The pathophysiology of penicillamine‐induced myasthenia gravis
Identifieur interne : 002A95 ( Istex/Corpus ); précédent : 002A94; suivant : 002A96The pathophysiology of penicillamine‐induced myasthenia gravis
Auteurs : Ralph W. Kuncl ; Alan Pestronk ; Daniel B. Drachman ; Emanuel RechthandSource :
- Annals of Neurology [ 0364-5134 ] ; 1986-12.
English descriptors
- Teeft :
- Acetylcholine, Acetylcholine receptor, Acetylcholine receptors, Achr, Achr blockade, Achr degradation, Achr degradation rate, Achrs, Antibody titer, Autoimmune response, Autoimmune state, Available achrs, Binding sites, Biopsy, Bootstrap nonparametric method, Brain damage, Brief communication, Control cultures, Decremental responses, Degradation, Deltoid, Drachman, Dysregulatory state, Epileptic brain damage, Functional activities, Gravis, High antibody titer, Initial serum, Junctional, Junctional acetylcholine receptors, Junctional achrs, Magnetic resonance, Magnetic resonance imaging, Massachusetts institute, Muscle nerve, Myasthenia, Myasthenia gravis, Neurol, Neurology, Neuromuscular, Neuromuscular junction, Neuromuscular junctions, Normal number, Ongoing, Ongoing autoimmunity, Ongoing subclinical, Pars compacta, Pars compacta signal, Pars reticulata, Penicillamine, Penicillamine administration, Penicillamine myasthenia, Present patient, Receptor, Repetitive stimulation, Rheumatoid, Rheumatoid arthritis, Serial studies, Significant difference, Skeletal muscle, Status epilepticus, Systemic factors, Temporal course, Whitaker college.
Abstract
The temporal course and pathophysiology of penicillamine‐induced myasthenia gravis were studied in detail in a typical case. Our results suggest that this disorder and idiopathic autoimmune myasthenia gravis share the same essential pathophysiological features, including the presence of anti–acetylcholine receptor (AChR) antibody, serum‐induced blockade of AChRs, antibody‐mediated accelerated degradation of AChRs, and a resultant quantitative reduction in available junctional AChRs. An initial severe reduction in junctional AChRs was reversed and the patient recovered, both within 8 months of stopping penicillamine. Our data suggest that penicillamine probably produced myasthenia gravis by initiating a new autoimmune response rather than by enhancing ongoing autoimmunity.
Url:
DOI: 10.1002/ana.410200617
Links to Exploration step
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registered="yes">10.1002/ana.410200617</doi><idGroup><id type="unit" value="ANA410200617"></id></idGroup><countGroup><count type="pageTotal" number="5"></count></countGroup><titleGroup><title type="articleCategory">Brief Communication</title><title type="tocHeading1">Brief Communications</title></titleGroup><copyright ownership="thirdParty">Copyright © 1986 American Neurological Association</copyright><eventGroup><event type="manuscriptReceived" date="1985-12-02"></event><event type="manuscriptRevised" date="1986-05-02"></event><event type="manuscriptAccepted" date="1986-05-10"></event><event type="firstOnline" date="2004-10-08"></event><event type="publishedOnlineFinalForm" date="2004-10-08"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.4.7 mode:FullText source:HeaderRef result:HeaderRef" date="2011-02-24"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-03"></event><event type="xmlConverted" 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corresponding="yes"><personName><honorifics>Dr</honorifics><givenNames>Ralph W.</givenNames><familyName>Kuncl</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Alan</givenNames><familyName>Pestronk</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Daniel B.</givenNames><familyName>Drachman</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Emanuel</givenNames><familyName>Rechthand</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe St, Baltimore, MD 21205</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The temporal course and pathophysiology of penicillamine‐induced myasthenia gravis were studied in detail in a typical case. Our results suggest that this disorder and idiopathic autoimmune myasthenia gravis share the same essential pathophysiological features, including the presence of anti–acetylcholine receptor (AChR) antibody, serum‐induced blockade of AChRs, antibody‐mediated accelerated degradation of AChRs, and a resultant quantitative reduction in available junctional AChRs. An initial severe reduction in junctional AChRs was reversed and the patient recovered, both within 8 months of stopping penicillamine. Our data suggest that penicillamine probably produced myasthenia gravis by initiating a new autoimmune response rather than by enhancing ongoing autoimmunity.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The pathophysiology of penicillamine‐induced myasthenia gravis</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Penicillamine Myasthenia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The pathophysiology of penicillamine‐induced myasthenia gravis</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr</namePart><namePart type="given">Ralph W.</namePart><namePart type="family">Kuncl</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe St, Baltimore, MD 21205</affiliation><affiliation>Correspondence address: Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe St, Baltimore, MD 21205</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alan</namePart><namePart type="family">Pestronk</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe St, Baltimore, MD 21205</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Daniel B.</namePart><namePart type="family">Drachman</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe St, Baltimore, MD 21205</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Emanuel</namePart><namePart type="family">Rechthand</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe St, Baltimore, MD 21205</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="brief-communication" displayLabel="shortCommunication" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-S9SX2MFS-0">brief-communication</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1986-12</dateIssued><dateCaptured encoding="w3cdtf">1985-12-02</dateCaptured><dateValid encoding="w3cdtf">1986-05-10</dateValid><copyrightDate encoding="w3cdtf">1986</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">0</extent><extent unit="tables">3</extent><extent unit="references">18</extent></physicalDescription><abstract lang="en">The temporal course and pathophysiology of penicillamine‐induced myasthenia gravis were studied in detail in a typical case. Our results suggest that this disorder and idiopathic autoimmune myasthenia gravis share the same essential pathophysiological features, including the presence of anti–acetylcholine receptor (AChR) antibody, serum‐induced blockade of AChRs, antibody‐mediated accelerated degradation of AChRs, and a resultant quantitative reduction in available junctional AChRs. An initial severe reduction in junctional AChRs was reversed and the patient recovered, both within 8 months of stopping penicillamine. 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Patients with penicillamine‐induced myasthenia or idiopathic myasthenia of recent onset</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Vincent</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Newsom‐Davis</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Vincent A, Newsom‐Davis J: Acetylcholine receptor antibody characteristics in myasthenia gravis. II. Patients with penicillamine‐induced myasthenia or idiopathic myasthenia of recent onset. Clin Exp Immunol 49: 266–272, 1982</note><part><date>1982</date><detail type="volume"><caption>vol.</caption><number>49</number></detail><extent unit="pages"><start>266</start><end>272</end></extent></part><relatedItem type="host"><titleInfo><title>Clin Exp Immunol</title></titleInfo><part><date>1982</date><detail type="volume"><caption>vol.</caption><number>49</number></detail><extent unit="pages"><start>266</start><end>272</end></extent></part></relatedItem></relatedItem><identifier type="istex">749B964B372BA05951E3C9EC53F8B8076B1287BE</identifier><identifier type="ark">ark:/67375/WNG-T752TF25-K</identifier><identifier type="DOI">10.1002/ana.410200617</identifier><identifier type="ArticleID">ANA410200617</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1986 American Neurological Association</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Converted from (version ) to MODS version 3.6.</recordOrigin><recordCreationDate encoding="w3cdtf">2019-11-13</recordCreationDate></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-T752TF25-K/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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