Contributions
Abstract: P597
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Introduction: Netrin-1 (NTN-1) belongs to laminin-related proteins that regulate glial cell migration, axon guidance, oligodendroglial maturation and angiogenesis. More recently, experimental studies on NTN-1 suggested that this protein may also play an important role in regulating blood-brain barrier (BBB) integrity and inflammation. Contrast enhanced MRI is an important tool to detect MS lesions with BBB breakdown and ongoing inflammation (active lesions). As serum NTN-1 values have recently been reported to be increased in MS we speculated that this might be a consequence of active lesions.
Objective: To compare serum NTN-1 between MS patients with active vs. non-active lesions and patients with other non-inflammatory neurological diseases and to investigate the temporal dynamics of serum NTN-1 in MS patients in relation to MRI and clinical activity.
Methods: 79 patients (clinically isolated syndrome, n=32; early RR MS, n=47), mean age 33.9 (SD 8.8) years, median Expanded Disability Status Scale (EDSS) score 1.0 (IQR 0.0-2.5) underwent gadolinium (Gd) enhanced 3 T MRI and simultaneous blood sampling at baseline and clinical and MRI follow-up (n=70, median follow-up time 1.4 years, IQR=1.0-2.3 years). 30 patients with other non-inflammatory neurological diseases, mean age 37.1 (SD 10.2) years, served as controls. Serum NTN-1 levels were assessed by ELISA (Cusabio Biotech, Wuhan, China).
Results: At baseline serum NTN-1 levels were similar in the MRI active, i.e. Gd+ positive patients (n=47) and in MRI non-active (n=32) MS patients and we observed no difference to controls. In the subgroup of Gd+ patients serum NTN-1 was significantly decreased in those who were also clinically active (n=9) when compared to clinically non-active patients (n=38) (p=0.034). Longitudinally collected blood samples during MRI with non-active lesions showed no temporal dynamics of serum NTN-1 in either initially MRI active or non-active subgroups. Serum NTN-1 was also unrelated to age, physical disability at remission and disease duration.
Conclusion: Serum NTN-1 cannot serve as body fluid biomarker for subclinical disease activity as evidenced by contrast enhancing lesions on MRI. How NTN-1 levels change during a relapse may deserve further examination.
Disclosure:
Ms. Voortman, MSc reports no disclosers.
Ms. Bachmayer reports no disclosers.
Dr. Seifert-Held received speaker honoraria and support from Teva, Novartis, Biogen, Eisai.
Dr. Archelos reports no disclosers.
Dr. Ropele reports no disclosers.
Dr. Pichler reports no disclosers.
Dr. Enzinger has received funding for travel and speaker honoraria from Biogen Idec, Bayer Schering Pharma, Merck Serono, Novartis Genzyme and Teva Pharmaceutical Industries Ltd./sanofi-aventis; research support from Merck Serono, Biogen Idec., and Teva Pharmaceutical Industries Ltd./sanofi-aventis; serving on scientific advisory boards for Bayer Schering Pharma, Biogen Idec, Genzyme, Merck Serono, Novartis, and Teva Pharmaceutical Industries Ltd./sanofiaventis; academic editor for PLOSOne.
Dr. Fuchs serves on scientific advisory boards for Biogen Idec, Novartis, Genzyme, Merck Serono, TEVA Pharmaceutical Industries and has received funding for travel and speaker honoraria from Bayer Schering, Merck Serono, Biogen Idec and Sanofi Aventis.
Dr. Fazekas serves on scientific advisory boards for Biogen Idec, Genzyme, Merck Serono, Novartis, Roche and Teva Pharmaceutical Industries Ltd.; serves on the editorial boards of Multiple Sclerosis, the Polish Journal of Neurology and Neurosurgery, and the Swiss Archives of Neurology and Psychiatry; provides services for Actelion and Parexel and has received speaker honoraria and support from Almirall, Merck Serono, Novartis, Pfizer, Roche, Shire and Teva Pharmaceutical Industries Ltd.
Dr. Khalil has received funding for travel and speaker honoraria from Bayer Schering Pharma, Novartis Genzyme, Merck Serono, Biogen Idec, and Teva Pharmaceutical Industries.
Abstract: P597
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Introduction: Netrin-1 (NTN-1) belongs to laminin-related proteins that regulate glial cell migration, axon guidance, oligodendroglial maturation and angiogenesis. More recently, experimental studies on NTN-1 suggested that this protein may also play an important role in regulating blood-brain barrier (BBB) integrity and inflammation. Contrast enhanced MRI is an important tool to detect MS lesions with BBB breakdown and ongoing inflammation (active lesions). As serum NTN-1 values have recently been reported to be increased in MS we speculated that this might be a consequence of active lesions.
Objective: To compare serum NTN-1 between MS patients with active vs. non-active lesions and patients with other non-inflammatory neurological diseases and to investigate the temporal dynamics of serum NTN-1 in MS patients in relation to MRI and clinical activity.
Methods: 79 patients (clinically isolated syndrome, n=32; early RR MS, n=47), mean age 33.9 (SD 8.8) years, median Expanded Disability Status Scale (EDSS) score 1.0 (IQR 0.0-2.5) underwent gadolinium (Gd) enhanced 3 T MRI and simultaneous blood sampling at baseline and clinical and MRI follow-up (n=70, median follow-up time 1.4 years, IQR=1.0-2.3 years). 30 patients with other non-inflammatory neurological diseases, mean age 37.1 (SD 10.2) years, served as controls. Serum NTN-1 levels were assessed by ELISA (Cusabio Biotech, Wuhan, China).
Results: At baseline serum NTN-1 levels were similar in the MRI active, i.e. Gd+ positive patients (n=47) and in MRI non-active (n=32) MS patients and we observed no difference to controls. In the subgroup of Gd+ patients serum NTN-1 was significantly decreased in those who were also clinically active (n=9) when compared to clinically non-active patients (n=38) (p=0.034). Longitudinally collected blood samples during MRI with non-active lesions showed no temporal dynamics of serum NTN-1 in either initially MRI active or non-active subgroups. Serum NTN-1 was also unrelated to age, physical disability at remission and disease duration.
Conclusion: Serum NTN-1 cannot serve as body fluid biomarker for subclinical disease activity as evidenced by contrast enhancing lesions on MRI. How NTN-1 levels change during a relapse may deserve further examination.
Disclosure:
Ms. Voortman, MSc reports no disclosers.
Ms. Bachmayer reports no disclosers.
Dr. Seifert-Held received speaker honoraria and support from Teva, Novartis, Biogen, Eisai.
Dr. Archelos reports no disclosers.
Dr. Ropele reports no disclosers.
Dr. Pichler reports no disclosers.
Dr. Enzinger has received funding for travel and speaker honoraria from Biogen Idec, Bayer Schering Pharma, Merck Serono, Novartis Genzyme and Teva Pharmaceutical Industries Ltd./sanofi-aventis; research support from Merck Serono, Biogen Idec., and Teva Pharmaceutical Industries Ltd./sanofi-aventis; serving on scientific advisory boards for Bayer Schering Pharma, Biogen Idec, Genzyme, Merck Serono, Novartis, and Teva Pharmaceutical Industries Ltd./sanofiaventis; academic editor for PLOSOne.
Dr. Fuchs serves on scientific advisory boards for Biogen Idec, Novartis, Genzyme, Merck Serono, TEVA Pharmaceutical Industries and has received funding for travel and speaker honoraria from Bayer Schering, Merck Serono, Biogen Idec and Sanofi Aventis.
Dr. Fazekas serves on scientific advisory boards for Biogen Idec, Genzyme, Merck Serono, Novartis, Roche and Teva Pharmaceutical Industries Ltd.; serves on the editorial boards of Multiple Sclerosis, the Polish Journal of Neurology and Neurosurgery, and the Swiss Archives of Neurology and Psychiatry; provides services for Actelion and Parexel and has received speaker honoraria and support from Almirall, Merck Serono, Novartis, Pfizer, Roche, Shire and Teva Pharmaceutical Industries Ltd.
Dr. Khalil has received funding for travel and speaker honoraria from Bayer Schering Pharma, Novartis Genzyme, Merck Serono, Biogen Idec, and Teva Pharmaceutical Industries.