Intravenous immunoglobulin in the treatment of autoimmune neuromuscular diseases: Present status and practical therapeutic guidelines
1999; Wiley; Volume: 22; Issue: 11 Linguagem: Inglês
10.1002/(sici)1097-4598(199911)22
ISSN1097-4598
Autores Tópico(s)Myasthenia Gravis and Thymoma
ResumoMuscle & NerveVolume 22, Issue 11 p. 1479-1497 Invited Review Intravenous immunoglobulin in the treatment of autoimmune neuromuscular diseases: Present status and practical therapeutic guidelines† Marinos C. Dalakas MD, Corresponding Author Marinos C. Dalakas MD [email protected] Neuromuscular Diseases Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 10, Room 4N248, 10 Center Drive MSC 1382, Bethesda, Maryland 20892-1382, USANeuromuscular Diseases Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 10, Room 4N248, 10 Center Drive MSC 1382, Bethesda, Maryland 20892-1382, USASearch for more papers by this author Marinos C. Dalakas MD, Corresponding Author Marinos C. Dalakas MD [email protected] Neuromuscular Diseases Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 10, Room 4N248, 10 Center Drive MSC 1382, Bethesda, Maryland 20892-1382, USANeuromuscular Diseases Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 10, Room 4N248, 10 Center Drive MSC 1382, Bethesda, Maryland 20892-1382, USASearch for more papers by this author First published: 07 October 1999 https://doi.org/10.1002/(SICI)1097-4598(199911)22:11 3.0.CO;2-BCitations: 117 † This article is a US Government work and, as such, is in the public domain in the United States of America. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Abstract This review summarizes the current status of intravenous immunoglobulin (IVIg) in the treatment of autoimmune neuromuscular disorders and the possible mechanisms of action of the drug based on work in vivo, in vitro, and in animal models. Supply of idiotypic antibodies, suppression of antibody production, or acceleration of catabolism of immunoglobulin G (IgG) are relevant in explaining the efficacy of IVIg in myasthenia gravis (MG), Lambert–Eaton myasthenic syndrome (LEMS), and antibody-mediated neuropathies. Suppression of pathogenic cytokines has putative relevance in inflammatory myopathies and demyelinating neuropathies. Inhibition of complement binding and prevention of membranolytic attack complex (MAC) formation are relevant in dermatomyositis (DM), Guillain–Barré syndrome (GBS), and MG. Modulation of Fc receptors or T-cell function is relevant in chronic inflammatory demyelinating polyneuropathy (CIDP), GBS, and inflammatory myopathies. The clinical efficacy of IVIg, based on controlled clinical trials conducted in patients with GBS, CIDP, multifocal motor neuropathy (MMN), DM, MG, LEMS, paraproteinemic IgM anti-myelin-associated glycoprotein (anti-MAG) demyelinating polyneuropathies, and inclusion body myositis is summarized and practical issues related to each disorder are addressed. The present role of IVIg therapy in other disorders based on small controlled or uncontrolled trials is also summarized. Finally, safety issues, risk factors, adverse reactions, spurious results or serological tests, and practical guidelines associated with the administration of IVIg in the treatment of neuromuscular disorders are presented. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 1479–1497, 1999 REFERENCES 1Abe Y, Horiuchi A, Miyake M, Kimura S. Anti-cytokine nature of natural human immunoglobulin: one possible mechanism of the clinical effect of intravenous immunoglobulin therapy. Immunol Rev 1994; 139: 5–19. 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