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Neurology 2003;60:S2-S7
© 2003 American Academy of Neurology

Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represent the opinions of the authors and are not endorsed by nor do they reflect the views of the American Academy of Neurology, Editor-in-Chief, or Associate Editors of Neurology.

The pathogenesis of CIDP

Rationale for treatment with immunomodulatory agents

Klaus V. Toyka, MD and Ralf Gold, MD

From the Department of Neurology, Clinical Research Unit for Multiple Sclerosis and Neuroimmunology, Julius-Maximilians University, Würzburg, Germany.

Address correspondence and reprint requests to Dr. Klaus V. Toyka, Department of Neurology, Julius-Maximilians University, Josef-Schneider-Strasse 11, D-97080 Würzburg, Germany; e-mail: kv.toyka{at}mail.uni-wuerzburg.de

Current knowledge about the pathogenic mechanisms involved in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) supports an autoimmune etiology. Some of the cell and humorally mediated immune responses that contribute to the development of CIDP resemble those implicated in multiple sclerosis (MS). The effector role of circulating antibodies has recently been revisited. In addition, similar to the situation in MS, histopathologic studies support the heterogeneity of disease mechanisms in CIDP, with variants showing axon damage. In addition to intravenous immunoglobulin (IVIg), prednisone, and plasma exchange, immunomodulatory drugs also were used to treat CIDP, although no definitive trial data are available. One class of immunomodulators, interferon beta formulations, has proven efficacy in the treatment of MS, and because of clinical similarities between the two diseases it is attractive to investigate whether some agents that are effective in the treatment of MS would also be effective in CIDP. Preliminary studies have evaluated the effects of interferon beta formulations in the treatment of CIDP, one of which has shown promising results and warrants further investigation.




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