Exacerbation of Chronic Inflammatory Demyelinating Polyradiculoneuropathy during Interferon.BETA.-1b Therapy in a Patient with Childhood-onset Multiple Sclerosis

Matsuse, Dai; Ochi, Hirofumi; Tashiro, Kotaro; Nomura, Takuo; Murai, Hiroyuki; Taniwaki, Takayuki; Kira, Jun Ichi

doi:10.2169/internalmedicine.44.68

Cited by 21 publications

(9 citation statements)

References 23 publications

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“…The predominant or exclusive demyelinating nature of neuropathy (5/6 patients) suggested an immune-mediated pathogenesis of nerve damage. In another report, a patient with childhood-onset MS and asymptomatic demyelinating neuropathy, developed clinically overt CIDP 2 months into IFNβ-1b therapy [73]. Management entailed IFNβ-withdrawal and an oral steroid course, with subsequent patient recovery to baseline function and marked electrophysiological improvement.…”

Section: Interferon Betamentioning

confidence: 99%

Drug-induced dysimmune demyelinating neuropathies

Stübgen

2011

Journal of the Neurological Sciences

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Section: Interferon Betamentioning

confidence: 99%

Drug-induced dysimmune demyelinating neuropathies

Stübgen

2011

Journal of the Neurological Sciences

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“…She was treated for MS before the onset of “CIDP”. Interferon (IFN) beta‐1b was administrated to prevent MS relapse, which might have influenced the onset of PNS symptoms . Previous reports have also suggested the existence of relationships between IFN beta and CIDP onset .…”

Section: Anti‐neurofascin Antibody In Ccpdmentioning

confidence: 99%

Anti‐neurofascin antibody in combined central and peripheral demyelination

Yamasaki

2013

Clinical & Exp Neuroim

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Neurofascin (NF), a cell adhesion molecule expressed in both the central nervous system (CNS) and the peripheral nervous system (PNS), plays important roles in developing and maintaining neural structures. There are several subtypes of NF resulting from post-translational modifications: NF155, 166, 180 and 186. Among them, NF155 and NF186 are expressed in the mature CNS/PNS. NF155 is present on the oligodendroglial cell surface in the CNS and on the Schwann cell surface in the PNS at paranodes, where it tightly connects with contactin and caspr on the axonal surface of the paranode, and acts as a stabilizer of the nodes of Ranvier. NF186 exists on the axonal surface at the nodes of Ranvier. NF186 is associated with voltage-gated Na channels (Nav), whereas both NF186 and Nav are anchored by ankyrin G. NF186 contributes to the clustering of Nav at the node. Combined central and peripheral demyelination (CCPD) is an inflammatory demyelinating disorder affecting both the CNS and PNS tissues. Distinct mechanisms including multiple sclerosis and chronic inflammatory demyelinating polyradiculoneuropathy have been hypothesized to play a role in this condition on the basis of distinctive clinical and laboratory findings. We detected anti-NF155 antibody by cell-based assay, enzyme-linked immunosorbent assay, and western blot in both the sera and cerebrospinal fluids of CCPD patients at high frequencies, but did not detect it in patients with other neurological disease or healthy controls. Herein, basic aspects and the clinical significance of NF as indispensable regulators and autoimmune target molecules are summarized. (Clin. Exp. Neuroimmunol.

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“…Two case reports of patients with multiple sclerosis developing CIDP after interferon beta-1b treatment have been published. 111,112 These adverse events, together with its doubtful efficacy and high costs, must lead to the conclusion that there is no place for interferon beta treatment in CIDP.…”

Section: Tacrolimusmentioning

confidence: 99%

Chronic Inflammatory Demyelinating Polyradiculoneuropathy - An Overview of Existing Treatment Options and Prospects for the Future

Schaik¹,

Eftimov²

2011

European Neurological Review

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Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an immune-mediated polyneuropathy. CIDP can cause prolonged periods of disability with many patients becoming severely debilitated at some time during their illness. Several open, uncontrolled studies and blinded, randomised clinical trials have shown that immunomodulatory therapy has a beneficial effect in CIDP. This paper reviews existing treatment options, provides a treatment algorithm and discusses prospects for the future. Corticosteroids, intravenous immunoglobulin, plasma exchange, immunosuppressive agents such as azathioprine, methotrexate, mycophenolate mofetil, cyclophosphamide, cyclosporine A, rituximab, alemtuzumab, etanercept, tacrolimus, interferon beta and alpha and autologous stem cell transplantation have been used in CIDP. Only corticosteroids, intravenous immunoglobulin and plasmapheresis have been proven to be effective in randomised controlled trials, however. As non-responsiveness to treatment seems to be associated with a greater degree of axonal dysfunction, finding therapies aimed at protecting the axon and restoring axonal damage are needed.

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Exacerbation of Chronic Inflammatory Demyelinating Polyradiculoneuropathy during Interferon.BETA.-1b Therapy in a Patient with Childhood-onset Multiple Sclerosis

Abstract: Interferon -1b (IFN -1b) is commonly used for relapsing-remitting multiple sclerosis (MS).

Cited by 21 publications

References 23 publications

Drug-induced dysimmune demyelinating neuropathies

Drug-induced dysimmune demyelinating neuropathies

Anti‐neurofascin antibody in combined central and peripheral demyelination

Chronic Inflammatory Demyelinating Polyradiculoneuropathy - An Overview of Existing Treatment Options and Prospects for the Future

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