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Growth-differentiation factor 15 (GDF-15) is increased in serum of stable multiple sclerosis patients
Author(s): ,
A. Amstad
Affiliations:
Department of Biomedicine
,
C. Frick
Affiliations:
Department of Biomedicine
,
C. Barro
Affiliations:
Neurologic clinic and Policlinic, Departments of Medicine, Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland
,
M. Recher
Affiliations:
Department of Biomedicine
,
C. Berger
Affiliations:
Department of Biomedicine
,
J. Wischhusen
Affiliations:
Department of Gynaecology, University Hospital Würzburg, Würzburg, Germany
,
L. Kappos
Affiliations:
Neurologic clinic and Policlinic, Departments of Medicine, Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland
,
Y. Naegelin
Affiliations:
Neurologic clinic and Policlinic, Department of Medicine, University Hospital and University of Basel
,
J. Kuhle
Affiliations:
Neurologic clinic and Policlinic, Departments of Medicine, Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland
M. Mehling
Affiliations:
Neurologic clinic and Policlinic, DNeurologic clinic and Policlinic, Departments of Medicine, Biomedicine and Clinical Researepartments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, University Hospital Basel and University of Basel, Basel, Switzerland
ECTRIMS Online Library. Mehling M. Oct 12, 2018; 229015
Matthias Mehling
Matthias Mehling
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Abstract: P1175

Type: Poster Sessions

Abstract Category: Pathology and pathogenesis of MS - Biomarkers

Background: Extensive infiltrations of blood-derived immune cells into the central nervous system are the cornerstone of immunopathology in relapsing multiple sclerosis (rMS). The cytokine Growth differentiation factor-15 (GDF-15) exerts anti-inflammatory properties by inhibiting adhesion of immune cells to endothelial cells. No blood biomarkers are available that allow differentiation of inflammatory disease activity or stability in individual patients with rMS.
Objective: To assess the relation of serum concentrations of GDF-15 with clinically and MRI defined disease activity in patients with rMS.
Methods: Serum and CSF GDF-15 concentrations were measured by ELISA in a cohort (cohort 1) of patients with rMS, patients with non-inflammatory neurological diseases (NIND) and patients with other inflammatory neurological disease (OIND, containing acute inflammatory CNS disorders). Serum GDF-15 was measured in two independent cohorts (cohorts 2 and 3) of patients with rMS and healthy controls (HC) at the University Hospital Basel.
Results: In cohort 1, median serum GDF-15 concentration were higher in patients with OIND (n=16; 497pg/ml, IQR=320-900) vs patients with NIND (n=46; 304pg/ml, IQR=245-304; p=0.012) or rMS (n=42; 356pg/ml, IQR=245-460; p=0.023). GDF-15 CSF concentrations correlated with serum concentrations (r=0.43, 95%CI=0.24-0.59, p< 0.0001). In cohort 2, median serum GDF-15 concentrations were higher in patients with clinically stable rMS treated with interferon (IFN)-beta (n=24; 587pg/ml, IQR=345-728; p=0.0007) or fingolimod (n=42; 557pg/ml, IQR=420-666; p< 0.0001) vs HC (n=29; 319pg/ml, IQR=271-414). In the longitudinally sampled and clinically and radiologically monitored cohort 3 (mean observation time 5.9 years), median GDF-15 concentrations were higher in IFN-beta treated patients with stable disease course (n=56; 384pg/ml, IQR=238-629) vs HC (n=39; 302pg/ml, IQR=248-364; p=0.03) but also vs patients with signs of MRI activity (gadolinium enhancing lesions (n=49; 324pg/ml, IQR=263-421; p=0.04) or new T2 lesions (n=51; 292pg/ml, IQR=206-394; p=0.007)).
Conclusions: Serum concentrations of GDF-15 were increased during acute inflammatory CNS disorders. In MS, a chronic inflammatory CNS disorder, increased levels of GDF-15 were found in treated patients with a stable disease course, possibly reflecting an anti-inflammatory mechanism. GDF-15 has the potential to serve as a biomarker for a stable disease course in MS.
Disclosure: This study was supported by the Swiss Multiple Sclerosis Society. Andrea Amstad was supported by the Goldschmidt Jacobson Foundation. Christian Barro received conference travel grant from Teva and Novartis. Mike Recher, Christoph Berger, Jörg Wischhusen and Yvonne Naegelin have nothing to disclose. Ludwig Kappos' Institution (University Hospital Basel) received in the last 3 years and used exclusively for research support at the Department: steering committee, advisory board and consultancy fees from Actelion, Alkermes, Almirall, Bayer, Biogen, Celgene/Receptos, df-mp, Excemed, GeNeuro SA, Genzyme, Japan Tobacco, Merck, Minoryx, Mitsubishi Pharma, Novartis, Roche, sanofi-aventis, Santhera, Teva, Vianex and royalties for Neurostatus-UHB products. The Research of the MS Center in Basel has been supported by grants from Bayer, Biogen, Novartis, the Swiss MS Society, the Swiss National Research Foundation, the European Union and Roche Research Foundations. Jens Kuhle received speaker fees, research support, travel support, and/or served on advisory boards by ECTRIMS, Swiss MS Society, Swiss National Research Foundation, (320030_160221), University of Basel, Bayer, Biogen, Genzyme, Merck, Novartis, Protagen AG, Roche, Teva. Matthias Mehling received received in the last 3 years speaker fees, travel support, and/or served on advisory boards by Swiss MS Society, University of Basel, Actelion, Genzyme, Merck and Novartis and is supported by the Swiss National Science Foundation (PZ00P3_154733).

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