Clinical trial NCT05735067: The Impact of Body Weight on Clinical and Immunological Outcomes in Relapse-Remitting Multiple Sclerosis Patients
Official title: The Impact of Body Weight on Clinical and Immunological Outcomes in Relapse-Remitting Multiple Sclerosis Patients
Study type: OBSERVATIONAL
Overall status: ACTIVE_NOT_RECRUITING
Conditions: Multiple Sclerosis
Keywords: Multiple Sclerosis, IFB 1a
Lead sponsor: German University in Cairo
Sponsor class: OTHER
First posted: 2023-02-21
Enrollment: 138
Sex: ALL
Minimum age (years): 18
Maximum age (years): 50
Standard ages: ADULT
Accepts healthy volunteers: no
Observational model: COHORT
Time perspective: CROSS_SECTIONAL
Sampling method: PROBABILITY_SAMPLE
Study population: Egyptian Relapsing-Remitting Multiple Sclerosis Patients

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

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.

Eligibility 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.
* Kurtzke EDSS step 0.0 - 6.0.
* At the time of screening, being treated with a stable dose of Interferon Beta 1a for at least 6 months.

Exclusion Criteria:

* they had been treated in the last 30 days with methylprednisolone
* they had changed their IFN-β preparation within the last 18 months
* they had other chronic diseases associated with MS
* they had been previously treated with immunosuppressive agents

Primary outcomes:
measure: Correlation between IL17 levels and patients' response to interferon beta 1a as measured by ELISA
timeFrame: Patients were treated with INF B 1a for at least 6 months
Secondary outcomes:
measure: Correlation between IL 22 levels and patients' response to interferon beta 1a, measured by ELISA
timeFrame: Patients were treated with INF B 1a for at least 6 months
measure: Correlation between Expanded Disability Status Scale and patients' response to interferon beta 1a
timeFrame: Patients were treated with INF B 1a for at least 6 months
measure: Correlation between malondialdehyde levels and patients' response to interferon beta 1a
timeFrame: Patients were treated with INF B 1a for at least 6 months
measure: Correlation between MRI load and Patients' response to interferon beta 1a
timeFrame: Patients were treated with INF B 1a for at least 6 months
measure: Correlation between body mass index and patients' response to interferon beta 1 a
timeFrame: Patients were treated with INF B 1a for at least 6 months
Other outcomes:
Locations:
city: Cairo
country: Egypt
facility: Nasser Institute for Research and Treatment
Study officials:
References:
citation: 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.
citation: 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.
citation: 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.
citation: 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.
citation: 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.