Pathogenic mechanisms in inflammatory and paraproteinaemic peripheral neuropathies

Rinaldi, Simon; Bennett, David L.H.

doi:10.1097/wco.0000000000000137

Cited by 11 publications

(7 citation statements)

References 77 publications

(18 reference statements)

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“…The disease is characterized by a growing list of auto-antibodies found in patient sera that target peripheral nerve components (Fehmi et al, 2018). CIDP autoantibodies may exert a pathogenic effect by directly interrupting the axonal-myelination structure, or complement-dependent cytotoxicity (Rinaldi and Bennett, 2014). There is also an appreciation of cellular immune component to CIDP (Mathey et al, 2015).…”

Section: Cellular Immunity In Inflammatory Neuropathiesmentioning

confidence: 99%

Cytotoxic Immunity in Peripheral Nerve Injury and Pain

et al. 2020

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Section: Cellular Immunity In Inflammatory Neuropathiesmentioning

confidence: 99%

Cytotoxic Immunity in Peripheral Nerve Injury and Pain

et al. 2020

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“…* These patients were included in a previous publication [33]. 1 AZA=azathioprine, CPM=cyclophosphamide, MPM=mycophenolate-mofetil, MTX=methotrexate.…”

Section: Acknowledgmentsmentioning

confidence: 99%

“…The inflammatory neuropathies are a heterogeneous group of disorders in which peripheral nerve function and structure are disturbed by largely ill-defined immunological mechanisms [1]. They can broadly be divided into acute and chronic forms, typified by the umbrella terms Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP), respectively.…”

Section: Introductionmentioning

confidence: 99%

Immunoadsorption and Plasma Exchange in Seropositive and Seronegative Immune-Mediated Neuropathies

Davies

Fehmi

Şenel

et al. 2020

JCM

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The inflammatory neuropathies are disabling conditions with diverse immunological mechanisms. In some, a pathogenic role for immunoglobulin G (IgG)-class autoantibodies is increasingly appreciated, and immunoadsorption (IA) may therefore be a useful therapeutic option. We reviewed the use of and response to IA or plasma exchange (PLEx) in a cohort of 41 patients with nodal/paranodal antibodies identified from a total of 573 individuals with suspected inflammatory neuropathies during the course of routine diagnostic testing (PNAb cohort). 20 patients had been treated with PLEx and 4 with IA. Following a global but subjective evaluation by their treating clinicians, none of these patients were judged to have had a good response to either of these treatment modalities. Sequential serology of one PNAb+ case suggests prolonged suppression of antibody levels with frequent apheresis cycles or adjuvant therapies, may be required for effective treatment. We further retrospectively evaluated the serological status of 40 patients with either Guillain-Barré syndrome (GBS) or chronic inflammatory demyelinating polyneuropathy (CIDP), and a control group of 20 patients with clinically-isolated syndrome/multiple sclerosis (CIS/MS), who had all been treated with IgG-depleting IA (IA cohort). 32 of these patients (8/20 with CIDP, 13/20 with GBS, 11/20 with MS) were judged responsive to apheresis despite none of the serum samples from this cohort testing positive for IgG antibodies against glycolipids or nodal/paranodal cell-adhesion molecules. Although negative on antigen specific assays, three patients’ pre-treatment sera and eluates were reactive against different components of myelinating co-cultures. In summary, preliminary evidence suggests that GBS/CIDP patients without detectable IgG antibodies on routine diagnostic tests may nevertheless benefit from IA, and that an unbiased screening approach using myelinating co-cultures may assist in the detection of further autoantibodies which remain to be identified in such patients.

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“…Recently, CIDP associated with paraproteinemia is viewed as a distinct entity, since the clinical course and management strategies vary [1,7,8]. Paraproteinemic demyelinating neuropathy (PDN) may be an appropriate term, despite there is no consensus as to whether it should be considered the same as CIDP [9].…”

Section: Discussionmentioning

confidence: 99%

Remission of Chronic Acquired Demyelinating Polyneuropathy Associated With Paraproteinemia After Removal of Skull Plasmacytoma

2017

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Chronic acquired demyelinating polyneuropathy can be caused by various etiologies. Although chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is the most common chronic acquired demyelinating polyneuropathy, currently there is no suitable biomarker to diagnose CIDP; hence misdiagnosis of CIDP has not been unusual. Herein, we present a patient with initially presumed CIDP, who maintains disease remission after early surgical removal of solitary plasmacytoma during 1-year follow-up. A 55-year-old woman was referred to our hospital due to progressive upper and lower extremity weakness from 6 months ago. Nerve conduction study findings were compatible with acquired demyelinating polyneuropathy, fulfilling electrodiagnostic criteria of CIDP. Serum electrophoresis suggested monoclonal gammopathy of lambda type, but the bone marrow biopsy showed no evidence of neoplastic plasma cell infiltration. Brain magnetic resonance imaging revealed an osteolytic mass involving the right parietal skull and adjacent dura mater. Total excision of the skull mass was performed. The biopsy result was compatible with plasmacytoma. Even without long term administration of high dose corticosteroid, the patient not only has continued to improve clinically, but also showed markedly improved electrophysiological findings during 1-year follow-up.

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Pathogenic mechanisms in inflammatory and paraproteinaemic peripheral neuropathies

Cited by 11 publications

References 77 publications

Cytotoxic Immunity in Peripheral Nerve Injury and Pain

Cytotoxic Immunity in Peripheral Nerve Injury and Pain

Immunoadsorption and Plasma Exchange in Seropositive and Seronegative Immune-Mediated Neuropathies

Remission of Chronic Acquired Demyelinating Polyneuropathy Associated With Paraproteinemia After Removal of Skull Plasmacytoma

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