Author Of 1 Presentation
P0422 - A Case of Multiple Sclerosis in an 18-year-old Female with Juvenile Idiopathic Arthritis on Abatacept (ID 207)
Abstract
Background
To date there are few case reports regarding the concurrence of Multiple Sclerosis (MS) and Juvenile Idiopathic Arthritis (JIA). Anti-tumor necrosis factor (TNF) agents, a staple of JIA treatment, have been associated with optic neuritis, MS, cranial nerve palsies, and peripheral neuropathies. In contrast, other biologic therapies – including anakinra, tocilizumab, and abatacept – are not thought to play a significant role in precipitating demyelinating disease.
Objectives
To describe a case of MS concurrent with JIA. To suggest a potential role for remote anti-TNF agents and current abatacept therapy in progression of demyelinating disease. To discuss the selection of disease-modifying therapy (DMT) for both MS and JIA in a patient who progressed to MS on abatacept.
Methods
We describe a case study of one patient. We also review the literature regarding the coincidence of JIA and MS and the occurence of demyelinating events with biological agents.
Results
We propose a case suggesting a potential role for abatacept in precipitating demyelinating disease. Our patient was diagnosed with JIA at age 15 and received methotrexate and etanercept without benefit. She was transitioned to infliximab briefly prior to abatacept monotherapy at age 16. She suffered a mild traumatic brain injury after a motor vehicle collision at age 17. MRI brain with and without contrast, obtained due to seizure, demonstrated multiple T2 hyperintensities in the periventricular and juxtacortical white matter without enhancement. Neurologic exam and workup at that time were unremarkable. One year later, she presented with left vision loss. MRI brain and spine without contrast revealed left optic neuritis and extensive new cortical, juxtacortical, basal ganglia, corpus callosum, and brainstem lesions, some with diffusion restriction suggesting active demyelination. Lab workup revealed 8 cerebrospinal fluid oligoclonal bands; aquaporin-4 and myelin oligodendrocyte glycoprotein antibodies were negative. Rheumatologic workup was negative. Abatacept was discontinued; she received methylprednisolone and was transitioned to ocrelizumab.
Conclusions
In a patient with concurrent JIA, we report the second described case of progression to MS on abatacept. While demyelinating syndromes are classically described as temporally related to initiation of anti-TNF agents, our patient had discontinued infliximab two years prior. Further investigation is needed in JIA to determine if remote anti-TNF therapy or non-TNF agents such as abatacept may also preclude an increased risk of demyelinating events.
Presenter Of 1 Presentation
P0422 - A Case of Multiple Sclerosis in an 18-year-old Female with Juvenile Idiopathic Arthritis on Abatacept (ID 207)
Abstract
Background
To date there are few case reports regarding the concurrence of Multiple Sclerosis (MS) and Juvenile Idiopathic Arthritis (JIA). Anti-tumor necrosis factor (TNF) agents, a staple of JIA treatment, have been associated with optic neuritis, MS, cranial nerve palsies, and peripheral neuropathies. In contrast, other biologic therapies – including anakinra, tocilizumab, and abatacept – are not thought to play a significant role in precipitating demyelinating disease.
Objectives
To describe a case of MS concurrent with JIA. To suggest a potential role for remote anti-TNF agents and current abatacept therapy in progression of demyelinating disease. To discuss the selection of disease-modifying therapy (DMT) for both MS and JIA in a patient who progressed to MS on abatacept.
Methods
We describe a case study of one patient. We also review the literature regarding the coincidence of JIA and MS and the occurence of demyelinating events with biological agents.
Results
We propose a case suggesting a potential role for abatacept in precipitating demyelinating disease. Our patient was diagnosed with JIA at age 15 and received methotrexate and etanercept without benefit. She was transitioned to infliximab briefly prior to abatacept monotherapy at age 16. She suffered a mild traumatic brain injury after a motor vehicle collision at age 17. MRI brain with and without contrast, obtained due to seizure, demonstrated multiple T2 hyperintensities in the periventricular and juxtacortical white matter without enhancement. Neurologic exam and workup at that time were unremarkable. One year later, she presented with left vision loss. MRI brain and spine without contrast revealed left optic neuritis and extensive new cortical, juxtacortical, basal ganglia, corpus callosum, and brainstem lesions, some with diffusion restriction suggesting active demyelination. Lab workup revealed 8 cerebrospinal fluid oligoclonal bands; aquaporin-4 and myelin oligodendrocyte glycoprotein antibodies were negative. Rheumatologic workup was negative. Abatacept was discontinued; she received methylprednisolone and was transitioned to ocrelizumab.
Conclusions
In a patient with concurrent JIA, we report the second described case of progression to MS on abatacept. While demyelinating syndromes are classically described as temporally related to initiation of anti-TNF agents, our patient had discontinued infliximab two years prior. Further investigation is needed in JIA to determine if remote anti-TNF therapy or non-TNF agents such as abatacept may also preclude an increased risk of demyelinating events.