therapy (HD-S) during acute stage. The HD-S treatment course referred to intravenous administration of 1 g of glucocorticoid daily for 3 consecutive days and continuous dose 240 mg reduction for 60mg oral administration. Immunomodulatory therapies are necessary for the remission stage. The treatment methods include: Azathioprine (start at 50 mg per day, add 50 mg per week to 2 mg/kg.d); Mycophenolate Mofetil (The initial dose was 0.25g bid, add 0.5g per week to 0.75g bid); and Rituximab (500 mg on the 1st day, the 15th day, then 500mg per half year).

MOGAD

Patients with myelin oligodendrocyte glycoprotein antibody-associated disease

Intravenous steroid

Intervention Type DRUG

This study does not limit treatment methods.patients commonly use high-dose intravenous steroid therapy (HD-S) during acute stage. The HD-S treatment course referred to intravenous administration of 1 g of glucocorticoid daily for 3 consecutive days and continuous dose 240 mg reduction for 60mg oral administration. Immunomodulatory therapies are necessary for the remission stage. The treatment methods include: Azathioprine (start at 50 mg per day, add 50 mg per week to 2 mg/kg.d); Mycophenolate Mofetil (The initial dose was 0.25g bid, add 0.5g per week to 0.75g bid); and Rituximab (500 mg on the 1st day, the 15th day, then 500mg per half year).

Healthy controls (HC)

Healthy people without any neuroinflammation disease

No interventions assigned to this group

Interventions

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Intravenous steroid

This study does not limit treatment methods.patients commonly use high-dose intravenous steroid therapy (HD-S) during acute stage. The HD-S treatment course referred to intravenous administration of 1 g of glucocorticoid daily for 3 consecutive days and continuous dose 240 mg reduction for 60mg oral administration. Immunomodulatory therapies are necessary for the remission stage. The treatment methods include: Azathioprine (start at 50 mg per day, add 50 mg per week to 2 mg/kg.d); Mycophenolate Mofetil (The initial dose was 0.25g bid, add 0.5g per week to 0.75g bid); and Rituximab (500 mg on the 1st day, the 15th day, then 500mg per half year).

Intervention Type DRUG

Other Intervention Names

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Azathioprine Mycophenolate Mofetil Rituximab

Eligibility Criteria

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Inclusion Criteria

* 16-75
* Diagnosis of neuroinflammatory and demyelination disease
* Availability of demographic and clinical data at the time disease onset
* Informed written consent obtained from the patient, and/or patient's parent(s), and/or legal representative. Assent, if old enough to grant, will be obtained from all patients under the age of 16 years.

Exclusion Criteria

* Patients for whom MRI is contra-indicated
* Patients included in an ongoing clinical trial where the product is blinded
Minimum Eligible Age

16 Years

Maximum Eligible Age

75 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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Beijing Tiantan Hospital

OTHER

Sponsor Role lead

Responsible Party

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Yaou Liu

Professor

Responsibility Role PRINCIPAL_INVESTIGATOR

Principal Investigators

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Yaou Liu, PhD

Role: PRINCIPAL_INVESTIGATOR

Beijing Tiantan Hospital

Locations

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Beijing Tiantan Hospital

Beijing, Beijing Municipality, China

Site Status RECRUITING

Countries

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China

Central Contacts

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Yaou Liu, PhD

Role: CONTACT

Phone: +86 1059975396

Email: [email protected]

Facility Contacts

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Yaou Liu, PHD

Role: primary

References

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Xu Y, Ren Y, Li X, Xu W, Wang X, Duan Y, Liu Y, Zhang X, Tian DC. Persistently Gadolinium-Enhancing Lesion Is a Predictor of Poor Prognosis in NMOSD Attack: a Clinical Trial. Neurotherapeutics. 2021 Apr;18(2):868-877. doi: 10.1007/s13311-020-00973-9. Epub 2021 Jan 19.

Reference Type DERIVED
PMID: 33469828 (View on PubMed)

Other Identifiers

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KY2024-309-04

Identifier Type: -

Identifier Source: org_study_id