Peripheral neuropathy associated with IgM monoclonal gammopathy: Correlations between M-protein antibody activity and clinical/electrophysiological features in 40 cases

Forty cases of polyneuropathy associated with IgM monoclonal gammopathy were retrospectively studied to investigate the relevance of clinical and electrophysiological features to M‐protein antibody activity. There were 26 men and 14 women; mean age was 65 ± 11.7 years at the time of the study. Thirt...

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Veröffentlicht in:Muscle & nerve 1998-01, Vol.21 (1), p.55-62
Hauptverfasser: Chassande, Bénédicte, Léger, Jean-Marc, Younes-Chennoufi, Amena Ben, Bengoufa, Djaouida, Maisonobe, Thierry, Bouche, Pierre, Baumann, Nicole
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container_title Muscle & nerve
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creator Chassande, Bénédicte
Léger, Jean-Marc
Younes-Chennoufi, Amena Ben
Bengoufa, Djaouida
Maisonobe, Thierry
Bouche, Pierre
Baumann, Nicole
description Forty cases of polyneuropathy associated with IgM monoclonal gammopathy were retrospectively studied to investigate the relevance of clinical and electrophysiological features to M‐protein antibody activity. There were 26 men and 14 women; mean age was 65 ± 11.7 years at the time of the study. Thirty‐nine patients had a symmetrical polyneuropathy, of whom 13 had a predominantly sensory and 17 a purely sensory neuropathy (i.e., 30 sensory neuropathies). The remaining patient had a multifocal mononeuropathy. Electrophysiological studies allowed the polyneuropathies to be classified as demyelinating in 33 cases (82.5%) and axonal in 6 cases. Antibody studies disclosed anti‐MAG antibodies in 65% and anti‐SGPG antibodies in 82.5% of patients. Anti‐MAG antibodies were associated with only demyelinating polyneuropathies. Anti‐SGPG antibodies were found in 91% of demyelinating polyneuropathies and 50% of axonopathies. In addition, anti‐MAG/SGPG antibody activity was significantly correlated with the subgroup of sensory neuropathies (P < 0.01). Last, antisulfatide antibodies were found at significant titers in 18 cases, and their presence was significantly correlated with anti‐MAG/SGPG antibody activity, but not with some clinical/electrophysiological features. © 1998 John Wiley & Sons, Inc. Muscle Nerve, 21: 55–62, 1998.
doi_str_mv 10.1002/(SICI)1097-4598(199801)21:1<55::AID-MUS8>3.0.CO;2-F
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Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction</topic><topic>Disease Progression</topic><topic>Electromyography</topic><topic>Electrophysiology - methods</topic><topic>Female</topic><topic>Humans</topic><topic>Immunoglobulin M</topic><topic>M-protein</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Muscle Proteins</topic><topic>Myelin-Associated Glycoprotein - immunology</topic><topic>Myeloma Proteins - immunology</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neural Conduction</topic><topic>Neurology</topic><topic>Paraproteinemias - complications</topic><topic>Paraproteinemias - immunology</topic><topic>Paraproteinemias - physiopathology</topic><topic>Paresthesia - etiology</topic><topic>Paresthesia - physiopathology</topic><topic>Patient Selection</topic><topic>Peripheral Nervous System Diseases - etiology</topic><topic>Peripheral Nervous System Diseases - immunology</topic><topic>Peripheral Nervous System Diseases - physiopathology</topic><topic>Recurrence</topic><topic>Retrospective Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chassande, Bénédicte</creatorcontrib><creatorcontrib>Léger, Jean-Marc</creatorcontrib><creatorcontrib>Younes-Chennoufi, Amena Ben</creatorcontrib><creatorcontrib>Bengoufa, Djaouida</creatorcontrib><creatorcontrib>Maisonobe, Thierry</creatorcontrib><creatorcontrib>Bouche, Pierre</creatorcontrib><creatorcontrib>Baumann, Nicole</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Muscle &amp; nerve</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chassande, Bénédicte</au><au>Léger, Jean-Marc</au><au>Younes-Chennoufi, Amena Ben</au><au>Bengoufa, Djaouida</au><au>Maisonobe, Thierry</au><au>Bouche, Pierre</au><au>Baumann, Nicole</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peripheral neuropathy associated with IgM monoclonal gammopathy: Correlations between M-protein antibody activity and clinical/electrophysiological features in 40 cases</atitle><jtitle>Muscle &amp; nerve</jtitle><addtitle>Muscle Nerve</addtitle><date>1998-01</date><risdate>1998</risdate><volume>21</volume><issue>1</issue><spage>55</spage><epage>62</epage><pages>55-62</pages><issn>0148-639X</issn><eissn>1097-4598</eissn><coden>MUNEDE</coden><abstract>Forty cases of polyneuropathy associated with IgM monoclonal gammopathy were retrospectively studied to investigate the relevance of clinical and electrophysiological features to M‐protein antibody activity. There were 26 men and 14 women; mean age was 65 ± 11.7 years at the time of the study. Thirty‐nine patients had a symmetrical polyneuropathy, of whom 13 had a predominantly sensory and 17 a purely sensory neuropathy (i.e., 30 sensory neuropathies). The remaining patient had a multifocal mononeuropathy. Electrophysiological studies allowed the polyneuropathies to be classified as demyelinating in 33 cases (82.5%) and axonal in 6 cases. Antibody studies disclosed anti‐MAG antibodies in 65% and anti‐SGPG antibodies in 82.5% of patients. Anti‐MAG antibodies were associated with only demyelinating polyneuropathies. Anti‐SGPG antibodies were found in 91% of demyelinating polyneuropathies and 50% of axonopathies. In addition, anti‐MAG/SGPG antibody activity was significantly correlated with the subgroup of sensory neuropathies (P &lt; 0.01). Last, antisulfatide antibodies were found at significant titers in 18 cases, and their presence was significantly correlated with anti‐MAG/SGPG antibody activity, but not with some clinical/electrophysiological features. © 1998 John Wiley &amp; Sons, Inc. Muscle Nerve, 21: 55–62, 1998.</abstract><cop>New York</cop><pub>John Wiley &amp; Sons, Inc</pub><pmid>9427224</pmid><doi>10.1002/(SICI)1097-4598(199801)21:1&lt;55::AID-MUS8&gt;3.0.CO;2-F</doi><tpages>8</tpages></addata></record>
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subjects Adult
Aged
Aged, 80 and over
Analysis of Variance
anti-MAG
antibodies
antisulfatide antibodies
Autoantibodies - blood
Axons - physiology
Biological and medical sciences
Connectin
Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction
Disease Progression
Electromyography
Electrophysiology - methods
Female
Humans
Immunoglobulin M
M-protein
Male
Medical sciences
Middle Aged
Muscle Proteins
Myelin-Associated Glycoprotein - immunology
Myeloma Proteins - immunology
Nervous system (semeiology, syndromes)
Neural Conduction
Neurology
Paraproteinemias - complications
Paraproteinemias - immunology
Paraproteinemias - physiopathology
Paresthesia - etiology
Paresthesia - physiopathology
Patient Selection
Peripheral Nervous System Diseases - etiology
Peripheral Nervous System Diseases - immunology
Peripheral Nervous System Diseases - physiopathology
Recurrence
Retrospective Studies
title Peripheral neuropathy associated with IgM monoclonal gammopathy: Correlations between M-protein antibody activity and clinical/electrophysiological features in 40 cases
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