Natalizumab Treatment in a Patient With Chronic Inflammatory Demyelinating Polyneuropathy

Wolf, Christian; Menge, Til; Stenner, Max-Philipp; Hörste, Gerd Meyer zu; Saleh, Andreas; Hartung, Hans‐Peter; Wiendl, Heinz; Kieseier, Bernd C.

doi:10.1001/archneurol.2010.143

Cited by 45 publications

(24 citation statements)

References 9 publications

(6 reference statements)

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“…In that case, and as for MS [26], we wondered if this severe relapse might have been due to the interruption of Natalizumab. For patient 3, the course of the disease was slowly progressive: Natalizumab apparently stopped the worsening, and the total ONLS score (6/12) seems to have been stabilized; considering this last patient, it has to be stressed that Natalizumab has been prescribed after 13 years (with severe axonal loss), so that significant clinically palpable nerve lesions and on a lumbar MRI presence of a significant (an important) and diffuse hypertrophy of the root nerves were observed, as for the case of Wolf et al [14]. It is known that axonal loss, correlated with a higher disability and a worst response to treatments, is the major long-term prognostic factor of CIDP [27].…”

Section: Discussionmentioning

confidence: 82%

“…The experimental immunological blockade of VCAM-1 can reduce damage on peripheral nerve myelin (in animals with experimental autoimmune neuritis), but without offering a total protection for the nerve [25]. Recently, T cells expressing α4-integrin were demonstrated in the peripheral nerve of a CIDP patient [14]. However, despite a good targeting of T cells by Natalizumab, no positive clinical response was observed for this patient with a highly active form of CIDP.…”

Section: Discussionmentioning

confidence: 99%

“…Some of these drugs act by selectively suppressing T cells (Alemtuzumab), B cells (Rituximab) or complement (Eculizumab), with various clinical efficacies [13]. Among these alternative drugs, Natalizumab (used in the treatment of multiple sclerosis), acting against cellular adhesion and T-cell migration (by acting directly on the α4β1-integrin (also known as ‘very late antigen-4' or VLA4) on leukocytes), might be a promising treatment for some immune-mediated neuropathies, even though it was found to be ineffective in one case of CIDP [14]. According to this rationale, we used Natalizumab in three patients with CIDP who presented very severe and frequent recurrent relapses over a number of years.…”

Section: Introductionmentioning

confidence: 99%

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Natalizumab as a Disease-Modifying Therapy in Chronic Inflammatory Demyelinating Polyneuropathy - A Report of Three Cases

Vallat

Mathis²,

Ghorab³

et al. 2015

Eur Neurol

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Background: Several treatments are available to treat the immune-mediated chronic inflammatory demyelinating polyneuropathy (CIDP). Among these treatments, intravenous immunoglobulins, corticosteroids and plasma exchanges are validated and widely used. A few immunosuppressive drugs have been tried, but they had little efficiency. Methods: We describe three CIDP patients treated by Natalizumab (acting against cellular adhesion and T-cell migration) after a failure of the validated treatments. Results: We observed a long-term improvement in one patient, a dramatic improvement over a significant duration in another patient and stabilization in the last one. Conclusion: This open label study provides evidence for the value of Natalizumab as second-line treatment for individual patients with a high dependency on waning efficacy of first-line therapies. CIDP is characterized by heterogeneity of clinical phenotypes, electrophysiological and pathological features, and various variable courses types of evolution. The different responses to drugs of our patients are consistent with some reported cases and may reflect the spectrum of lesional mechanisms and the molecular dysfunctions in CIDP.

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Section: Discussionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Natalizumab as a Disease-Modifying Therapy in Chronic Inflammatory Demyelinating Polyneuropathy - A Report of Three Cases

Vallat

Mathis²,

Ghorab³

et al. 2015

Eur Neurol

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“…31 In a rat model of EAN, α4-integrin-blockade led to apoptosis of peripheral nerve infiltrating T-lymphocytes and improvement of clinical disease. 32 In the single literature report, a single 300 mg intravenous dose of natalizumab was ineffective in a patient with refractive CIDP, 33 …”

Section: T-lymphocytesmentioning

confidence: 99%

Biological Agents for Chronic Inflammatory Demyelinating Polyradiculoneuropathy

Stübgen¹

2014

US Neurology

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Chronic inflammatory demyelinating polyneuropathy (CIDP) denotes a spectrum of acquired, chronically progressive, or recurrent, immunemediated disorders of the peripheral nervous system with variable pathology and pathogenesis. 1 The estimated prevalence may be up to nine per 100,000 Due to the unpredictable efficacy, financial burden, and/or toxicity of 'broad-spectrum' immunomodulatory/-suppressive drugs, a need exists to develop effective and safe therapeutic strategies. 19,20 Research is hindered by the current lack of consensus on appropriate outcome measures and definition of treatment failure, as well as the tendency to study potentially effective therapy exclusively on refractive CIDP patients. 21,22 In order to realize the full potential of any new drug/agent, it may be advisable to identify and exclude from future drug trials any patients with predictably unresponsive (chronically stable and inactive) disease. 20 The future development and application of biomarkers could assist in the selection of effective therapy at initiation and long-term. 23 This review offers an updated summary and analysis of the genetically engineered, biological therapeutic agents considered potentially useful in patients with CIDP. Specific recommendations on management strategies are not proposed, as reviews on this subject have been published. [24][25][26][27][28] Biological therapeutics may rarely induce dysimmune inflammatory neuropathies (discussed elsewhere). 29 T-lymphocytesActivated T-lymphocytes invade peripheral nerve and partake in the pathogenesis of CIDP. 6,7,30 Natalizumab Natalizumab (Tysabri®) is a monoclonal antibody (mAb) targeted at the α4 subunit of α4β1 (VLA4) and α4β7 integrins that are expressed on AbstractChronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a term for a group of acquired, immune-mediated inflammatory demyelinating disorders of the peripheral nervous system. Most patients with CIDP respond to 'first-line' therapy with intravenous immunoglobulin (IVIG), plasmapheresis, and/or corticosteroids. 'Conventional' immunosuppressive drugs are of no proven benefit. Biological agents directed at key aspects of the CIDP immunopathogenic pathway have gained increasing attention due to the unpredictable efficacy and overall health risks of non-targeted immunosuppressive drugs. Presently, there exists insufficient clinical experience with biological therapy to allow specific treatment recommendations for CIDP. The challenge remains to identify drug-naïve or treatment-resistant CIDP patients who will most likely respond to targeted immunotherapy.

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“…In one case of CIDP, clinical and paraclinical effects of natalizumab treatment were studied [61]. T cells expressing the α4-integrin were found in the inflamed peripheral nerve, and natalizumab bound with high affinity to the α4-integrin on T lymphocytes.…”

Section: Natalizumab and Firategrastmentioning

confidence: 99%

Disease-modifying therapy in multiple sclerosis and chronic inflammatory demyelinating polyradiculoneuropathy: common and divergent current and future strategies

Melzer

Meuth

2014

Clin Exp Immunol

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OTHER ARTICLES PUBLISHED IN THIS SERIESParaneoplastic neurological syndromes. Clinical and Experimental Immunology 2014, 175: 336-48. Diagnosis, pathogenesis and treatment of myositis: recent advances. Clinical and Experimental Immunology 2014, 175: 349-58. Monoclonal antibodies in treatment of multiple sclerosis. Clinical and Experimental Immunology 2014, 175: 373-84 SummaryMultiple sclerosis (MS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) represent chronic, autoimmune demyelinating disorders of the central and peripheral nervous system. Although both disorders share some fundamental pathogenic elements, treatments do not provide uniform effects across both disorders. We aim at providing an overview of current and future disease-modifying strategies in these disorders to demonstrate communalities and distinctions.

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Natalizumab Treatment in a Patient With Chronic Inflammatory Demyelinating Polyneuropathy

Abstract: To study clinical and paraclinical effects of natalizumab in a patient with chronic inflammatory demyelinating polyneuropathy (CIDP).

Cited by 45 publications

References 9 publications

Natalizumab as a Disease-Modifying Therapy in Chronic Inflammatory Demyelinating Polyneuropathy - A Report of Three Cases

Natalizumab as a Disease-Modifying Therapy in Chronic Inflammatory Demyelinating Polyneuropathy - A Report of Three Cases

Biological Agents for Chronic Inflammatory Demyelinating Polyradiculoneuropathy

Disease-modifying therapy in multiple sclerosis and chronic inflammatory demyelinating polyradiculoneuropathy: common and divergent current and future strategies

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