The Impact of Interferon Beta 1a on Egyptian Relapse-Reemitting Multiple Sclerosis Patients
Study Details
Study Description
Brief Summary
Our study aimed to investigate the effect of interferon beta 1a on the clinical and immunological parameters in Egyptian relapse-remitting multiple sclerosis patients
| Condition or Disease | Intervention/Treatment | Phase |
|---|---|---|
|
N/A |
Detailed Description
Until recently, relapsing-remitting multiple sclerosis (RRMS) was considered a homogeneous form of multiple sclerosis (MS). Variability both in the immunopathology of active demyelinating lesions in MS and in response to immunomodulatory treatments has demonstrated that RRMS is a heterogeneous form of MS. An overwhelming number of trials have supported the use of interferon-β (IFN-β) as a first-line immunomodulatory treatment in RRMS. Approximately 30% of IFN-β treated RRMS patients are non-responders (NR) to treatment. Despite vast clinical experience in the use of IFN-β, its mechanisms of action have not been fully clarified. Interleukin-17 (IL-17) is a proinflammatory cytokine that is secreted by a lineage of T cells named Th17 cells. The Th17 chemokine pathways are essential for the development of central nervous system (CNS) autoimmune diseases such as MS. A high IL-17 concentration in the serum. of people with RRMS is associated with nonresponse to IFN-β therapy. Some animal and human studies have shown that IFN-β inhibits the activity of Th17 cells.
Study Design
Arms and Interventions
| Arm | Intervention/Treatment |
|---|---|
| Experimental: Group 1 RRMS patients who received Interferon beta 1a |
Other: Blood sample collection
5 ml of blood samples were withdrawn from RRMS patients
|
Outcome Measures
Primary Outcome Measures
- Correlation between IL17 levels and patients' response to interferon beta 1a as measured by ELISA [Patients were treated with INF B 1a for at least 6 months]
Anti-inflammatory and disease activity biomarkers
Secondary Outcome Measures
- Correlation between IL 22 levels and patients' response to interferon beta 1a, measured by ELISA [Patients were treated with INF B 1a for at least 6 months]
Anti-inflammatory and disease activity biomarkers
- Correlation between Expanded Disability Status Scale and patients' response to interferon beta 1a [Patients were treated with INF B 1a for at least 6 months]
Determination disability level (0 - 6), The lowest value means that it is best outcome and the highest value is the worst outcome.
- Correlation between malondialdehyde levels and patients' response to interferon beta 1a [Patients were treated with INF B 1a for at least 6 months]
oxidative stress biomarkers
- Correlation between MRI load and Patients' response to interferon beta 1a [Patients were treated with INF B 1a for at least 6 months]
Determination of T2 lesions
- Correlation between body mass index and patients' response to interferon beta 1 a [Patients were treated with INF B 1a for at least 6 months]
Body weight measurement
Eligibility Criteria
Criteria
Inclusion Criteria:
-
Age between 18 and 50 years at time of signing informed consent form.
-
Relapsing- remitting multiple sclerosis as per the McDonald 2017 criteria, including an MRI brain satisfying the 2017 radiological criteria.
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Full-field visual evoked potential (VEP) P100 latency in at least one eye of ≥118 ms.
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Kurtzke EDSS step 0.0 - 6.0.
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At the time of screening, being treated with a stable dose for at least 6 months of a category 1 multiple sclerosis DMT or for at least 2 years with a category 2 DMT.
Exclusion Criteria:
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they had been treated in the last 30 days with methylprednisolone
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they had changed their IFN-β preparation within the last 18 months
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they had other chronic diseases associated with MS
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they had been previously treated with immunosuppressive agents
Contacts and Locations
Locations
| Site | City | State | Country | Postal Code | |
|---|---|---|---|---|---|
| 1 | Nasser Institute for Research and Treatment | Cairo | Egypt | 1053 |
Sponsors and Collaborators
- German University in Cairo
Investigators
None specified.Study Documents (Full-Text)
None provided.More Information
Publications
- Axtell RC, Raman C, Steinman L. Interferon-beta exacerbates Th17-mediated inflammatory disease. Trends Immunol. 2011 Jun;32(6):272-7. doi: 10.1016/j.it.2011.03.008. Epub 2011 Apr 29.
- Brucklacher-Waldert V, Stuerner K, Kolster M, Wolthausen J, Tolosa E. Phenotypical and functional characterization of T helper 17 cells in multiple sclerosis. Brain. 2009 Dec;132(Pt 12):3329-41. doi: 10.1093/brain/awp289.
- Hesse D, Krakauer M, Lund H, Sondergaard HB, Langkilde A, Ryder LP, Sorensen PS, Sellebjerg F. Breakthrough disease during interferon-[beta] therapy in MS: No signs of impaired biologic response. Neurology. 2010 May 4;74(18):1455-62. doi: 10.1212/WNL.0b013e3181dc1a94.
- Lucchinetti C, Bruck W, Parisi J, Scheithauer B, Rodriguez M, Lassmann H. Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination. Ann Neurol. 2000 Jun;47(6):707-17. doi: 10.1002/1531-8249(200006)47:63.0.co;2-q.
- Rudick RA, Polman CH. Current approaches to the identification and management of breakthrough disease in patients with multiple sclerosis. Lancet Neurol. 2009 Jun;8(6):545-59. doi: 10.1016/S1474-4422(09)70082-1.
- MSINF