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Treatment of immune-mediated, dysimmune neuropathies.
Acta Neurol Scand. 2005 Aug; 112(2):115-25.AN

Abstract

This review focuses on the actual status and recent advances in the treatment of immune-mediated neuropathies, including: Guillain-Barre syndrome (GBS) with its subtypes acute inflammatory demyelinating polyradiculoneuropathy, acute motor axonal neuropathy, acute motor and sensory axonal neuropathy, Miller Fisher syndrome, and acute pandysautonomia; chronic inflammatory demyelinating polyneuropathy (CIDP) with its subtypes classical CIDP, CIDP with diabetes, CIDP/monoclonal gammopathy of undetermined significance (MGUS), sensory CIDP, multifocal motor neuropathy (MMN), multifocal acquired demyelinating sensory and motor neuropathy or Lewis-Sumner syndrome, multifocal acquired sensory and motor neuropathy, and distal acquired demyelinating sensory neuropathy; IgM monoclonal gammopathies with its subtypes Waldenstrom's macroglobulinemia, myelin-associated glycoprotein-associated gammopathy, polyneuropathy, organomegaly, endocrinopathy, M-protein, skin changes syndrome, mixed cryoglobulinemia, gait ataxia, late-onset polyneuropathy syndrome, and MGUS. Concerning the treatment of GBS, there is no significant difference between intravenous immunoglobulins (IVIG), plasma exchange or plasma exchange followed by IVIG. Because of convenience and absent invasiveness, IVIG are usually preferred. In treating CIDP corticosteroids, IVIG, or plasma exchange are equally effective. Despite the high costs and relative lack of availability, IVIG are preferentially used. For the one-third of patients, who does not respond, other immunosuppressive options are available. In MMN IVIG are the treatment of choice. Inadequate response in 20% of the patients requires adjunctive immunosuppressive therapies. Neuropathies with IgM monoclonal gammopathy may respond to various chemotherapeutic agents, although the long-term effects are unknown. In addition, such treatment may be associated with serious side effects. Recent data support the use of rituximab, a monoclonal antibody against the B-cell surface-membrane-marker CD20.

Authors+Show Affiliations

Department of Neurology, Krankenanstalt Rudolfstiftung, Vienna, Austria. duarte@aonmail.at

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

16008538

Citation

Finsterer, J. "Treatment of Immune-mediated, Dysimmune Neuropathies." Acta Neurologica Scandinavica, vol. 112, no. 2, 2005, pp. 115-25.
Finsterer J. Treatment of immune-mediated, dysimmune neuropathies. Acta Neurol Scand. 2005;112(2):115-25.
Finsterer, J. (2005). Treatment of immune-mediated, dysimmune neuropathies. Acta Neurologica Scandinavica, 112(2), 115-25.
Finsterer J. Treatment of Immune-mediated, Dysimmune Neuropathies. Acta Neurol Scand. 2005;112(2):115-25. PubMed PMID: 16008538.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Treatment of immune-mediated, dysimmune neuropathies. A1 - Finsterer,J, PY - 2005/7/13/pubmed PY - 2005/9/10/medline PY - 2005/7/13/entrez SP - 115 EP - 25 JF - Acta neurologica Scandinavica JO - Acta Neurol. Scand. VL - 112 IS - 2 N2 - This review focuses on the actual status and recent advances in the treatment of immune-mediated neuropathies, including: Guillain-Barre syndrome (GBS) with its subtypes acute inflammatory demyelinating polyradiculoneuropathy, acute motor axonal neuropathy, acute motor and sensory axonal neuropathy, Miller Fisher syndrome, and acute pandysautonomia; chronic inflammatory demyelinating polyneuropathy (CIDP) with its subtypes classical CIDP, CIDP with diabetes, CIDP/monoclonal gammopathy of undetermined significance (MGUS), sensory CIDP, multifocal motor neuropathy (MMN), multifocal acquired demyelinating sensory and motor neuropathy or Lewis-Sumner syndrome, multifocal acquired sensory and motor neuropathy, and distal acquired demyelinating sensory neuropathy; IgM monoclonal gammopathies with its subtypes Waldenstrom's macroglobulinemia, myelin-associated glycoprotein-associated gammopathy, polyneuropathy, organomegaly, endocrinopathy, M-protein, skin changes syndrome, mixed cryoglobulinemia, gait ataxia, late-onset polyneuropathy syndrome, and MGUS. Concerning the treatment of GBS, there is no significant difference between intravenous immunoglobulins (IVIG), plasma exchange or plasma exchange followed by IVIG. Because of convenience and absent invasiveness, IVIG are usually preferred. In treating CIDP corticosteroids, IVIG, or plasma exchange are equally effective. Despite the high costs and relative lack of availability, IVIG are preferentially used. For the one-third of patients, who does not respond, other immunosuppressive options are available. In MMN IVIG are the treatment of choice. Inadequate response in 20% of the patients requires adjunctive immunosuppressive therapies. Neuropathies with IgM monoclonal gammopathy may respond to various chemotherapeutic agents, although the long-term effects are unknown. In addition, such treatment may be associated with serious side effects. Recent data support the use of rituximab, a monoclonal antibody against the B-cell surface-membrane-marker CD20. SN - 0001-6314 UR - https://www.unboundmedicine.com/medline/citation/16008538/Treatment_of_immune_mediated_dysimmune_neuropathies_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0001-6314&date=2005&volume=112&issue=2&spage=115 DB - PRIME DP - Unbound Medicine ER -