
Contributions
Abstract: P699
Type: Poster
Abstract Category: Therapy - disease modifying - 26 Immunomodulation/Immunosuppression
Objective: Secukinumab is a fully human monoclonal antibody against interleukin-17A which is approved for the treatment of patients with moderate-to-severe plaque psoriasis, psoriatic arthritis, and ankylosing spondylitis (AS). Based on several studies supporting a central role for IL-17 in multiple sclerosis (MS) pathophysiology, a phase 2 trial showed that secukinumab reduced significantly the number of cumulative new gadolinium-enhancing T1 lesions (Gd+) compared to placebo. We present 2 patients with AS and concomitant MS treated with secukinumab.
Material and methods: We describe the clinical features, neurological examination, neuroimaging and clinical-radiological follow-up.
Results: A 46-year-old woman diagnosed with AS at age 22 years treated with etanercept from 2013 to mid-2016. In April 2016, she presented symptoms consistent with a brainstem relapse. Neurological examination revealed a residual Kurtzke scale (EDSS) of 1.5. A cranial MRI showed abundant demyelinating lesions with Gd+ being diagnosed of MS according to the McDonald 2010 criteria. The cerebrospinal fluid (CSF) showed the presence of oligoclonal IgG bands (BOCG+). Secukinumab was started in September 2016. She is remaining clinically stable so far without any new neurological symptoms. A control cranial MRI showed improvement in inflammatory activity.
A 41-year-old man diagnosed with AS at age 25 years treated with infliximab from 2009 to 2012 and etanercept from 2012 to 2016. In May 2016, he presented symptoms consistent with a spinal relapse. Neurological examination revealed a residual EDSS of 2.0. A craniospinal MRI showed abundant demyelinating lesions with Gd+ being diagnosed of MS according to the McDonald 2010 criteria. The CSF showed BOCG+. Secukinumab was started in November 2016. He is remaining clinically stable so far without any new neurological symptoms.
Conclusions: The role of Tumour Necrosis Factor-α blockers inducing demyelination (either with a progressive or a monophasic course) or triggering pre-existing demyelinating predisposition (as it might be for these patients), still remains controversial. Secukinumab may be an optimizing, feasible and cost-benefit therapeutic approach for patients with concurrence of MS and other rheumatologic diseases reducing, thereby, overexposure to other biological treatments as well as the incidence of adverse effects.
Disclosure:
Robles-Cedeño, René reports no disclosures.
Perkal Rug, Héctor reports no disclosures.
Armengol Pérez, Eulàlia, reports no disclosures.
Valls García, Ramón reports no disclosures.
Belchí Guillamón, Olga reports no disclosures.
Ramió-Torrentà, Lluís has received compensation for consulting services and speaking honoraria from Biogen Idec, Novartis, Bayer, Merck-Serono, Genzyme, Teva Pharmaceutical Industries Ltd and Almirall.
Abstract: P699
Type: Poster
Abstract Category: Therapy - disease modifying - 26 Immunomodulation/Immunosuppression
Objective: Secukinumab is a fully human monoclonal antibody against interleukin-17A which is approved for the treatment of patients with moderate-to-severe plaque psoriasis, psoriatic arthritis, and ankylosing spondylitis (AS). Based on several studies supporting a central role for IL-17 in multiple sclerosis (MS) pathophysiology, a phase 2 trial showed that secukinumab reduced significantly the number of cumulative new gadolinium-enhancing T1 lesions (Gd+) compared to placebo. We present 2 patients with AS and concomitant MS treated with secukinumab.
Material and methods: We describe the clinical features, neurological examination, neuroimaging and clinical-radiological follow-up.
Results: A 46-year-old woman diagnosed with AS at age 22 years treated with etanercept from 2013 to mid-2016. In April 2016, she presented symptoms consistent with a brainstem relapse. Neurological examination revealed a residual Kurtzke scale (EDSS) of 1.5. A cranial MRI showed abundant demyelinating lesions with Gd+ being diagnosed of MS according to the McDonald 2010 criteria. The cerebrospinal fluid (CSF) showed the presence of oligoclonal IgG bands (BOCG+). Secukinumab was started in September 2016. She is remaining clinically stable so far without any new neurological symptoms. A control cranial MRI showed improvement in inflammatory activity.
A 41-year-old man diagnosed with AS at age 25 years treated with infliximab from 2009 to 2012 and etanercept from 2012 to 2016. In May 2016, he presented symptoms consistent with a spinal relapse. Neurological examination revealed a residual EDSS of 2.0. A craniospinal MRI showed abundant demyelinating lesions with Gd+ being diagnosed of MS according to the McDonald 2010 criteria. The CSF showed BOCG+. Secukinumab was started in November 2016. He is remaining clinically stable so far without any new neurological symptoms.
Conclusions: The role of Tumour Necrosis Factor-α blockers inducing demyelination (either with a progressive or a monophasic course) or triggering pre-existing demyelinating predisposition (as it might be for these patients), still remains controversial. Secukinumab may be an optimizing, feasible and cost-benefit therapeutic approach for patients with concurrence of MS and other rheumatologic diseases reducing, thereby, overexposure to other biological treatments as well as the incidence of adverse effects.
Disclosure:
Robles-Cedeño, René reports no disclosures.
Perkal Rug, Héctor reports no disclosures.
Armengol Pérez, Eulàlia, reports no disclosures.
Valls García, Ramón reports no disclosures.
Belchí Guillamón, Olga reports no disclosures.
Ramió-Torrentà, Lluís has received compensation for consulting services and speaking honoraria from Biogen Idec, Novartis, Bayer, Merck-Serono, Genzyme, Teva Pharmaceutical Industries Ltd and Almirall.